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Full length article| Volume 98, ISSUE 2, SUPPLEMENT 1, 76S-88S, February 27, 1995

The dilemma of osteoporosis in men

  • Ego Seeman
    Correspondence
    Requests for reprints should be addressed to Ego Seeman, M.D., University of Melbourne, Austin Hospital, Heidelberg, 3084, Melbourne, Australia.
    Affiliations
    Austin Hospital, University of Melbourne, Melbourne, Australia
    Search for articles by this author
DOI:https://doi.org/10.1016/S0002-9343(05)80082-8
The dilemma of osteoporosis in men
Previous ArticleWhy elderly women should be screened and treated to prevent osteoporosis
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      Abstract

      Hip fractures in men account for one third of all hip fractures and have a higher mortality than in women. The age-specific incidence of hip fractures is increasing so that the public health burden will increase out of proportion to the burden imposed by the increase in the numbers of elderly men in the community. Vertebral fractures are a public health problem of lesser magnitude in terms of morbidity, mortality, and cost, but they are debilitating and are seen commonly in clinical practice. (Forearm fractures should probably not be regarded as a public health problem.) The pattern of earlier gain/later loss of bone during ageing in healthy men is well documented. Peak bone mass is higher in men than women because men have bigger bones. Peak bone density is the same. The absolute 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. It is less because endocortical resorption is less, and periosteal formation is greater, in men. Bone loss may accelerate in elderly men and women (rather than decelerate), perhaps because endocortical resorption and increasing cortical porosity increase the effective surface available for resorption in cortical bone. Thus, bone fragility is less in men because (a) the cross-sectional surface of the vertebral body 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 bone density in men with fractures may be due to reduced peak bone density and bone loss. As found in women with spine fractures, men with fractures have smaller bone size. Bone loss occurs by reduced bone formation and increased bone resorption. Loss of connectivity appears to predominate in men with vertebral fractures; trabecular thinning appears to predominate in men with hip fractures. 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 insulinlike growth factor 1 may be concomitants of ageing or may contribute to reduced bone formation and bone loss. Men with vertebral fractures may be more deficient in growth hormone and insulin-like growth factor 1. They often have illness, hypogonadism, or illnesses associated with hypogonadism that should be sought with a high index of suspicion. Secondary hyperparathyroidism may contribute to bone loss by activating bone turnover and so increasing the number of bone remodeling units with impaired bone formation. There is no known treatment for osteoporosis in men because there have been no trials using antifracture efficacy as an endpoint and few using other endpoints. Decisions are based on studies in women; on endpoints such as bone densitometry, markers of bone turnover, and histomorphometry; and on studies in animal models of osteoporosis.
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        (Suppl 1)in: Sixteenth Annual Meeting of the American Society for Bone and Mineral Research. J Bone Min Res. 9. 1994: S267-s2

      Article Info

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      DOI: https://doi.org/10.1016/S0002-9343(05)80082-8

      Copyright

      © 1995 Reed Publishing USA. Published by Elsevier Inc.

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