Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/13239
Full metadata record
DC FieldValueLanguage
dc.contributor.authorSeeman, Egoen
dc.date.accessioned2015-05-16T03:03:26Z
dc.date.available2015-05-16T03:03:26Z
dc.date.issued1994-05-16en
dc.identifier.citationOsteoporosis International : A Journal Established As Result of Cooperation Between the European Foundation For Osteoporosis and the National Osteoporosis Foundation of The Usa; 4 Suppl 1(): 15-25en
dc.identifier.govdoc8081052en
dc.identifier.otherPUBMEDen
dc.identifier.urihttp://ahro.austin.org.au/austinjspui/handle/1/13239en
dc.description.abstractOsteoporosis is regarded as a disease of the elderly because fractures occur late in life. Although excessive bone loss during aging is likely to contribute to the deficit in bone density, patients with fractures do not consistently have more rapid bone loss, greater bone resorption or lower bone formation (measured using biochemical or histomorphometric markers of bone turnover). The pathogenesis of the low bone density and bone fragility that characterize osteoporosis may begin during the first two decades of life. There are differences in the hormonal regulation of regional growth and mineral accrual, differences in the age of onset, rate and duration of linear growth and mineral accrual of the axial and appendicular skeleton, of cortical and trabecular bone, and of proximal and distal limb segments. Illnesses, risk or protective factors, and disorders of hormonal deficiency or excess may affect longitudinal growth, mineral accrual, or both, depending on the timing of exposure. Quantitatively larger and qualitatively different effects on bone density may result when exposure occurs during growth rather than during adulthood. The magnitude of these deficits and their location are likely to establish the relevance of regional age-related and sex hormone dependent bone loss. Thus, any unifying hypothesis concerning the epidemiology and pathogenesis of osteoporosis must consider the relative contributions of low peak bone density and bone loss to the deficit in bone density in adulthood. A great deal of research is needed to examine the physiology of longitudinal growth and mineral accrual as the pathogenesis of osteoporosis is at least partly explained by events occurring during the first 20 years of life.en
dc.language.isoenen
dc.subject.otherAge Factorsen
dc.subject.otherAgeden
dc.subject.otherAging.physiologyen
dc.subject.otherBone Density.physiologyen
dc.subject.otherCalcification, Physiologic.physiologyen
dc.subject.otherFemaleen
dc.subject.otherFractures, Bone.epidemiology.physiopathologyen
dc.subject.otherHip Fractures.epidemiology.physiopathologyen
dc.subject.otherHumansen
dc.subject.otherMaleen
dc.subject.otherMiddle Ageden
dc.subject.otherOsteoporosis.epidemiology.physiopathologyen
dc.subject.otherRisk Factorsen
dc.subject.otherSex Factorsen
dc.subject.otherSpinal Fractures.epidemiology.physiopathologyen
dc.titleReduced bone density in women with fractures: contribution of low peak bone density and rapid bone loss.en
dc.typeJournal Articleen
dc.identifier.journaltitleOsteoporosis Internationalen
dc.identifier.affiliationDepartment of Medicine, Austin Hospital, University of Melbourne.en
dc.description.pages15-25en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/8081052en
dc.type.austinJournal Articleen
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.fulltextNo Fulltext-
item.cerifentitytypePublications-
item.grantfulltextnone-
item.languageiso639-1en-
item.openairetypeJournal Article-
crisitem.author.deptEndocrinology-
Appears in Collections:Journal articles
Show simple item record

Page view(s)

4
checked on Feb 5, 2023

Google ScholarTM

Check


Items in AHRO are protected by copyright, with all rights reserved, unless otherwise indicated.