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This Article Full Text Full Text (PDF) All Versions of this Article: JME-08-0142v1 42/4/269    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Bassett, J H D. Articles by Williams, G. R Search for Related Content PubMed PubMed Citation Articles by Bassett, J H D. Articles by Williams, G. R

Molecular Endocrinology Group, Division of Medicine, Imperial College London, MRC Clinical Sciences Centre, Hammersmith Hospital, 5th Floor, Clinical Research Building, Du Cane Road, London W12 0NN, UK

(Correspondence should be addressed to J H D Bassett; Email: d.bassett{at}imperial.ac.uk; G R Williams; Email: graham.williams{at}imperial.ac.uk)

Analysis of mice harbouring deletions or mutations of T₃ receptor (TR) and β (TRβ) have clarified the complex relationship between central and peripheral thyroid status and emphasised the essential but contrasting roles of T₃ in skeletal development and adult bone. These studies indicate that TR1 is the predominant TR expressed in bone and that T₃ exerts anabolic actions during growth but catabolic actions in the adult skeleton. Examination of key skeletal regulatory pathways in TR mutant mice has identified GH, IGF-1 and fibroblast growth factor signalling and the Indian hedgehog/parathyroid hormone-related peptide feedback loop as major targets of T₃ action in chondrocytes and osteoblasts. Nevertheless, although increased osteoclastic resorption is a major feature of thyrotoxic bone loss and altered osteoclast activity is central to the skeletal phenotype of TR mutant mice, it remains unclear whether T₃ has direct actions in osteoclasts. Detailed future analysis of the molecular mechanisms of T₃ action in bone will enhance our understanding of this emerging field and has the potential to identify novel strategies for the prevention and treatment of osteoporosis.