Bone Abstracts

TSH exerts both antiresorptive and anabolic effects on bone remodeling in aged ovariectomized rats and TSH^−/− mice, supported by clinical results demonstrating that low TSH level is associated with increased bone loss. To further explore the effect of TSH on bone metabolism we here introduced a rat model with removed thyroid and parathyroid glands to obtain low serum concentrations of thyroid and parathyroid hormone, calcitonin and 1,25(OH)₂D₃ (approval for the experiment was obtained from ethical committee of University of Zagreb)_. Surgery resulted in hypocalcemia, low parathyroid and thyroid hormone, 1,25(OH)₂D₃, C-telopeptide and osteocalcin serum level. Intermittent administration of TSH resulted in a further decrease of serum calcium and decreased level of serum C-telopeptide due to the suppression of bone resorption, while serum osteocalcin level was higher indicating an increased bone formation rate. MicroCT analyses of the distal femur and proximal tibia showed that rats treated with 1,25(OH)₂D₃ alone or in a combination with TSH had an increased trabecular bone volume, and enhanced trabecular bone quality. Biomechanical testing of the trabecular bone showed an increased maximal load for 105 and 235%, respectively, in rats treated with 1,25(OH)₂D₃ alone, or in a combination with TSH. Rats treated with TSH had a significantly decreased number of osteoclasts in comparison to TPTx control animals. The decline of the osteoclast number was even greater in rats treated with a combination of TSH and 1,25(OH)₂D₃, despite the fact that 1,25(OH)₂D₃ increased the number of osteoclasts. Addition of TSH to osteoblasts increased the production of the bone specific alkaline phosphatase and had a synergistic effect when combined with 1,25(OH)₂D₃. We suggest that TSH independently of calciotropic hormones suppressed bone resorption and stimulated bone formation, while in combination with 1,25(OH)₂D₃ acted synergistically on bone formation resulting in an increased bone volume.