Propagation of surface fissures in articular cartilage in response to cyclic loading in vitro

Mechanical overloading of synovial joints can damage the articular cartilage surface and may lead to osteoarthritis. However, causal links between mechanical and biological events in cartilage are poorly understood.

To test the hypothesis that surface fissures in cartilage can propagate mechanically if the joint surface is subjected to vigorous cyclic loading.

Thirty-five cartilage-on-bone specimens, 15-mm square, were removed from mature bovine knee and shoulder joints. Specimens were loaded by means of a 9-mm-diameter flat indenter with a beveled edge, and their compressive strength determined. Failure occurred in the cartilage surface at an average stress of 36 MPa. Cartilage fissures were marked with Indian ink, photographed, and their length and width measured using image analysis software. Each damaged specimen was subjected to cyclic loading at 40% of its compressive strength, at 0.5 Hz, for up to 5 h. Fissure length and width were measured at regular intervals. After testing, fissure depth was measured from histological sections, and compared with measurements from damaged cartilage which was not cyclically loaded.

Cyclic loading caused cartilage fissures to increase in length (mean 353%, P<0.01) and width (360%, P<0.01) but not depth. Propagation was rapid at first, but approached equilibrium after several hundred cycles. Rehydration in saline had no effect on fissure length, but width returned to pre-cyclic loading values.

Cartilage fissures can propagate mechanically when a joint surface is subjected to cyclic compressive loading in vitro. The transient opening-up of fissures to form wide surface "wounds" during cyclic loading could be of biological significance if it occurred in living people.

In living joints, wide open fissures in the cartilage surface could promote degenerative changes in the tissue.