Abstract

The mechanism of action as well as the clinical effects of thyroid hormones on bone has been of interest for more than a century. With the appearance of new treatment modalities for thyroid function disorders, the accompanying alterations in bone metabolism appeared to be rare. However, the introduction of new diagnostic tools, such as osteodensitometry and biochemical bone markers, has changed our view since they were able to show smaller but important changes in bone mineral metabolism associated with thyroid function disorders. Now, we know that hyperthyroidism is associated with an increased life-time risk for fractures, even after achieving euthyroidism. This fact may play an important role in the higher mortality rate among previously hyperthyroid patients later in life. Subclinical hyperthyroidism may also affect bone density, however, its effect on fracture rate remains to be established. The lack of thyroid hormones will alter normal growth during childhood. Adult hypothyroid patients tend to exhibit higher than normal bone density. Despite rather increased bone quantity, hypothyroidism is accompanied with increased fracture risk before and after diagnosis. The effect of thyroid hormone treatment on bone tissue is somewhat controversial. Nevertheless, only patients with suppressed thyroid-stimulating hormone (TSH) appear to loose bone and have higher fracture incidence, whereas patients with a TSH level in the normal range seem to have similar bone mineral content and fracture rate as euthyroid subjects. In summary, most of thyroid function disorders may result in reduced bone density and/or increased fracture rate that should be taken into consideration at clinical evaluation.

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