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Osteoporosis due to hyperthyroidism is worse when TSH signaling is lost
DOI:10.1038/bonekey.2012.253
Baliram et al. investigated whether low levels of thyroid-stimulating hormone (TSH) contribute to the bone loss and subsequent osteoporosis observed in human hyperthyroidism.
Wild-type mice and mice in which the gene for the TSH receptor was knocked out (Tshr−/− mice) were implanted with slow-release thyroxine (T4) pellets to model hyperthyroidism. Both groups of mice showed a clear reduction in areal bone mineral density (BMD), volumetric BMD, bone volume/trabecular volume, trabecular number, trabecular thickness and connectivity density, but the bone loss observed was significantly greater in the Tshr−/− mice. The Tshr knockout mice also showed increased rates of bone resorption and bone formation, elevated serum C-telopeptide levels and higher serum osteocalcin levels.
These findings may explain why T4-treated patients whose TSH levels are suppressed show greater bone loss than similarly treated patients with normal TSH levels; lowering serum TSH levels to levels that are undetectable should be avoided, recommend the authors. However, they admit that it was not possible, due to the short-term nature of the experiments included, to find out whether having consistently elevated TSH was osteoprotective.
Editor’s comment: The authors also identified a TSHβ splice variant produced by bone marrow CD11b-positive cells. They imply that as production of this factor is enhanced by T4, it may confer osteoprotection, but if this were the case its level should change reciprocally with the serum TSH level.
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