Abstract
Fibronectin is an essential component of the extracellular matrix. The role of fibronectin in craniofacial surgery has not been previously reviewed. Fibronectin mediates bone differentiation and development of the skull. Studies have shown that normal development of the skull requires a specific pattern of expression around the epithelial-mesenchymal interface of the neurocranium. Fibronectin is also essential in mediating the migration of neural crest cells to form the facial skeleton. The calvaria of patients with Apert and Crouzon syndromes have an abnormally elevated collagen level. However, fibronectin levels are elevated in the former syndrome and decreased in the latter syndrome. The significance of this requires further research. Fibronectin gene expression is increased in port wine-derived fibroblasts in patients with Sturge-Weber syndrome. Normal palatogenesis also requires a specific pattern of expression of fibronectin around the maxillary process as well as the roof of the stomodeum, and several studies have linked the development of cleft lip/palate to an imbalance of fibronectin content of the extracellular matrix. Fibronectin mediates cell-to-cell attachment during repair of calvarial defects; hence, fibronectin has been used as a carrier for bone morphogenetic proteins to treat calvarial defects. Finally, fibronectin is now an essential component in stem cell technology related to craniofacial surgery.