title: Models of cranial suture biology.
abstract: 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 advancing 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.
authors.affiliation: Hagey Laboratory for Pediatric Regenerative Medicine, Department of Surgery, Plastic and Reconstructive Surgery Division, Stanford University School of Medicine, Stanford, CA 94305, USA.
authors.forename: Monica
authors.initials: M
authors.lastname: Grova
authors.forename: David D
authors.initials: DD
authors.lastname: Lo
authors.forename: Daniel
authors.initials: D
authors.lastname: Montoro
authors.forename: Jeong S
authors.initials: JS
authors.lastname: Hyun
authors.forename: Michael T
authors.initials: MT
authors.lastname: Chung
authors.forename: Derrick C
authors.initials: DC
authors.lastname: Wan
authors.forename: Michael T
authors.initials: MT
authors.lastname: Longaker
mesh_terms: D000818:Animals; D001695:Biology; D003393:Cranial Sutures / Q000196:embryology / Q000254:growth & development / Q000502:physiology*; D003398:Craniosynostoses / Q000209:etiology; D004195:Disease Models, Animal; D036341:Intercellular Signaling Peptides and Proteins / Q000502:physiology; D023421:Models, Animal; D015398:Signal Transduction / Q000502:physiology
chemical_list: D036341:Intercellular Signaling Peptides and Proteins