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Craniofacial sutures: development, diseases and treatment: by David P. Rice

By David P. Rice

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Additional resources for Craniofacial sutures: development, diseases and treatment: 10 tables

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Endocrinology 2005;146:1012–1017. Ducy P, Zhang R, Geoffroy V, Ridall AL, Karsenty G: Osf2/Cbfa1: a transcriptional activator of osteoblast differentiation. Cell 1997;89:747–754. Ducy P, Karsenty G: Two distinct osteoblast-specific cis-acting elements control expression of a mouse osteocalcin gene. Mol Cell Biol 1995;15:1858–1869. Yoshida CA, Furuichi T, Fujita T, Fukuyama R, Kanatani N, Kobayashi S, Satake M, Takada K, Komori T: Core-binding factor beta interacts with Runx2 and is required for skeletal development.

Although the source and nature of these signals are largely unknown, it is known that cues from the adjacent epithelium can stimulate the process. Mesenchymal cells then react by a combination of enhanced cell turnover, aggregation toward a focus and failure to disperse away from that focus [2]. A variety of extracellular matrix and cell surface molecules including syndecans, neural cell adhesion molecule (NCAM) and neural cadherin (N-cadherin) are all thought to be important in mesenchymal condensate formation [3].

The exception is the intermaxillary suture which starts to fuse between the age of 30 and 35 years [66]. In the mouse, all calvarial sutures, except for the posterior section of the interfrontal suture, remain patent. The posterior section of the interfrontal suture fuses between 25 and 45 days postnatal, and it does this in an anterior to posterior manner [67]. The Sprague-Dawley rat exhibits a similar pattern with posterior section of the interfrontal suture fusing between 12 and 30 days postnatal.

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