Steven L Goudy, MD
Director, Division of Pediatric Otolaryngology
Emory University School of Medicine
Cleft and craniofacial disorders are my primary clinical and basic research interests. Even though the surgical repair of cleft lip and palate is highly effective, patients will continue to be faced with ongoing medical, dental, and surgical care. Surgical outcomes can be variable, and the patient's facial growth and development is primarily the result of their genetic composition. Therefore, much of my research focuses on the problems that can develop during the years that follow surgery.
Underdevelopment of the upper jaw is one of the main sequelae of cleft palate repair and causes maxillary hypoplasia. To uncover why this happens, I have assembled a team of collaborators that includes Drs. Nick Willett (Emory Department of Orthopedics), Gregory Gibson (Center for Integrative Genomics, Georgia Institute of Technology), and Michael Davis (Coulter Department of Biomedical Engineering at Georgia Tech and Emory University), all of whom are experts in the fields of bone and vascular biology. Our goal is to determine how cell autonomous and non-cell autonomous Jagged1 signaling during maxillary development contributes to final maxillary formation.
I worked closely with Dr. Joey Barnett of the Department of Pharmacology at Vanderbilt while I was there, and he will continue to be my senior advisor as I evaluate the integration of Jagged1 and TgfßR3 signaling during maxillary mesenchymal cell differentiation and ossification.
With assistance from Drs. Scott Boden (Emory Department of Orthopedics), Roberto Pacifici (Emory Department of Medicine), and Bob Taylor (Emory Department of Medicine), I am examining how intramembranous ossification of the maxillary and palatine bones contributes to later maxillary morphology. Dr. Greg Gibson (Director of the Center for Integrative Genomics, Georgia Tech) will help plan, execute, and analyze the RNA-seq data to identify the targets of Jagged1 signaling. We have already published our observations involving the bony phenotype and our conclusion that Wnt1-Cre;Jagged1 F/F mice are a viable model of post-natal maxillary hypoplasia. Once we have a wider understanding of maxillary development, we plan on developing targeted therapies for future in vitro and in vivo correction of maxillary hypoplasia in the Jag1CKO mice