All ETDs from UAB

Advisory Committee Chair

Amjad Javed

Advisory Committee Members

Haiyan Chen

Michael McCracken

Somsak Sittitavornwong

Document Type


Date of Award


Degree Name by School

Master of Science (MS) School of Dentistry


The development of the orofacial structure in mammals is a highly ordered process that is coordinated activity of epithelial and mesenchymal cells. Chondrocytes and osteoblasts work in close association for development of many cartilaginous skeletal structures and cartilaginous orofacial structures. Two major orofacial structures are the palate and the temporomandibular joint (TMJ). The transcription factor, Runx2, is obligatory for differentiation of mesenchymal cells into chondrocytes and osteoblasts. However, specific contributions of chondrocyte in cartilaginous and mineralized structures of the craniofacial skeleton are not known. Thus, the objective of this study was to discover the regulatory role of Runx2 in chondrocyte for craniofacial development, palatogenesis, and formation of TMJ. Runx2 floxed mice were used to conditionally ablate Runx2 gene in developing chondrocytes. Cellular, histological, immuno-histochemical and 3D laser scanning microscopy were utilized to evaluate development of craniofacial bone, palate and TMJ. Deletion of Runx2 specifically in chondrocyte results in failed endochondral ossification and death shortly after birth. Surprisingly, sever defects in development of craniofacial elements were observed suggesting interplay between chondrocyte and osteoblast. Skull bones that are derived through endochondral ossification were absent. Intramembranous ossification derived craniofacial bones were developed in Runx2 mutant mice but they were poorly formed. Interestingly, we observed normal tongue and jaw formation in Runx2 mutant animals. However, Runx2 deletion in chondrocyte delayed palatogenesis that was monitored at key transitional time points. At E14 the mutant mice showed a significant gap (40% more space) between the tongue and nasal septum. At E15.5, the wild type was observed to have a normal and well contoured palate. In contrast the mutant palate was flatter and not contoured properly. Moreover the medial epithelial seam (MES) was poorly formed with disorganized cell organization in the mutant. At the new born stage, palate width was significantly decreased and palatal ridges were shallow in the mutant mice. Together, these findings suggest that Runx2 deletion in chondrocyte delayed palatogenesis. Although, chondrocyte arrangement appeared slightly disorganized in the mutant TMJ, formation and maturation appeared to be unaffected throughout its development. Thus, Runx2 exerts differential activity in chondrocyte for development of TMJ, palate and craniofacial bones.

Included in

Dentistry Commons



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