Osteochondral allograft transplantation is a useful technique to manage larger articular cartilage injuries. One factor that
may compromise the effectiveness of this procedure is chondrocyte cell death that occurs during the storage, preparation,
and implantation of the osteochondral grafts. Loss of viable chondrocytes may negatively affect osteochondral edge integration
and long-term function. A better understanding of the mechanisms responsible for chondrocyte loss could lead to interventions
designed to decrease cell death and improve results. Recent studies indicate that apoptosis, or programmed cell death, is
responsible for much of the chondrocyte death associated with osteochondral allograft transplantation. Theoretically, some
of these cells can be rescued by blocking important apoptotic mediators. We review the role of apoptosis in cartilage degeneration,
focusing on apoptosis associated with osteochondral transplantation. We also review the pathways thought to be responsible
for regulating chondrocyte apoptosis, as well as experiments testing inhibitors of the apoptotic pathway. These data suggest
that key contributors to the apoptotic process can be manipulated to enhance chondrocyte survival. This knowledge may lead
to better surgical outcomes for osteochondral transplantation.
This research was performed at the San Francisco VA Medical Center.
One or more of the authors (HTK) has received funding from the Musculoskeletal Transplant Foundation, the Orthopaedic Research
and Education Foundation, VA Medical Research, and the University of California, San Francisco.
Each author certifies that his or her institution has approved the animal protocol for this investigation and that all investigations
were conducted in conformity with ethical principles of research.