Puberty is a period of dynamic changes mediated by GH and the gonadal steroid hormones. Although these substances exert important independent effects, their interaction is vital to normal pubertal growth and development. This is supported by observations of blunted growth and diminished levels of GH and IGF-1 during adolescence in individuals with panhypopituitarism in whom adequate replacement with both hormones had not been achieved. The independent roles of androgens and estrogens in mediating the rise in GH secretion at puberty have been studied in individuals with complete androgen insensitivity and through the administration of nonaromatizable androgens and the use of selective androgen- or estrogen-receptor blockade. The preponderance of evidence from studies of nonaromatizable (pure) androgens suggests that GH secretion is not enhanced as it is under the influence of testosterone. In addition, studies have shown increased GH secretion following androgen-receptor blockade and diminished GH release after estrogen-receptor blockade. Together these studies suggest a facilitory role of estrogen receptor-mediated processes on GH secretion and IGF-1 production. If androgens influence the GH/IGF-1 axis, it is most likely by an inhibitory mechanism. Observations of delayed skeletal maturation and deficient bone mineralization in individuals with estrogen receptor defects or mutations of the aromatase gene demonstrate the essential role of estrogen in promoting normal bone maturation, the accrual and maintenance of BMD, and control of the rate of bone turnover.