Poster 2: Cell and Tissue Studies

Stephanie Richardson-Solorzano (1), Travis Block (2), and Justin Parreno (1)

1 Department of Biology, University of Delaware; 2 StemBioSys, San Antonio

Articular cartilage is incapable of self-repair. Even small defects to cartilage results in Osteoarthritis progression where eventually total joint replacements would be necessary. Therefore, repairing small focal defects to prevent Osteoarthritis is critical, especially for young patients that injure their cartilage. Autologous Chondrocyte Implantation (ACI) is a gold standard therapy to heal small focal defects. In ACI, a small portion of cartilage is removed from a healthy cartilage site and primary chondrocytes are isolated from donor cartilage. The chondrocytes are then expanded and then reimplanted into the damage joint. Two major issues assoicated with ACI are donor site morbidity and the loss of phenotype during monolayer expansion of chondrocytes. In this study, we attempt to address these issues by investigating the use of another autologous cell source, skin fibroblasts, for ACI. We test the hypothesis that skin fibroblasts can be stimulated to express chondrogenic matrix.
To stimulate chondrogenic expression, we culture embryonic fibroblasts (NIH3T3) on decellularized extracellular matrix. I have determined that short-term exposure stimulates chondrogenic gene expression. Transdifferentiation of fibroblasts into chondrocytes would result in a potential cell source for cartilage repair.

Research Area: Cartilage