Parathyroid hormone (PTH) is the principal regulator of bone remodeling in the adult skeleton. The acute in vivo effect of PTH is to increase bone resorption, although sustained increases in its circulating levels accelerate both formation and resorption. These divergent effects have focused attention on PTH as a factor contributing to bone loss in some postmenopausal women, as well as interest in its role as therapy for the disease. Sustained increases in PTH are classically seen in primary hyperparathyroidism. While still controversial, increasing evidence suggests that primary hyperparathyroidism is associated with increased rates of bone loss, particularly from cortical sites in the skeleton. It is clear that the remodeling space is increased in primary hyperparathyroidism, and that surgical correction of the disease leads to substantial increases in bone mass in patients with osteoporosis. Recently, secondary hyperparathyroidism has emerged as an important contributor to increased rates of bone turnover and bone loss in postmenopausal women. The etiology of secondary hyperparathyroidism in postmenopausal women is complex, and is probably related to alterations in vitamin D metabolism and tissue responsiveness to 1,25(OH)2vitamin D. PTH has emerged at the forefront of anabolic therapies for the treatment of postmenopausal osteoporosis. When given as a single agent, intermittent daily subcutaneous administration of PTH induces consistent gains in trabecular bone mass with more varying effects on the cortical envelope. However, recent therapeutic trials employing a second agent, most notably estrogen, give hope that this approach may provide the first truly efficacious anabolic therapy for this devastating disease.