Craniosynostosis is a common congenital defect caused by premature fusion of cranial sutures. The severe morphologic abnormalities and cognitive deficits resulting from craniosynostosis and the potential morbidity of surgical correction espouse the need for a deeper understanding of the complex etiology for this condition. Work in animal models for the past 20 years has been pivotal in zadvancing our understanding of normal suture biology and elucidating pathologic disease mechanisms. This article provides an overview of milestone studies in suture development, embryonic origins, and signaling mechanisms from an array of animal models including transgenic mice, rats, rabbits, fetal sheep, zebrafish, and frogs. This work contributes to an ongoing effort toward continued development of novel treatment strategies.
From the *Hagey Laboratory for Pediatric Regenerative Medicine, Department of Surgery, Plastic and Reconstructive Surgery Division, Stanford University School of Medicine; and †Institute for Stem Cell Biology and Regenerative Medicine, Stanford University, Stanford, California.
Received February 16, 2012.
Accepted for publication April 2, 2012.
Address correspondence and reprint requests to Michael T. Longaker, MD, MBA, Hagey Laboratory for Pediatric Regenerative Medicine, Stanford University School of Medicine, 257 Campus Dr, Stanford, CA 94305-5148; E-mail: Longaker@stanford.edu
The authors report no conflicts of interest.