Relation of mandible growth to palate closure in mice

The role of mandible growth in normal palate closure and the effects on the mandible of three teratogens‐—cortisone, 6‐aminonicotinamide (6‐AN), and hypervitaminosis A — during palate closure in A/J (susceptible to cleft palate induction by these teratogens) and in C57BL (resistant) inbred strains of mice were investigated. The rate of mandible growth in the control embryos of the two strains was similar during the period of palate closure. Mandible length in A/Js was greater than that in C57BLs at the initial stage of palate closure and this remained true when it was adjusted for palate stage and for body weight. The mandibles were not shortened at the beginning of palate closure by any of the teratogens in either strain. In the cortisone‐treated groups the mandibles of C57BL embryos were consistently longer than those of controls whereas the mandibles of A/J embryos did not differ from those of control embryos at comparable body weights. It is concluded that cortisone, 6‐aminonicotinamide, and hypervitaminosis‐A do not cause cleft palate by reducing the length of the mandible at palate‐closure time.