Joint injury results in cartilage lesions that are characterized by a poor
repair response, and such lesions often progress to osteoarthritis. Acute j
oint injury or chronic exposure of cartilage to an abnormal biochemical or
biomechanical environment results in the activation of chondrocytes. This c
hondrocyte response is manifested by enhanced cell proliferation and death,
matrix degradation, and new matrix synthesis. Cytokines are important stim
uli of this chondrocyte activation response and trigger joint inflammation
that can accompany cartilage injury. The presence of cytokines in cartilage
is associated with abnormal extracellular matrix remodeling and loss, ther
efore defining them as a class of targets for therapeutic interventions. In
sight into intracellular signaling mechanisms that are activated by cytokin
es; may provide the basis for pharmacologic interventions that promote cart
ilage repair.