Acta Clin Croat, Vol. 46, No. 1, 2007 41 V. Altabas et al. Bone remodeling and thyroid function Acta Clin Croat 2007; 46:41-47 Review BONE REMODELING AND THYROID FUNCTION Velimir Altabas, Maja Berkoviæ, Branko Beèejac and Miljenko Solter Department of Endocrinology, Diabetes and Metabolic Diseases, University Department of Medicine, Sestre milosrdnice University Hospital, Zagreb, Croatia SUMMARY  Many diseases are associated with more rapid bone loss and an increased risk of osteoporosis and fractures. Both hyperthyroidism and hypothyroidism as well as use of thyroid hormones or thyrosuppressant treatment influence bone turnover rates and may alter the risk of future fractures. Markers of bone remodeling are good indicators to determine bone turnover rates and potential bone loss, and correlate well with thyroid hormone levels. Untreated hyperthyroidism accelerates bone turnover resulting in net bone loss, while untreated hypothyroidism in adult humans slows down bone turnover resulting in net bone gain. In both cases, damage in bone microarchitecture occurs, leading to an increased relative risk of fractures. Effective therapies for both states are available, and in ideal case, full recovery of mineralized tissue may occur over time. Controversies are still present in patients receiving suppressive thyroxin treatment for thyroid carcinoma. It seems that suppressed thyroid-stimulating hormone with normal levels of peripheral thyroid hormones may increase the relative fracture risk in postmenopausal but not in premenopausal women. However, the exact molecular mechanisms of thyroid hormone and thyroid-stimulating hormone action on bone are not completely understood yet. Key words: Bone remodeling  physiology; Bone and bones  physiology; Bone and bones  metabolism; Thyroid hormones  physiology; Thyroid hormones  deficiency Corresponding address: Velimir Altabas, MD, MS, Department of Endocrinology, Diabetes and Metabolic Diseases, University Department of Medicine, Sestre milosrdnice University Hospital, Vinogradska c. 29, HR-10000 Zagreb, Croatia E-mail: velimir.altabas@zg.t-com.hr Received August 24, 2006, accepted in revised form February 5, 2007 Introduction The skeleton continually undergoes a process of bone remodeling by which old bone is removed and replaced by new bone in two different but coupled processes  bone formation and bone resorption. Bone remodeling in adult humans is thought to have two functions: to provide a means of maintaining normal serum calcium level and to repair microdamage within the skeleton to maintain skeletal integrity and strength 1 . This process can result in one of the following: net gain of bone mass, e.g. during the growth period; constant bone mass in most adult people; and net loss of bone mass, e.g., in osteoporosis. Net loss of bone is an increasing problem in public health due to aging of the entire population but also due to other risk factors such as smoking, alcohol abuse and chronic diseases 1 . Bone Turnover and Bone Mineral Density Bone formation and bone resorption exist simulta- neously in the healthy bone, as a consequence of syn- chronous and coupled action of osteoblasts and osteo- clasts forming remodeling units. The normal bone re- modeling cycle lasts for approximately 200 days. During this period, all bone resorbed by osteoclasts should be replaced by new bone produced by osteoblasts. Activa- tion of both cell types is necessary for effective bone remodeling. The cytokine responsible for communication be- tween the osteoblast (cell responsible for bone forma- tion) and osteoclast (cell responsible for bone resorp- tion) has been identified as a receptor activator of NFkB (RANK) ligand. Osteoprotegerin is a circulating decoy for the RANK receptor. Modulation of osteoclast recruit- ment and activity appears to be a function of interplay