Assistant Scientist, Hospital for Special Surgery
Assistant Professor, New York Center for Biomedical Engineering
Visiting Assistant Professor, Department of Biomedical Engineering, City College of New York, City University of New York
Chen C. T., Burton-Wurster N. I., Borden C., Hueffer K., Bloom S. E., and Lust G. (2001) Chondrocyte necrosis and apoptosis in impact damaged articular cartilage. J. Orthopaedic Research 19: 703-711.
Chen C.T., Bhargava M., Lin P. M., and Torzilli P. A. (2003) Time, stress, and location dependent chondrocyte death and collagen damage in cyclically loaded articular cartilage. J. Orthopaedic Research 21:888-898.
Chen C. T., Torzilli P. A., Fishbein K. W., Spencer R. G. S., Hilger A. and Horton W.E., Jr. (2003) Matrix fixed charge density as determined by magnetic resonance microscopy of bioreactor-derived hyaline cartilage correlates with biochemical and biomechanical properties. Arthritis & Rheumatism 48(4):1047-56.
Williams R., McCarthy D., and Chen C.T. (2004) Chondrocyte survival and biomechanical Properties of fresh cold-stored whole femoral condyles: An evaluation of tissue used in osteochondral allograft transplantation. Am J Sports Med. 32:132-9.
Levin, A.S., Chen, CT. and Torzilli, P.A. (2005) Effect of Tissue Maturity on Cell Viability in Mechanically Loaded Articular Cartilage. Osteoarthritis and Cartilage, 13:488-496.
Gulotta L., Rudzki J.R., Kovacevic D., Milentijevic D., Chen C.T.; Williams R. (2009) Chondrocyte Death and Cartilage Degradation Following Autologous Osteochondral Transplantation Surgery in a Rabbit Model. Am J Sports Med 2009; 37(7):1324-33
Torzili PA., Bhargava M, Park S, Chen C.T. (2009) Mechanical Load Inhibits IL-1Induced Matrix Degradation in Articular Cartilage. Osteoarthritis & Cartilage. (In Press)
For more publications, please see the PubMed listing.
My current research is focused on defining the molecular mechanisms by which mechanical load mediates cartilage degradation induced by pro-inflammatory cytokines or trauma injury. Normal joint load is essential for the homeostasis of articular cartilage where an alternation of joint loading due to immobilization or joint instability can often lead to progressive degradation of cartilage matrix. Although many intracellular signaling pathways have been found activated by mechanical force, the molecular mechanisms by which chondrocytes mediated mechanical related homeostasis are not clear. Recently, our and other groups found that mechanical load can counteract cartilage degradation induced by pro-inflammatory cytokines through the inhibition of NF-kB signaling pathway. Since NF-kB pathway is the master pro-inflammatory pathway responsible for the production of aggrecanase and collagenase that cleaves proteoglycan and collagen, the main building components of cartilage, the inhibition of NF-kB pathway suggests that joint loading plays a key role on regulating matrix degradation and cartilage homeostasis. In other words, joint load in daily exercises and activities may help prevent the cartilage degradation in an inflamed joint. Currently, we are focused on defining the key players and regulatory sequences of NF-kB inhibition mediated by mechanical loading. In a related study, we are also studying how mechanical load mediated cartilage degradation after trauma injury, another important risk factor for the progressive degradation of cartilage and the onset of osteoarthritis.