It is now established that adults with growth hormone (GH) deficiency, of childhood or adult onset, have reduced bone mass. GH deficiency is believed to interfere with acquisition of bone mass, although an alternative mechanism is required to explain the reduction in bone mass present in adults who acquire GH deficiency after peak bone mass has been achieved. GH replacement increases bone turnover and may increase bone mass in the longer term, although short-term studies show a decrease in bone mass which can be explained by an increase in bone resorption before new bone formation occurs. Abnormalities of GH secretion have also been implicated in the development of osteoporosis, but the effect of GH treatment on bone mass in such patients is disappointing. Sex steroids have an important role to play in the acquisition of bone mass, and reduced sex steroid levels during adolescence have a deleterious effect on bone mass. The importance of sex steroids in the maintenance of bone mass is illustrated by the development of osteopenia in men and women with hypogonadism, and by the preservation of bone mass by restoration of normal endogenous sex steroid levels, or by treatment with exogenous sex steroid. Sex steroids also influence circulating levels of GH and insulin-like growth factor-1, and the inter-action between these hormones is likely to be important in the acquisition and maintenance of normal bone mass.