Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/10624
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dc.contributor.authorSeeman, Egoen
dc.date.accessioned2015-05-16T00:08:26Z-
dc.date.available2015-05-16T00:08:26Z-
dc.date.issued2008-07-01en
dc.identifier.citationRheumatology (oxford, England); 47 Suppl 4(): iv2-8en
dc.identifier.govdoc18556646en
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/10624en
dc.description.abstractIf bone strength was the only requirement of skeleton, it could be achieved with bulk, but bone must also be light. During growth, bone modelling and remodelling optimize strength, by depositing bone where it is needed, and minimize mass, by removing it from where it is not. The population variance in bone traits is established before puberty and the position of an individual's bone size and mass tracks in the percentile of origin. Larger cross-sections have a comparably larger marrow cavity, which results in a lower volumetric BMD (vBMD), thereby avoiding bulk. Excavation of a marrow cavity thus minimizes mass and shifts the cortex radially, increasing rigidity. Smaller cross-sections are assembled by excavating a smaller marrow cavity leaving a relatively thicker cortex producing a higher vBMD, avoiding the fragility of slenderness. Variation in cellular activity around the periosteal and endocortical envelopes fashions the diverse shapes of adjacent cross-sections. Advancing age is associated with a decline in periosteal bone formation, a decline in the volume of bone formed by each basic multicellular unit (BMU), continued resorption by each BMU, and high remodelling after menopause. Bone loss in young adulthood has modest structural and biomechanical consequences because the negative BMU balance is driven by reduced bone formation, remodelling is slow and periosteal apposition continues shifting the thinned cortex radially. But after the menopause, increased remodelling, worsening negative BMU balance and a decline in periosteal apposition accelerate cortical thinning and porosity, trabecular thinning and loss of connectivity. Interstitial bone, unexposed to surface remodelling becomes more densely mineralized, has few osteocytes and greater collagen cross-linking, and accumulates microdamage. These changes produce the material and structural abnormalities responsible for bone fragility.en
dc.language.isoenen
dc.subject.otherAgeingen
dc.subject.otherBoneen
dc.subject.otherFragilityen
dc.subject.otherGrowthen
dc.subject.otherModellingen
dc.subject.otherRemodellingen
dc.subject.otherStrengthen
dc.subject.otherAdolescenten
dc.subject.otherAdulten
dc.subject.otherAgeden
dc.subject.otherBone Densityen
dc.subject.otherBone Development.physiologyen
dc.subject.otherBone Remodeling.physiologyen
dc.subject.otherBone and Bones.physiopathologyen
dc.subject.otherChilden
dc.subject.otherChild, Preschoolen
dc.subject.otherFemaleen
dc.subject.otherHumansen
dc.subject.otherInfanten
dc.subject.otherMaleen
dc.subject.otherMiddle Ageden
dc.subject.otherOsteoporosis.physiopathologyen
dc.subject.otherSex Factorsen
dc.titleStructural basis of growth-related gain and age-related loss of bone strength.en
dc.typeJournal Articleen
dc.identifier.journaltitleRheumatology (Oxford, England)en
dc.identifier.affiliationDepartment of Endocrinology and Medicine, Austin Health, University ofMelbourne, Melbourne, Australiaen
dc.identifier.doi10.1093/rheumatology/ken177en
dc.description.pagesiv2-8en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/18556646en
dc.type.austinJournal Articleen
local.name.researcherSeeman, Ego
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.fulltextNo Fulltext-
item.grantfulltextnone-
item.languageiso639-1en-
item.openairetypeJournal Article-
crisitem.author.deptEndocrinology-
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