sutures' deposition of bone (with consequent expansion and modeling of the skull) was growth of the underlying brain. This was termed the "functional matrix theory" .
Further work by Persson and others endeavored to clarify the primary locus of craniosynostosis. Persson et al. demonstrated that experimental restriction of a suture's growth produced skull deformities that mimicked craniosynostosis in humans . In addition, cranial base and facial abnormalities appeared to occur in response to the cranial suture restriction . This suggested that craniofacial anomalies were primarily the result of suture fusion - not the cranial base, as Moss had proposed. Marsh and Vannier reported that preexisting cranial base abnormalities resolved after surgery in which only cranial vault alteration was undertaken . Collectively, considerable data have accrued against Moss's stance that suggest, at least in most cases of non-syn-dromic craniosynostosis, that the cranial vault sutures assume a major inciting role in the pathogenesis of craniosynostosis. In states of syndromic craniosynostosis (e.g. Apert or Crouzon syndromes), however, a more generalized pathologic process involving the cranial vault sutures and cranial base may exist.
Work by Opperman and colleagues emphasized the critical influences of mesenchymal tissues, including the dura mater and periosteum, at the suture site in regulating and maintaining suture patency during development [17-18]. Recognition of this dynamic interaction and the existence of factors, including matrix and cytokine influences (fibroblast growth factors (FGF), fibroblast growth factor receptors (FGFR) and transforming growth factor beta (TGF-p), have been instrumental in the refinement of our contemporary molecular understanding of craniosynostosis .
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