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Although fragility fractures are less common in men than in women, when they occur, these fractures are associated with higher morbidity and death during one year after fracture.Overall, one in five men over the age of 50 will have an osteoporosis related fracture in their remaining lifetime.Each year, about 80,000 men will break a hip in United States and many more worldwide.While men share certain traditional risk factors of osteoporosis with women, they are also subject to unique factors that contribute to their bone loss.First, there is clear evidence that declining levels of bioavailable estrogen level with age contribute to bone loss and fracture risk in men.Studies have shown that estrogen plays an important, and likely dominant, role in regulating bone mineral density (BMD) and bone resorption in men.There seems to be a threshold serum estradiol level below which the male skeleton becomes estrogen deficient.In recent and largest study, following 2,639 men for longer then three years and after multivariable proportional hazards regression analysis, free estradiol, but not free testosterone,were independently associated with fracture risk.In men with prostate cancer and on gonadotropin releasing hormone (GnRH) agonists, total and free testosterone/estradiol levels are profoundly supressed, causing rapid decline in BMD and increased fracture risk.From Medicare data base study risk of hip, spine and any fractures were increased by 46%, 63% and 25%, respectively.This is a group of men we should pay more attention to.Second group of men are ones with prostate hyperplasia on 5-reductase inhibitors.Prostatic hyperplasia is common, affecting 40% to 50% of men aged 51 to 60 and more than 80% of men older than 80 years.When men are treated with finasteride or dutasteride, plasma dihydrotestosterone (DHT) levels decline by 60%-95% and testosterone levels increase by 15-22% as well as estradiol level.Markers of bone turnover and bone mineral density do not change with the use of these agents, and use of finasteride is not associated with increased fracture risk suggesting that DHT by itself has little effect on bone or that increased levels of testosterone and estradiol negate profound decline of DHT caused by this group of drugs.Third group are men on testosterone replacement therapy.In the Massachusettss male aging study, 20% of men were found to be biochemically hypogonadal by age 60.Hypogonadism has driven a marked increase in the use of testosterone replacement with prescriptions increasing from 692 000 in 2000 to 2.66 million in 2008.Testosterone replacement in most short term studies have produced increased bone mineral density, yet no fracture data is available.More gain of BMD is reached in men with lowest testosterone levels.Because skin expresses high 5-reductase activity, testosterone gel applied on skin achieves much higher DHT levels than a comparable dose of testosterone enanthate, yet it remains unclear if that has any influence on BMD.Replacement with non-aromatizable and rogen DHT in hypogonadal men,caused reduction of spinal bone mineral density, likely due to decrease in estradiol level.In one study increase in BMD was similar in group of men treated with alendronate and testosterone.In our discussion we also will review studies currently underway in men with use of denosumab and odanacatib.