Postmenopausal osteoporosis and hyperparathyroidism are to two common forms of bone loss caused primarily by an expansion of the osteoclastic pool only partially compensated by a stimulation of bone formation. The intimate mechanisms by which estrogen deficiency and excessive production of PTH cause bone loss remain to be determined in part because in vitro studies do not provide the means to adequately reproduce the effects of ovx and PTH overproduction observed in vivo. This article examines the connection between T cells and bone in health and disease and reviews the evidence in favor of the hypothesis that T cells play an unexpected critical role in the mechanism of action of estrogen and PTH in bone.