title: The pathogenesis, treatment and prevention of osteoporosis in men.
abstract: Testosterone stimulates longitudinal and appositional growth during childhood, whereas estrogen induces epiphysial closure. During adulthood, testosterone continues to stimulate periosteal growth, whereas estrogen is important for the maintenance of trabecular bone mass and structure. In males, testosterone is aromatized to estradiol. Both free and bioavailable plasma levels of testosterone and estradiol decrease with age in males, and fracture risk is associated with low estradiol levels. Testosterone may increase muscle mass and prevent fractures related to falls. Younger hypogonadal males should be treated with testosterone to attain peak bone mass and increase bone mineral density (BMD). Older hypogonadal males should be treated in cases of osteoporosis, reduced muscle strength and increased risk of falling. Secondary hyperparathyroidism caused by calcium and vitamin D insufficiency may reduce bone mass and strength and increase fracture risk and should be avoided. Since calcium supplementation has been associated with an increased risk of cardiovascular complications and renal stones, the dose should be tailored to the habitual daily calcium intake. Lifestyle-related risk factors (smoking, alcohol consumption, lack of physical activity and low body weight) should be addressed. The antifracture efficacy of antiresorptive and anabolic treatment for osteoporosis has not been documented in larger randomized controlled studies. However, changes in BMD and bone markers suggest similar effects in males and females of bisphosphonates (alendronate, risedronate, ibandronate, zoledronic acid), nasal calcitonin, denosumab and teriparatide (parathyroid hormone [1-34]). The antiresorptive drugs should be used in males with BMD T-score less than -2.5 and one or more risk factors, or with hip and vertebral fractures. It seems appropriate to recommend a higher cut-off T-score (e.g. less than -1.0 standard deviation [SD]) in glucocorticoid-induced osteoporosis and in patients receiving androgen deprivation therapy because of the fast initial bone loss. Anabolic treatment should be used in more severe spinal fracture cases, including glucocorticoid-induced osteoporosis.
authors: Faculty of Health Science, Aarhus University, Denmark. leimos@rm.dk
authors: Leif
authors: L
authors: Mosekilde
authors: Peter
authors: P
authors: Vestergaard
authors: Lars
authors: L
authors: Rejnmark
mesh_terms: D000367:Age Factors; D015519:Bone Density / Q000502:physiology; D050071:Bone Density Conservation Agents / Q000627:therapeutic use; D004967:Estrogens / Q000627:therapeutic use; D005260:Female; D050723:Fractures, Bone / Q000517:prevention & control; D006801:Humans; D008297:Male; D010024:Osteoporosis / Q000188:drug therapy / Q000209:etiology / Q000517:prevention & control; D012307:Risk Factors; D013739:Testosterone / Q000627:therapeutic use; D013997:Time Factors
chemical_list: D050071:Bone Density Conservation Agents; D004967:Estrogens; D013739:Testosterone