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Article
June 3, 1988

Thyroid Hormone and the Skeleton: A Bone of Contention

Author Affiliations

Sinai Hospital of Baltimore The Johns Hopkins University School of Medicine Baltimore

Sinai Hospital of Baltimore The Johns Hopkins University School of Medicine Baltimore

JAMA. 1988;259(21):3175. doi:10.1001/jama.1988.03720210065033
Abstract

In 1891, von Recklinghausen1 reported severe skeletal demineralization in a 23-year-old woman with thyrotoxicosis. Since then, numerous studies have detailed the abnormal bone and mineral dynamics in states of thyroid hormone excess. (See reference 2 for a review.) Briefly stated, thyroid hormones directly stimulate osteoclasts to enhance bone resorption. This leads to mild hypercalcemia, with concomitant suppression of serum parathyroid hormone levels, modest elevations in levels of bone alkaline phosphatase, and negative calcium balance. While clinically overt thyrotoxic bone disease is uncommon, numerous studies have demonstrated decreased bone mineral content in hyperthyroidism, using a variety of noninvasive techniques2; not surprisingly, postmenopausal women are the most severely affected. Several reports also document that the bone loss in hyperthyroidism may be partially reversible with treatment of the underlying thyroid disorder.3

See also p 3137.

Although the decline in skeletal mass associated with endogenous thyrotoxicosis is interesting from a pathophysiological

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