Thyroid hormones exert multiple effects on bone and have a physiologic role in the development of the skeleton. The mechanisms by which thyroid hormones affect bone are poorly defined, but the presence of thyroid hormone receptors on bone cells suggests that their actions may be directly mediated. Thyrotoxicosis is associated with bone loss and increased risk for fracture at the hip and possibly other sites; subclinical endogenous hyperthyroidism may have adverse skeletal effects in postmenopausal women. In general, thyroxine replacement therapy does not seem to result in clinically significant bone loss, although postmenopausal women with a past history of thyrotoxicosis may be particularly susceptible. Hypothyroidism is associated with growth retardation in children but does not result in symptomatic bone disease in adults. Bone densitometry should be offered to all patients with prolonged, overt hyperthyroidism and to postmenopausal women with subclinical endogenous hyperthyroidism or those with a prior history of thyrotoxicosis who are receiving replacement thyroxine therapy. Hormone replacement therapy should be advised for those in the latter group who are found to have low bone mineral density and bisphosphonate therapy may also be considered as a therapeutic option.