Traumatic injury to a joint is known to increase the risk for the developme
nt of secondary osteoarthritis, but it is unclear how this process occurs.
The existence of such a discrete event that can lead to an increased risk o
f osteoarthritis has spurred interest in developing in vitro models of trau
matic joint injury. The current authors review some of the recent insights
gained from these model systems into the pathogenesis of osteoarthritis, in
cluding the evidence for an initial, irreversible insult to chondrocytes du
ring mechanical injury, the occurrence of apoptotic chondrocyte death, and
attempts to identify the effects of trauma on chondrocyte metabolic respons
e. Results also are presented from the authors' ongoing studies of the degr
adative pathways initiated by traumatic mechanical loads, the mechanism by
which chondrocytes are affected during compression, and possible contributi
ons of the joint capsule to posttraumatic cartilage degradation.