SOURCE: New York Group for Plastic Surgery, LLP
TARRYTOWN, NY–(Marketwire – June 30, 2010) – A new study holds promising evidence that monitoring certain molecules during fetal growth may potentially permit doctors to reverse a cleft palate before birth. Published in the journal Development, researchers at the USC School of Dentistry found that an excess of a specific protein resulted in the formation of a cleft palate. “There are exciting developments on the horizon regarding our understanding of cleft palates,” noted plastic surgeon Dr. Tae Ho Kim of the New York Group for Plastic Surgery in Tarrytown, New York. “Breakthroughs like these could one day help us successfully prevent or treat this condition early on in babies,” Kim continued.
Dr. Kim, a craniofacial and pediatric plastic surgeon, has worked for many years treating patients with craniofacial deformities. He restores the natural symmetry and balance of the human face for those born with complex physical deformities. His work is not limited to cleft palates, as he also works with cases of craniosynostoses, hemangiomas, vascular malformations, jaw deformities, burns and traumatic injuries. In addition to his work as the Chief of Craniofacial and Pediatric Plastic Surgery at the Maria Fareri Children’s Hospital and the Westchester Medical Center, Dr. Kim runs an informational website on cleft palates at www.craniofacialhealing.com.
The protein, sonic hedgehog homolog (SHH), which is regulated by two genes, the Msx1 and the Dlx5, must be maintained within a certain level in order for proper palate formation in a fetus. If the protein is not properly balanced, a cleft palate could form. The Msx1 and Dlx5 genes both encourage and discourage the protein’s growth respectively and are needed for the development of the main facial structures, such as the skull, teeth and the palate.
In the study, originating from the School of Dentistry’s Center for Craniofacial Molecular Biology, fetal mice were purposely bred with an Msx1 deficiency, which suppressed SHH protein growth and promoted the formation of cleft palates. However, when the researchers also suppressed the Dlx5 gene, SHH was expressed and the palate experienced a regrowth. After birth, the palates of the mice were intact, with small differences as compared to the palates of healthy mice. The “regulated” palates, however, functioned as normally as the healthy palates.
Dr. Kim states that cleft palates are one of the most common congenital birth defects in humans. They occur in 1 of every 700 newborns, and are seen more in males than females. The treatment is very complex, taking many years before it is completed. Initial repair is done early, with a subsequent repair happening a year later, then about every 2 to 4 years until the age of 16, if necessary. However, these treatments are not without complications, such as problems with eating or speaking.
Dr. Kim is hopeful. “The proper balance of these genes and their influence on the protein is an exciting concept that could have positive implications on this troubling condition,” he said.
Contact:
New York Group for Plastic Surgery, LLP
http://www.nygplasticsurgery.com/
(800) 433-7410
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