10 20 30 40 FRAX (osteoporosis) without BMD (%) 50 Non-African-American African-American (a) 10 20 30 FRAX (Hip) without BMD (%) 40 Non-African-American African-American (b) Figure 1 so the predictive ability of FRAX scores with or without BMD, for hip versus osteoporotic, and across ethnic groups could be analyzed. Our study demonstrated that discovery of incidental vertebral fractures on routine spine ﬁlms increased the predictive ability for vertebral fracture of all types of FRAX scores. Another novel ﬁnding was that vertebral fracture in men with prostate cancer was better Journal of Osteoporosis 5 50 ) 40 % ( D M B ith 30 w ) s i s o r o eop 20 t s o ( X A FR10 0 0 40 30 ) % ( D M B h itw 20 ) p i H ( X A R F 10 0 0 2 1.8 1.6 2) 1.4 m c /m1.2 g (D 1 eBM0.8 n iSp0.6 0.4 0.2 0 0 2 4 10 20 40 60 80 6 8 PSA (ng/mL) Non-African-American African-American Figure 2 predicted by osteoporotic FRAX than hip FRAX. The FRAX score (without knowledge of spine fractures) calculated with BMD underestimated therapeutic threshold in nine men with previously unknown spine fractures in our study. As a result we feel that most men with prostate cancer on ADT, and with any height loss, should have spine X-rays taken to estimate their future fracture risk accurately. It should be mentioned that hypogonadism is one of the “secondary causes” in the FRAX calculator but does not change the FRAX score if and when BMD of the femoral neck is used in calculation. We believe that patients with prostate cancer on ADT may be diﬀerent from “typical” patients with hypogonadism. It is well known that patients with prostate cancer on ADT have mostly undetectable levels of testosterone and as the result have low estradiol levels. Both testosterone and estradiol are imperative in preserving bone density, quality, and in predicting the risk of future fractures. Moreover, the eﬀects of ADT on BMD and fracture risk persist for years after ADT is completed [6]. The positive correlation of age and spine BMD may be an artifact of falsely elevated BMD in lumbar spine due to vertebral body degeneration since the group with- out vertebral fractures had lower spine T scores (higher spine BMD) than the group with vertebral fractures. The signiﬁcance of the positive correlation of PSA level and lumbar spine BMD is unclear. PSA accounted for 9% of the variability in lumbar BMD. The mechanism by which PSA aﬀects bone metabolism is not clearly deﬁned, but it seems to regulate the biologic activity of parathyroid- hormone-related protein (PTHrP). PSA speciﬁcally cleaves PTHrP, which subsequently eliminates the ability of PTHrP to stimulate cAMP production [14]. Moreover, PSA appears to promote osteoblast diﬀerentiation via transcription factor Cbfa1 [15]. PSA prevents bone resorption by inducing osteo- protegerin activity and inhibiting the receptor activator of nuclear factor-kB ligand (RANKL) expression on osteoblasts