The thyroid hormones L-thyroxine und 3,3',5-triiodo-L-thyronine are critical regulators of skeletal development and maintenance of a healthy bone in adults. While direct actions of thyroid hormones on osteoblasts are well established, only little is known about thyroid hormone signaling in osteoclasts and especially osteocytes. Thyroid hormones increase osteoblast differentiation and function in vitro. Three main factors determine their biological activity: their import via specific transporter proteins, their activation or inactivation mediated by deiodinases and the thyroid hormone receptor availability. Preclinical studies using transgenic mouse models demonstrated that every one of these factors determines bone quality, structure and mineral density. Thyroid disorders can cause distinct skeletal changes during childhood and adulthood that usually can be medically treated. During childhood, untreated hypothyroidism and hyperthyroidism both can cause short stature. In adults, hyperthyroidism is a known cause of secondary osteoporosis with an increased fracture risk due to enhanced bone formation and especially bone resorption. In contrast, hypothyroid patients display a prolonged bone remodeling cycle and increased secondary mineralization. Given that thyroid hormones directly affect bone turnover, they can also regulate the whole-body calcium and phosphate homeostasis. Thus, thyroid hormones play an important role in bone and mineral metabolism.