Androgen receptors are present at low densities in osteoblasts. Androg
ens are also metabolized in bone. (Non)aromatizable androgens probably
induce proliferation of osteoblasts and differentiation. A direct eff
ect of androgens on osteoclasts has not been demonstrated. Androgens m
ay however inhibit bone resorption indirectly, by an inhibition of the
recruitment of osteoclast precursors from bone marrow, by decreased s
ecretion of interleukin-6 and/or prostaglandin E(2), and/or by an incr
eased sensitivity of marrow cells or osteoblasts for bone resorption s
timulating factors such as PTH. The recent demonstration of androgen r
eceptors in bone marrow stromal and osteoclast-like cells opens new pe
rspectives in this respect. During puberty, androgens stimulate bone g
rowth both directly and indirectly. Observations in androgen-resistant
animals clearly demonstrated that the sexual dimorphism of bone depen
ds on the presence of a functional androgen receptor. Optimal peak bon
e mass seems related to an appropriately timed androgen secretion. In
adults, androgens are also involved in maintenance of the male skeleto
n. Androgen replacement may prevent further bone loss in hypogonadal m
en, however, it seems difficult to fully correct bone mass in these me
n.