Functional anatomy of cranial synostosis.
An understanding of how sutural growth processes relate to the totality of cranial growth is necessary to cure the cause and not just the symptoms of cranial synostosis. There is no direct genetic determination for the origin, growth, size, shape or maintenance of bones. Rather, phenotypic expression of skeletal tissues is regulated via genetic information encoded in the cells of functional matrices. The primary morphogenetic event in neurocranial growth is the volumetric expansion of the neural mass, which causes the surrounding neurocranial capsule to expand. Calvarial bones arise at widely separated ossification centers and spread centrifugally towards each other. Premature synostosis of the human metopic suture was noted as a frequent characteristic of the cleft-palate skull. Primary morphological event associated with premature synostosis was a cranial base malformation. Cranial sutures permit passage of the neonatal head through the birth canal, permit slight relative variations between adjacent bones while keeping these same bones relatively approximated. All morphological attributes of carnial bones and of their sutures are extrinsically determined and regulated, including both the normal and premature synostosis of the cranial sutures. It seems reasonable to the author that premature synostosis originates in the early embryonic prosencephalic head organizer, which makes it developmentally understandable.
D000818:Animals; D003398:Craniosynostoses / Q000503:physiopathology*; D051381:Rats; D012886:Skull / Q000254:growth & development*