Bone Abstracts

There is increasing evidence for the key role of osteocytes in the regulation of bone remodeling. One of the main products of these cells, sclerostin, inhibits bone formation and may also stimulate bone resorption. To our knowledge, there are few data in prostate cancer (PC) patients especially in patients with hypogonadism related to androgen deprivation therapy (ADT). The aim of this study was to compare serum levels of sclerostin in ADT-treated and untreated PC patients with healthy controls, and to evaluate their relationship with sex steroids and bone metabolism. Our study was a cross-sectional one including 81 subjects: 25 patients with PC treated with ADT, 34 PC patients without ADT treatment, and 22 healthy controls. We measured serum sclerostin concentrations, bone turnover markers and BMD in all subjects, and also sex steroids levels in PC patients. PC patients had increased serum sclerostin compared to control subjects. ADT treated patients had significantly higher sclerostin levels than PC patients without treatment: ADT: 64.52±27.21 pmol/l; non ADT: 48.24±15.93 pmol/l; healthy controls: 38.48±9.19 pmol/l, P<0.05 for all comparisons. In PC patients, there was an inverse relationship between serum sclerostin levels and androgens after age-adjustment (total testosterone: r=−0.309, P=0.029; bioavailable testosterone: r=−0.280, P=0.049; free testosterone: r=−0.299, P=0.035). In addition, we observed a positive association between sclerostin and estradiol/testosterone ratio (total: r=0.470, P=, bioavailable: r=0.524 and free: r=0.523; P<0.001). Serum sclerostin were not related to bone turnover markers or BMD in any group.

In conclusion, circulating sclerostin levels are significantly increased in patients with prostate cancer and particularly in those with androgen deprivation therapy. The inverse relationship between serum sclerostin and testosterone in these patients suggests that androgens are key regulators of bone metabolism in this population.