Submitted to: Plastic and Reconstructive Surgery
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 4/19/2007
Publication Date: 4/1/2008
Citation: Weinzweig, J., Panter, K.E., Patel, J., Smith, D.M., Spangenberger, A., Freeman, B. 2008. The Fetal Cleft palate: V. Elucidation of the Mechanism of Palatal Clefting in the Congenital Caprine Model. Plastic and Reconstructive Surgery, pp.1328-1334
Interpretive Summary: Cleft palate is part of a group of congenital anomalies produced by various poisonous plants containing toxins that cause contracture type birth defects. A Spanish goat model was developed to study the mechanism of action and determine the fetoxic effects of these plants. It was determined that fetal movement was inhibited and when this occurred during the time of palatal shelf closure, days 32-41 of gestation, a high incidence of cleft palate resulted. This cleft palate goat model has been utilized over the last decade to study the human anomaly and develop new techniques and procedures to improved treatment of cleft palate in children.
Technical Abstract: Maternal ingestion of Nicotiana glauca from gestation days 32 through 41 results in a high incidence of cleft palate in Spanish goats. This caprine cleft palate model was used to evaluate the temporal sequence of palatal shelf fusion throughout the period of cleft induction with the poisonous plant, Nicotiana glauca. In normal goats palatal fusion is complete by gestation day 40. Using this model the "fetal movement theory" of cleft palate induction was postulated and demonstrated. Reduced fetal movement in the congenital caprine model results in neck hyperflexion causing the tongue to act as a mechanical obstruction to palatal shelf fusion resulting in a permanent cleft palate.