[Frontiers in Bioscience S1, 92-107, June 1, 2009]

Skeletal morphofunctional considerations and the pituitary-thyroid axis

Jameel Iqbal1, Terry F. Davies1, Li Sun, Etsuko Abe1, Angelo Carpi2, Jeffrey Mechanick1, Mone Zaidi1

1Mount Sinai Bone Program and Department of Medicine, Mount Sinai School of Medicine, New York 10029 and 2Department of Reproduction and Ageing, University of Pisa, Pisa, Italy


1. Abstract
2. Introduction
3. Limb patterning and joint formation
4. Endochondral bone formation
5. Bone formation
6. Bone resorption
7. Neurogenic control of bone mass
8. Endocrine regulation of bone mass
9. Bone loss from alterations in the pituitary or thyroid axis
10. Clinical correlations and recommendations
11. Acknowledgments
12. References


The past decade has unraveled novel molecular mechanisms not only of skeletal remodeling, which is the process by which the skeleton is restructured throughout adult life, but also the precision by which the skeleton is put together during embryogenesis and later modeled during growth. It is now possible to delete single genes in individual cells and during specified periods of life. This has allowed us to pin down specific molecular events that underlie individual cellular processes, and also importantly, to identify molecular defects underlying disorders of skeletal morphogenesis and remodeling. Particularly novel has been the demonstration of cross-talk, some of which is humoral, between the skeleton and organs as diverse as the brain, pituitary, and even adipose tissue and pancreas. The current review describes these molecular mechanisms in relation to the way thyroid hormones, and the pituitary hormone thyrotropin (TSH), regulate skeletal morphogenesis and remodeling.