Role of sex steroids hormones in the regulation of bone metabolism in men: Evidence from clinical studies

Abstract

Sex steroids regulate bone metabolism in young men during growth and consolidation. Their deficit during growth compromises longitudinal and radial growth of bones and has a negative impact on body height, bone width, peak areal bone mineral density (aBMD) and bone microarchitecture. In older men, the deficit of sex steroid hormones (mainly 17β-oestradiol) contributes to high bone turnover rate, low aBMD, poor bone microarchitecture, low estimated bone strength, accelerated bone loss and rapid decline of bone microarchitecture. The role of 17β-oestradiol is confirmed by the case of men with congenital oestrogen receptor deficit and with congenital aromatase deficiency. 17β-oestradiol inhibits bone resoption, whereas both hormones regulate bone formation. However, the associations are weak. Prospective data on the utility of blood 17β-oestradiol or testosterone for fracture risk assessment are inconsistent. Men with hypogonadism have decreased aBMD and poor bone microarchitecture. In men with hypogonadism, testosterone replacement therapy increases aBMD and improves bone microarchitecture. In men with prostate cancer, androgen deprivation therapy (gonadoliberin analogues) induces rapid bone loss and severe deterioration of bone microarchitecture.

Keywords: 17β-oestradiol; bone microarchitecture; bone mineral density; bone turnover markers; men; testosterone.