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Patients with thyroid cancer who are treated with suppressive dosage thyroxin may be at risk of developing accelerated bone loss and a decrease in bone density. High dosages of beta-blockers decreased hypercalcemia and bone resorption markers in patients with hyperthyroidism, suggesting that the beta adrenergic receptor might be involved in bone metabolism. The tumor necrosis factor (TNF) family members, OPG and RANKL, are essential regulators of bone resorption and bone mass. The OPG and RANKL system has changed our view of bone mineral metabolism, and allows us to detect smaller but important changes in bone mineral metabolism in hyperthyroid states due to suppressive doses of thyroxin. We hypothesize that there is accelerated bone loss in thyroid cancer patients receiving thyroid suppressive therapy, and that beta-blockade reduces bone loss in these patients through altered regulation of the OPG/RANKL system. As the incidence of thyroid cancer increased and thyroid cancer patient survives longer, more than 500,000 thyroid cancer patients will be on thyroid suppression therapy. Our current research thus may have a major clinical impact for management of these patients in the future.