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Updated: May 2, 2026

Skeletal Phenotype Analysis of a Conditional Stat3 Deletion Mouse Model
Published on: July 3, 2020
Thyroid-stimulating hormone maintains bone mass and strength by suppressing osteoclast differentiation
Wenwen Zhang1, Yanling Zhang1, Yuantao Liu2
1Department of Endocrinology, Shandong Provincial Hospital affiliated to Shandong University, Jinan, Shandong Province 250021, China; Shandong Clinical Medical Center of Endocrinology and Metabolism, Jinan, Shandong Province 250021, China; Institute of Endocrinology and Metabolism, Shandong Academy of Clinical Medicine, Jinan, Shandong Province 250021, China.
Thyroid-stimulating hormone (TSH) plays a crucial role in bone metabolism. This study found that TSH enhances bone volume and strength by inhibiting osteoclast activity, impacting bone remodeling.
Area of Science:
- Endocrinology
- Bone Biology
- Skeletal Physiology
Background:
- Pituitary hormones influence bone metabolism.
- The specific role of thyroid-stimulating hormone (TSH) in bone health requires further elucidation.
Purpose of the Study:
- To investigate the function of TSH in bone metabolism.
- To determine the effect of TSH on bone microarchitecture, strength, and osteoclastogenesis.
Main Methods:
- Utilized TSH receptor (TSHR) null mice (Tshr(-/-)) and wild-type controls (Tshr(+/+)).
- Administered thyroxine to Tshr(-/-) mice and performed histomorphometrical and biomechanical analyses on femurs.
- Examined TSH's effect on osteoclast differentiation in vitro using RAW264.7 cells.
Main Results:
- Tshr(-/-) mice exhibited reduced bone strength, decreased trabecular bone volume, and altered osteoblast and osteoclast surfaces compared to controls.
- Thyroxine replacement in Tshr(-/-) mice further modulated bone resorption and formation.
- TSH demonstrated an inhibitory effect on osteoclast differentiation in vitro.
Conclusions:
- TSH is confirmed to increase bone volume and improve bone microarchitecture and strength.
- TSH exerts its bone-protective effects, at least partly, through the inhibition of osteoclastogenesis.
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