**1. Introduction**

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Thyroid hormones play a crucial role in the skeletal growth, peak bone mass acquisition and maintenance of bone mass. Abnormalities in hypothalamic–pituitary–thyroid axis in infancy and childhood have been shown to interfere with a normal linear growth and skeletal maturation. Hypothyroidism compromises normal bone formation and results in slowing of linear growth. Thyrotoxicosis leads to growth acceleration, diminution of bone mass and advance in bone age. Studies in animal models have demonstrated the importance of thyroid hormone signaling in the maintenance of bone mass in adulthood. Increased risk of fracture has been demonstrated in both hypothyroidism and hyperthyroidism. The thyroid hormone, 3,5,3'-triiodothyronine (T3), has long been considered to play a primordial role in the skeletal homeostasis. However, recent studies have shown that TSH acts as a direct regulator of bone remodeling, highlighting the importance of integrity of the hypothalamopituitary-thyroid axis.

This chapter will review our current understanding regarding the action of thyroid hormones on the bone development and maintenance of bone mass, under normal conditions and as a result of thyroid gland dysfunction. Mechanism of thyroid hormone action will be illustrated in relation to bone with the focus on the genetic regulation and the molecular interactions between thyroid hormones and skeletal cells. Clinical consequences of thyroid dysfunction on the growth and skeletal maturation will be detailed. We will review the published literature regarding BMD in hyperthyroid and hypothyroid patients including patients on medical therapy, as well as the influence of sex and menopause on the maintenance of bone mass. The impact of treatments for thyroid dysfunction on the bone mineral metabolism will be discussed.

© 2012 Weryha et al., licensee InTech. This is an open access chapter distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2012 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
