Male osteoporosis is a significant clinical problem that is often not diagnosed until patients suffer a fragility fracture. Approximately 20% of the 44 million Americans with osteoporosis (defined as a DXA bone mineral density T-score below 2.5) are men (1). However, men disproportionately account for 30-40% of the osteoporotic fractures (1-2). In addition, mortality rates in men with hip fractures are two to three times greater than in women (3) and this difference increases with age (2). Hence, improvements in the diagnosis and treatment of men at high risk for osteoporosis would significantly improve both their quality of life and overall healthcare costs.
The risk factors for the development osteoporotic fragility fractures in males include: age, race, bone mineral density, alcohol consumption, smoking, corticosteroid use, a history of a prior fragility fracture within the past year, a family history of fragility fractures, a history of a fall within the past year and hypogonadism. Both the Endocrine Society and the National Osteoporosis Foundation recommend that all men over 70 undergo screening for osteoporosis by DXA (4-5). This is because epidemiologic data clearly demonstrates that the overall risk of a fragility fracture in men is significantly increased after this age (6). In addition, DXA screening should be performed on younger men if additional risk factors are present.
As in any patient being evaluated for osteoporosis, a careful history and physical are essential. In addition, serum 25 OH vitamin D levels and screening studies to rule out undiagnosed hyperparathyroidism or hematologic malignancy should be performed.
Approved pharmacologic therapies for male osteoporosis include a number of the available bisphosphonates, as well as denosumab and teriparatide. It is also interesting to speculate about the potential role of a selective estrogen receptor modulator (SERM) in male osteoporosis (7). In both men and women estrogens mediate the majority of the effects of sex steroids on bone mass (7). In males, aromatization of androgens to estrogens is critical since men who lack the enzyme for this conversion have a syndrome of low bone mass that is responsive to estrogen therapy (8). Hence, SERMs, which selectively mimic the effects of estrogen on bone but not on some other tissues, may have utility for the treatment of male osteoporosis. However, currently, no SERM is approved for this condition.
The use of androgens for treating male osteoporosis is more controversial. Profound hypogonadism produces significant symptoms. Therefore, androgen replacement therapy is indicated for this condition. However, testosterone levels in men generally decrease with age and there have been inconsistent effects on bone mass of androgen replacement therapy in an elderly population with mild androgen deficiency (7).
In summary, male osteoporosis is a condition that health care providers should be more aware of since early intervention in appropriate high-risk individuals can significantly decrease fracture rates, improve patients’ quality of life and lower overall health care costs.
Farmington, CT, USA
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