Craniofacial growth during human secondary palate formation and potential relevance of experimental cleft palate observations.

Although formation of the secondary palate is known to involve a complex sequence of developmental events, current concepts of palatal clefting emphasize alterations in the palatal shelves. The objective of this study was to identify similarities in facial growth and palatal formation in man and in rodent experimental models and to examine mechanisms of experimentally induced cleft palate that might be relevant to human clefting. Morphometric analyses of facial growth changes reveal similar patterns of mandibular prominence, head extension, and increased oronasal cavity vertical dimension during secondary palate development, with more pronounced changes in the human. Experimental studies of induced cleft palate in rats and mice show that interference with growth changes can contribute to cleft palate. Failure of palatal shelves to make contact, often associated with delayed horizontal movement, has been observed with increased tongue obstruction secondarily to mandibular retrognathia after either growth inhibition in Meckel's cartilage or morphologic deformation of Meckel's cartilage. In other experiments, failure of adequate shelf contact has been observed with reduced shelf growth or with altered craniofacial relations associated with abnormally flexed head posture resulting from fetal growth abnormalities or oligohydramnios. The results of these studies show that the etiology of cleft palate malformation can be related to interference with a number of different development events not immediately in the palatal shelves. Similar alterations of craniofacial growth that affect the palate secondarily appear to be associated with etiology of cleft palate in human syndromes such as Pierre Robin syndrome and the oligohydramnios syndrome.