Thyroid disease is common, and more than 10 percent of women over 65 years of age undergo thyroid hormone replacement therapy. Osteoporosis also affects a large proportion of this population, making it critical to understand the effects of thyroid hormone on bone. Hyperthyroidism accelerates bone turnover and shortens the normal bone remodeling cycle. Thyroid hormone appears to be more damaging to cortical bone (found in the hip and forearm) than to trabecular bone (found in the spine). The availability of noninvasive testing for bone loss and sensitive thyroid-stimulating hormone (TSH) assays has led to a greater understanding of the reduction in radial bone mineral density in women receiving suppressive doses of l-thyroxine. Greenspan and Greenspan reviewed the data on thyroid hormone and skeletal integrity, examining hyperthyroidism, exogenous or endogenous TSH suppression, and the effect of thyroid replacement therapy.

The main causes of hyperthyroidism are Graves' disease, toxic multinodular goiter and toxic thyroid nodule. Most studies have shown decreased bone density in patients with these disorders. Several studies have shown that bone mineral density improves in men and women after treatment changes hyperthyroidism to a euthyroid state. Because hyperthyroidism is associated with fractures, bone mineral density should be measured in patients, especially postmenopausal women, with this condition. The results may then be used to determine if treatment for osteopenia or osteoporosis is required.

Exogenous administration of l-thyroxine to fully suppress TSH (defined as a TSH measurement less than 0.1 μU per mL [0.1 mU per L]) is used to inhibit progression or recurrence of papillary or follicular thyroid cancer. Partial TSH suppression (TSH just below normal, between 0.2 and 0.5 μU per mL [0.2 and 0.5 mU per L]) has also been used to inhibit growth of thyroid nodules and goiters, although this use is controversial. Studies evaluating bone loss in these patients give contradictory results in premenopausal women but show clear loss of bone mineral in postmenopausal patients. Testing bone mineral density at a cortical site with follow-up every one to two years is advisable in post-menopausal women. Estrogen replacement or treatment with bisphosphonates should be considered in these women, along with calcium and vitamin D supplementation and exercise.

Thyroid replacement therapy, defined as supplementing l-thyroxine (50 to 150 μg per day) to maintain a normal TSH level of 0.5 to 5.0 μU per mL (0.5 to 5.0 mU per L) had no negative effect on bone mass in premenopausal or postmenopausal women. The influence of thyroid hormone therapy on bone density in men appears to be minimal.

The authors conclude that, although interpretation of all the clinical studies performed is complex, it is clear that hyperthyroidism can adversely affect bone and is associated with hip fractures. Assessment of bone mass is recommended in all hyperthyroid patients. Thyroid hormone suppression of TSH seems to have an adverse effect on bone, and this effect seems to be greatest in postmenopausal women, and greater in cortical bone than in trabecular bone. Thyroid hormone replacement therapy resulting in normal serum TSH levels apears to have minimal or no effect on bone density.