This research looked specifically at a gene called TBX22 that regulates important development events during normal palate formation. When defective this gene causes cleft palate, mainly in boys and can also be associated with tongue tie. Studying the effect of this gene in mice has provided significant insights as it closely mimics human palate closure. The palate of a mouse is similar to the human palate although it is not known yet if mice use the same muscles for communication as humans do.

Organ culture allows palate development to be followed in vivo. The image (above) shows the head of a cultured mouse embryo with the lower jaw removed to expose the palate. Here the rudimentary palatal shelves are still separated prior to closure. Within 48 hours of culture, the palatal shelves will converge and fuse to form the secondary palate.

The CLEFT funded study has shown that in mice with clefts, the closure of the palate can be potentially modified or augmented by growth factors or stem cells. If muscle stem cells are added to patients, it could possibly be useful in conditions such 22q11.2 Deletion Syndrome where palate muscles are less well developed.

Overall, the potential benefit for patients is the possible identification of the causes of cleft palate as well as the possible prevention.