Abstract
The relationship between the thyroid and the skeleton was first suggested in 1891 when Von Recklinghausen (1891) reported a patient with hyperthyroidism and multiple fractures. Thyroid disease is common; more than 1% of British women receive thyroxine treatment, increasing to over 3% in those over 50 years of age, and the concern is that patients with a history of hyperthyroidism or those receiving thyroxine treatment may be at increased risk of osteoporosis and fractures (Parle et al ., 1993). While the clinical consequences of overt hyperthyroidism on bone have been known for many years the molecular mechanism of action of thyroid hormone on bone has remained incompletely understood. Furthermore, earlier recognition of thyroid disease and effective treatment for clinical symptoms has meant that severe bone disease is now uncommonly seen. It is only in more recent years, with the development of more sensitive TSH assays and the recognition that even so-called subclinical thyroid disease, associated with a suppressed TSH but normal FT4 and FT3 levels, may have effects on fracture risk that there has been a renewed interest in the role of thyroid hormone in bone (Klee & Hay, 1988; Bauer et al ., 2001). The molecular actions of thyroid hormone in bone have recently been comprehensively reviewed (Harvey et al ., 2002; Bassett & Williams, 2003). This review will therefore only briefly summarize this information and instead concentrate in detail on some of the clinical aspects of thyroid hormone effects on bone growth and development in childhood and bone turnover and maintenance in adults. Tables are used to illustrate the effects of thyroid hormone suppressive therapy for thyroid cancer and thyroid hormone replacement on bone mineral density (BMD), and the effects of thyroid hormone on fracture risk. Each clinical section concludes with a summary of the salient points discussed. The role of calcitonin, a hormone also synthesized and secreted by the thyroid gland, and its effects on bone has recently been reviewed and will not be discussed further here (Inzerillo et al ., 2002). Bone biology and the skeletal consequences of thyroid disease
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