Osteoarthritis is the most common disabling condition of man in the Western world. Biologically, osteoarthritis implies the (symptomatic) degeneration of the whole joint with many structures involved such as subchondral bone and the periarticular soft tissues. Still, the degeneration of the articular cartilage appears to be the focus of the structural changes taking place during the osteoarthritic disease process.
Cartilage degeneration implies mostly a failure of the extracellular matrix of the articular cartilage. The matrix represents the functional component responsible for the biomechanical integrity of the tissue. Thus, many studies over decades in osteoarthritis and cartilage research have focused on the understanding of degenerative or degradative processes taking place within the matrix. This has led to significant continuous advances in our understanding of the biochemistry and pathobiochemistry of molecules and their assembly within the cartilage matrix.
The cells of the tissue, which do not exert per se structural functions within the tissue, were considered largely responsible for the proper matrix turnover. They were thought to react to external mediators and biomechanical stimuli or assaults and to be more or less able to compensate for continuous (bio)mechanical tissue destruction. More recently, however, besides matrix (patho)biochemistry, the cellular phenotype during the disease process has come more and more into the focus of interest. This was induced on the one hand by upcoming (molecular) technology, but also by increasing evidence that also the cells degenerate per se. Osteoarthritic chondrocytes are not only no longer able to compensate for matrix degeneration, but themselves are (co)initiators and (co)promoters of the disease process.