During craniofacial morphogenesis, suture patency (remaining open) and fusion (closing) are under the regulation of varied biological and mechanical factors. The sutures are the soft tissue regions that separate the cranial bony plates. They allow the skull to expand during growth; a subset of skull bones progress to fusion at the sutures during later development. Premature fusion of the skull bones at the sutures, or craniosynostiosis (1.2 out of 3,000 live births), is treated by surgically separating the bones soon after birth (Cohen, 1986). Previous studies have implicated an abnormal mechanical environment in the pathogenesis of craniosynostosis. Suggesting that abnormal tensile forces transmitted by a defective cranial base cause craniosynostiosis, Moss (1959) severed the connection between the cranial base and the developing calvaria, the falx cerebri, and found that sutures destined to fuse failed to do so. Similarly, increased compressive force as a result of intrauterine compression has also been implicated in human craniosynostosis. By physicalling delaying the birth of mice pups for 3 days, Koskinen-Moffett and Moffett (1989) showed that the increased intrauterine forces caused by the growing pups led to a higher incidence of craniosynostosis.
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