This study tests the hypothesis that the natural progression of osteoarthritis (OA) in human joints leads to an increase in the friction coefficient. This hypothesis is based on the expectation that the wear observed in OA may be exacerbated by higher friction coefficients. A corollary hypothesis is that healthy synovial fluid (SF) may help mitigate the increase in the friction coefficient in diseased joints.
The friction coefficient of human tibiofemoral joints with varying degrees of OA was measured in healthy bovine SF and physiological buffered saline (PBS). Two testing configurations were adopted, one that promotes sustained cartilage interstitial fluid pressurization to investigate the effectiveness of this mechanism with advancing OA, and another that allows interstitial fluid pressure to subside to investigate the effectiveness of boundary lubrication.
Seven specimens were visually staged to be normal or mildly degenerated (stages< or =2 on a scale of 1 to 4) and nine others had progressive degeneration (stages>2 and< or =3). No statistical differences were found in the friction coefficient with increasing OA, whether in migrating or stationary contact area configurations; however, the friction coefficient was significantly lower in SF than PBS in both configurations.
The friction coefficient of human tibiofemoral cartilage does not necessarily increase with naturally increasing OA, for visual stages ranging from 1 to 3. This outcome may be explained by the fact that interstitial fluid pressurization is not necessarily defeated by advancing degeneration. This study also demonstrates that healthy SF decreases the friction coefficient of OA joints relative to PBS.