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dc.contributor.authorSeeman, Egoen
dc.identifier.citationBaillie`re's Clinical Rheumatology; 11(3): 613-29en
dc.description.abstractHip fractures in men account for one third of all hip fractures and have a higher mortality than in women. The public health burden will increase as the increase in the numbers of elderly men in the community increases. In addition, the age-specific incidence of hip fractures may be increasing in some, but not all, countries. Vertebral fractures may be a public health problem as recent studies suggest that the prevalence in the community is 20-30%, similar to that reported in women. Forearm fractures should probably not be regarded as a public health problem. Peak bone mass is higher in men than women because men have bigger bones. Peak bone mineral density is the same. The amount of trabecular bone lost at the spine and iliac crest during ageing is similar in men and women. Cortical bone loss is less in men because endocortical resorption is less and periosteal formation is greater. Bone loss accelerates in elderly men because endocortical resorption and increasing cortical porosity increase the surface available for resorption. Bone fragility is less in men than women because: (a) the cross-sectional surface of the bone is larger; (b) trabecular bone loss is less as a percentage of the higher peak bone mass; (c) trabecular bone loss occurs by thinning rather than perforation; and (d) periosteal appositional growth compensates for endocortical resorption by maintaining the bending strength of bone. Reduced BMD in men with fractures may be due to reduced peak bone size and mass, and bone loss. Bone loss occurs by reduced bone formation. Whether men with fractures have increased bone fragility due to reduced periosteal appositional growth during ageing is unknown. The age-related decline in testosterone, adrenal androgens, growth hormone, and insulin-like growth factor 1 may contribute to reduced bone formation and bone loss. Men with vertebral fractures often have hypogonadism or illnesses with few clinical features that should be considered with a high index of suspicion (alcoholism, myeloma, malabsorption, primary hyperparathyroidism, haemochromatosis, Cushing's disease). Secondary hyperparathyroidism may contribute to bone loss by activating bone turnover and so increasing the number of bone remodelling units with impaired bone formation in each. There is no proven treatment for osteoporosis in men because there have been no trials using anti-fracture efficacy as an end point. Testosterone replacement should be considered in men with proven hypogonadism and vitamin D deficiency should be corrected if present. Calcium supplements and bisphosphonates are reasonable options given the lack of information.en
dc.subject.otherAccidental Fallsen
dc.subject.otherAged, 80 and overen
dc.subject.otherBone Density.physiologyen
dc.subject.otherBone Development.physiologyen
dc.subject.otherBone Resorption.physiopathologyen
dc.subject.otherFractures, Bone.etiology.pathology.prevention & controlen
dc.subject.otherOsteoporosis.etiology.pathology.prevention & controlen
dc.titleOsteoporosis in men.en
dc.typeJournal Articleen
dc.identifier.journaltitleBaillière's clinical rheumatologyen
dc.identifier.affiliationDepartment of Endocrinology, Austin and Repatriation Medical Centre, University of Melbourne, Heidelberg, Australiaen
dc.type.austinJournal Articleen, Ego
item.openairetypeJournal Article-
item.fulltextNo Fulltext-
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