Treatment Of Osteoporosis In Men Research Articles

Therapeutic role of androgens in the treatment of osteoporosis in men

There has been much recent interest in the relationship between androgens and bone mineralization in men. Increases in serum androgens during puberty allow for skeletal maturation and the attainment of peak bone mass, and the persistence of normal testosterone secretion during adulthood is important for the maintenance of bone density. Testosterone deficiency is associated with heightened bone turnover and is a major risk factor for osteoporosis in men. The administration of testosterone to androgen-deficient men leads to an increase in bone mass, particularly in the trabecular bone compartment, and a reduction in levels of surrogate markers of bone turnover, suggesting that androgens have a dampening effect on bone remodelling. In addition, the administration of androgens to eugonadal men with idiopathic osteoporosis, with resulting supraphysiological testosterone concentrations, may lead to increases in bone mineral density. The risk of osteopenia due to androgen deficiency and the benefits of testosterone substitution therapy or supraphysiological administration on bone will be reviewed.

9 Osteoporosis in men

Hip 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.

The dilemma of osteoporosis in men

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.