Journal Article

Molecular mechanisms in calvarial bone and suture development, and their relation to craniosynostosis

David P. C. Rice, Ritva Rice and Irma Thesleff

in The European Journal of Orthodontics

Published on behalf of European Orthodontics Society

Volume 25, issue 2, pages 139-148
Published in print April 2003 | ISSN: 0141-5387
Published online April 2003 | e-ISSN: 1460-2210 | DOI: http://dx.doi.org/10.1093/ejo/25.2.139
Molecular mechanisms in calvarial bone and suture development, and their relation to craniosynostosis

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The development and growth of the skull is a co‐ordinated process involving many different tissues that interact with each other to form a complex end result. When normal development is disrupted, debilitating pathological conditions, such as craniosynostosis (premature calvarial suture fusion) and cleidocranial dysplasia (delayed suture closure), can result. It is known that mutations in the fibroblast growth factor receptors 1, 2, and 3 (FGFR1, 2, and 3), as well as the transcription factors MSX2 and TWIST cause craniosynostosis, and that mutations in the transcription factor RUNX2 (CBFA1) cause cleidocranial dysplasia. However, relatively little is known about the development of the calvaria: where and when these genes are active during normal calvarial development, how these genes may interact in the developing calvaria, and the disturbances that may occur to cause these disorders. In this work an attempt has been made to address some of these questions from a basic biological perspective. The expression patterns of the above‐mentioned genes in the developing mouse skull are detailed. The microdissection and in vitro culture techniques have begun the task of identifying Fgfrs, Msx2, and Twist interacting in intricate signalling pathways that if disrupted could lead to craniosynostosis.

Journal Article.  0 words. 

Subjects: Restorative Dentistry and Orthodontics

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