Dr. Pavlin's academic activities include the functions of program director for Orthodontic Residency and the director of Orthodontic Clinic. He is the course director of several graduate courses at UT Health San Antonio and a lecturer in other didactic and clinical courses in our predoctoral program. He is also directing a laboratory involved in research projects in the area of bone biology, and he serves as a reviewer for several basic science and clinical journals.
Regulation of genes for bone cell (osteoblast) markers
The primary research interest in Dr. Pavlin's laboratory is in regulation of genes for bone cell (osteoblast) markers. In particular, the focus is on molecular mechanisms involved in mechanically-induced regulation of bone cell markers, including the type I collagen, osteocalcin, alkaline phosphatase, bone morphogenetic proteins and homeobox-containing genes. For these studies, his group has developed an animal model in which the pattern of gene expression is monitored in subsets of periodontal cells within mechanically stimulated periodontium of transgenic mice. This model system allows for monitoring of a temporal pattern of expression of osteoblast markers in vivo, with a long term goal of mapping the regions within the type I collagen and osteocalcin promoters involved in the process of transduction of an external mechanical signal into a gene regulatory event (mechanotransduction). His laboratory is also utilizing a cell culture model of immortalized bone cell lines from transgenic mice subject to different components of mechanical stress. These cell lines are supplementing the transgenic mouse model and allow for examination of the effects of single components of mechanical stress, i.e. the unilateral strain, hydrostatic pressure and fluid shear stress, on regulation of osteoblast-specific genes. Supplementing the animal model with cloned cell lines facilitates characterization of regulatory mechanisms involved in mechanotransduction in bone, which are essential for the process of bone remodeling in physiological conditions and in bone disease.