Thyroid hormones and bone metabolism: the Dkk1 role

It is well recognized that bone metabolism is linked to thyroid hormones. Indeed, there is an association between untreated juvenile hypothyroidism and complex skeletal alterations, as well as bone loss and fractures may be present in patients with hyperthyroidism. At molecular and cellular levels, this happens because the thyroid hormones T3 and T4 exert their actions also on bone cells increasing the activity of bone forming osteoblast and of bone eroding osteoclasts. However, the mechanism behind this link is not well defined, and the understanding of this relationship might have therapeutic relevance. The Wnt cellular signal, and its inhibitor Dickkopf-1 (Dkk1) molecule, are key regulators of osteoblast functions and are influenced by thyroid hormones. In a recent study by members of the ECTS Academy, Elena Tsourdi and Martina Rauner, published on Endocrinology, the role of Dkk1 in experimental models affected by thyroid hormone dysfunctions was investigated. Using experimental models of thyroid diseases, they found that Dkk1 regulates does not protected against bone alterations induced by hyper or hypothyroidism. Bone formation and erosion was found altered due to thyroid hormones influence and independently from the Dkk1 action. So, Dkk1 does not appear to be a master mediator in the alteration of bone metabolism occurring with dysbalanced thyroid hormones levels. In patients affected by thyroid hormone dysfunction, the blockade of this molecule appears unlikely to be an effective strategy to prevent pathological alterations in bone.

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