The classic bone disease of primary hyperparathyroidism, osteitis fibrosa cystica, was characterized by subperiosteal bone resorption, osteopenia, and "brown tumors." Since the description of this skeletal disorder, the clinical profile of primary hyperparathyroidism has evolved markedly. The disease today is often characterized by no more than asymptomatic hypercalcemia, and severe bone disease is a distinct rarity. However, as we have endeavored to show in this article, newer and more sensitive techniques show significant evidence of the effect of excess parathyroid hormone on the skeleton. Bone density as measured by photon absorptiometry and bone histomorphometry show a deficit of cortical bone and a preservation or increase in cancellous bone elements in mild primary hyperparathyroidism with no clinical evidence of skeletal disease. Important questions exist as to the therapeutic implications of these data. Does the presence of parathyroid hormone effect on sophisticated testing portend the development of clinical bone disease? Should these data be used as a rationale for surgical intervention in patients who might otherwise be followed conservatively with mild primary hyperparathyroidism? The answers to these questions must await further data collection and study.