**2. Diagnosis of osteoporosis in men**

Bone mineral density (BMD) is considered to be the gold standard for diagnosing and assessing the severity of osteoporosis and fracture risk in women. The role of BMD in men is less clear. BMD is measured most commonly by dual-energy X-ray absorptiometry (DXA), but quantitative computed tomography (QCT) of the lumbar spine also is used, particularly in research studies (Faulkner KG et al., 1998).

BMD of the wrist and hip, after adjusting for age, is a strong predictor of fracture risk (Melton L et al., 1998). Although the BMD criteria for diagnosing osteoporosis in men remain controversial (Binkley NC et al., 2002), a definition based on World Health Organization recommendations is accepted currently.

According to definition, osteoporosis exists when the BMD value is > 2.5 standard deviations (SD) below the peak young normal mean reference range (T-score < 2.5). Accurate T-score calculations in individual men can be obtained from bone densitometers using standardized software derived from reference databases for 'healthy' Caucasian men ages 20–40 years. In elderly men, it has been reported that advanced spondyloarthropathy, facet joint disease, and aortic calcification elevate spinal BMD falsely, as assessed by DXA (Zmuda JM et al., 2000)). Spinal BMD of the second through fourth lumbar vertebrae should be measured routinely to diagnose osteoporosis. Interpretation of the results often requires the addition of spinal radiographs to improve diagnostic accuracy. QCT of the lumbar spine, using the new three-dimensional multislice scanners, may overcome this problem, but it is not available at many centers; this technique has the ability to accurately define a region of interest unconfounded by extravertebral calcification (Faulkner KG et al., 1998; Weigert JM & Cann CE, 1988). Femoral neck DXA in elderly men, for practical purposes, is used routinely for the diagnosis of osteoporosis, especially if spinal BMD is pseudoelevated. Both spinal BMD and total hip BMD are the preferred sites for monitoring changes in BMD in response to therapies (Kaufman JM et al., 2000; Lenchik L et al., 2002). In a recent study, the relative risk of hip fracture in men was 3.0 (range, 1.7–5.4) for each SD decrease in femoral neck BMD (Delaet C et al., 1998). Longitudinal studies suggest that the rate of lumbar spine bone loss in elderly men is approximately 5–10% per decade, with acceleration after age 75 years. Femoral neck bone loss in normal elderly men is estimated at approximately 0.7% per year (Jones G et al., 2004). A number of factors may increase the bone loss normally associated with aging. These include physical immobility, poor nutrition, reduced calcium dietary intake and intestinal absorption, vitamin D deficiency, increased cytokines, reduced growth factors and osteoblastic activity, and a gradual decline in gonadal androgen production (Kaufman JM et al., 2000). Accelerated bone loss similar to that seen in women undergoing bilateral oophorectomy has been demonstrated in men with hypogonadism who undergo gonadectomy (Daniell HW, 1997) or who receive ADT (Bruder JM & Welch MD, 2002; Yaturu S et al., 2002). In male sex offenders who underwent surgical castration, spinal bone loss occurred at a rate of 4% per year (Stepan JJ et al., 1999). Because these rates of loss are higher compared with the rates of loss observed in otherwise healthy elderly men, the abrupt loss of sex steroids appears to initiate a period of rapid bone loss.
