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Introduction
There is immense current interest in the effects of thyroid hormones on bone. This is largely due to concern that patients on thyroxine replacement therapy are at increased risk of developing osteoporosis; this concern follows a number of reports describing reduced bone mineral density in this group of patients. The issue is, however, uncertain and the purpose of this review is (i) to summarize what is known about the effects of thyroid hormones on bone at both an experimental and clinical level and (ii) to try to reach a greater understanding of the problem and its implications for patient management.
Bone biology
Bone remodelling requires the tightly coupled actions of osteoclasts and osteoblasts. A normal bone remodelling cycle takes approximately 200 days. Each cycle begins with activation of cells which become osteoclasts and start resorbing bone. This phase lasts for about 50 days and is terminated
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ABSTRACT
Tri-iodothyronine (T3) increases bone resorption in vivo and in vitro. In order to understand further the mechanisms by which this occurs we studied the effects of T3 at concentrations in the range of 1 pmol/l–1 μmol/l on bone resorption by osteoclasts isolated from neonatal rat long bones. Osteoclasts were disaggregated and incubated either with or without UMR 106 cells or with mixed bone cells. We found that there was no effect of T3 on bone resorption by osteoclasts incubated alone or co-cultured with UMR 106 cells. However, in culture with mixed bone cells there was a significant relationship between the concentration of T3 and bone resorption (r = 0·54, P= 0·01) The greatest effect was observed at a T3 concentration of 1 μmol/l at which a 1·8-fold increase in resorption was seen compared with control (P <0·005; paired t-test). We conclude that the ability of T3 to increase osteoclastic bone resorption is not due to a direct action of T3 on osteoclasts but is mediated by another cell present in bone. The observation that UMR 106 cells are unable to mediate this effect suggests that either the mediating cell is not osteoblastic or the phenotype of UMR 106 does not conform to the phenotype of osteoblastic cells that mediate the T3 responsiveness of bone.
Journal of Endocrinology (1992) 133, 327–331
