Many systemic and local hormones influence bone growth and remodelling. These include calcium regulating hormones, systemic growth regulators and local growth factors. Parathyroid hormone (PHT) is a potent stimulator of osteoclastic bone resorption and a direct inhibitor of osteoblastic collagen synthesis. However, intermittent low-dose PTH administration can increase bone formation in vivo. PTH may act indirectly via local factors. It has been shown to increase prostaglandin E2 (PGE2) and transforming growth factor beta (TGF-beta) release from bone. Both PGE2 and TGF-beta have complex effects on bone metabolism and are likely to be physiological regulators of bone remodelling. Oestradiol has been shown to inhibit bone resorption in vivo but not in vitro. While there is evidence for oestrogen receptors in cultured bone cells, the effect could still be indirect. Oestradiol can inhibit bone PGE2 release in an in vivo-in vitro model in the rat. Glucocorticoids are potent inhibitors of bone formation and inhibit PGE2 and interleukin 1 production both in vivo and in vitro. While many regulatory factors affect prostaglandin production in bone, the complex effects of PGE2 on bone metabolism make it difficult to predict the ultimate response. The major effects of PGE2 are stimulation of bone formation and resorption and an increase in bone turnover. However, opposite effects can occur at certain times and concentrations. Interactions among these factors could explain some physiological, pathological, and therapeutic responses in skeletal tissue.