open access

Vol 60, No 5 (2009)
Review article
Published online: 2009-10-30
Submitted: 2013-02-15
Get Citation

Actions of thyroid hormones in bone

Graham R. Williams
Endokrynologia Polska 2009;60(5):380-388.

open access

Vol 60, No 5 (2009)
Review article
Published online: 2009-10-30
Submitted: 2013-02-15

Abstract

Thyroid hormones are required for skeletal development and establishment of peak bone mass. Hypothyroidism in children results in growth retardation with delayed skeletal development, whereas thyrotoxicosis accelerates bone maturation. In adults, T3 regulates bone turnover and bone mineral density, and normal euthyroid status is essential to maintain optimal bone strength. Population studies indicate that hypothyroidism and hyperthyroidism are both associated with an increased risk of fracture. Nevertheless, the mechanism of T3 action in bone is incompletely understood. Studies in mutant mice have demonstrated that T3 action in bone is mediated principally by T3 receptor α (TRα). T3 exerts anabolic actions during growth to stimulate peak bone mass acrrual, but has catabolic effects on the adult skeleton that increase bone turnover. Recent studies have also suggested that TSH may have direct actions in bone cells, but such effects are difficult to resolve in vivo because thyroid hormone and TSH concentrations are maintained in an inverse relationship by the hypothalamic-pituitary-thyroid axis. Current understanding is based on studies in mice that harbor germline mutations in the genes encoding TRα, TRβ or the TSH receptor and it is not clear whether the skeletal effects of these mutations result from disruption of primary T3 actions in bone cells or whether they are secondary to systemic effects on other endocrine pathways that regulate skeletal development and bone mass. Tissue-specific disruption of thyroid hormone signalling in bone cells will be required to address this issue. Such studies are likely to identify key components of the T3 signalling pathway that may represent suitable drug targets for treatment of osteoporosis.

Abstract

Thyroid hormones are required for skeletal development and establishment of peak bone mass. Hypothyroidism in children results in growth retardation with delayed skeletal development, whereas thyrotoxicosis accelerates bone maturation. In adults, T3 regulates bone turnover and bone mineral density, and normal euthyroid status is essential to maintain optimal bone strength. Population studies indicate that hypothyroidism and hyperthyroidism are both associated with an increased risk of fracture. Nevertheless, the mechanism of T3 action in bone is incompletely understood. Studies in mutant mice have demonstrated that T3 action in bone is mediated principally by T3 receptor α (TRα). T3 exerts anabolic actions during growth to stimulate peak bone mass acrrual, but has catabolic effects on the adult skeleton that increase bone turnover. Recent studies have also suggested that TSH may have direct actions in bone cells, but such effects are difficult to resolve in vivo because thyroid hormone and TSH concentrations are maintained in an inverse relationship by the hypothalamic-pituitary-thyroid axis. Current understanding is based on studies in mice that harbor germline mutations in the genes encoding TRα, TRβ or the TSH receptor and it is not clear whether the skeletal effects of these mutations result from disruption of primary T3 actions in bone cells or whether they are secondary to systemic effects on other endocrine pathways that regulate skeletal development and bone mass. Tissue-specific disruption of thyroid hormone signalling in bone cells will be required to address this issue. Such studies are likely to identify key components of the T3 signalling pathway that may represent suitable drug targets for treatment of osteoporosis.
Get Citation

Keywords

thyroid hormones; T3; T4; bone turnover; osteoporosis

About this article
Title

Actions of thyroid hormones in bone

Journal

Endokrynologia Polska

Issue

Vol 60, No 5 (2009)

Pages

380-388

Published online

2009-10-30

Bibliographic record

Endokrynologia Polska 2009;60(5):380-388.

Keywords

thyroid hormones
T3
T4
bone turnover
osteoporosis

Authors

Graham R. Williams

Important: This website uses cookies.tanya dokter More >>

The cookies allow us to identify your computer and find out details about your last visit. They remembering whether you've visited the site before, so that you remain logged in - or to help us work out how many new website visitors we get each month. Most internet browsers accept cookies automatically, but you can change the settings of your browser to erase cookies or prevent automatic acceptance if you prefer.

Via MedicaWydawcą serwisu jest  "Via Medica sp. z o.o." sp.k., ul. Świętokrzyska 73, 80–180 Gdańsk

tel.:+48 58 320 94 94, faks:+48 58 320 94 60, e-mail:  viamedica@viamedica.pl