Pituitary glycoprotein hormone receptors, including ACTH‐R, TSH‐R, and FSH‐R, occur in bone. Their skeletal expression reflects that central endocrine control is evolutionarily recent. ACTH receptors, in osteoblasts or the adrenal cortex, drive VEGF synthesis. VEGF is essential to maintain vasculature. In bone, ACTH suppression by glucocorticoids can cause osteonecrosis. TSH receptors occur on osteoblasts and osteoclasts, in both cases reducing activity. Thus, TSH directly reduces skeletal turnover, consistent with evolutionary adaptation to stress. FSH receptors accelerate bone resorption, whereas estrogen promotes bone formation, the forces usually balancing. With ovarian failure, low estrogen with high FSH causes rapid bone loss. The skeletal FSH effect in the menopause seems paradoxical, but it is a logical adaptation in lactation, where prolonged FSH elevation also occurs. In addition to receptors, there is some synthesis of pituitary glycoproteins at distributed sites; this is not well studied, but it may further modify the paradigm of central endocrine regulation.