Mandibular growth retardation as a cause of cleft palate in mice homozygous for the chondrodysplasia gene

Abstract

Defective chondrogenesis in C57BL mice homozygous for the chondrodysplasia gene leads to deformity of limbs, ribs, trachea, mandible and palate. Since formation of the secondary palate depends upon coordinated development of several craniofacial structures, the presence of micrognathia and cleft palate in cho/cho newborn mice suggested a cause-and-effect relation between these two deformities. To determine whether or not lower jaw shortening coincided with the time of palate closure, heads from mutant and control littermates previously rated morphologically were examined in median sagittal section. Of six parameters analyzed, growth rates for mutant mandible and anterior vertical dimension were significantly less than those of controls from the beginning of control palate closure. Since there is evidence that intrinsic shelf force is normal, these observations suggested that, during palatogenesis, growth retardation of Meckel’s cartilage did not allow forward displacement of the tongue, and that the consequent failure to straighten the tongue impaired shelf movement. The data support the concept that growth of Meckel’s cartilage is necessary for normal palate formation.