The studies reported in this thesis aim to validate a theoretical prediction of the mechanisms that maintain a low friction coefficient of articular cartilage for long periods of time.

It has been demonstrated that pressurization of the interstitial fluid is the mechanism that regulates the time-dependent response of the friction coefficient in articular cartilage. It is believed that in vivo the friction coefficient does not reach high values, and a theoretical model has been proposed.

The first study presented in this thesis validated the prediction that interstitial fluid pressurization is the mechanism that can maintain a low friction coefficient in articular cartilage for a long period of time. The Peclet number Pe = Vb / H_+Ak = is the dimensionless ratio of the speed of articular surfaces to the diffusive velocity of the fluid inside the cartilage. The experiments verified that when Pe«1 the fluid under the contact area does not have time to escape, and with most of the load supported by the pressurized interstitial fluid, only a small fraction would be transferred via collagen-against-collagen contact, thus producing a very small frictional force for as long as the interstitial fluid pressure remains elevated. When Pe«1 the fluid escapes from underneath the contact area, the interstitial fluid pressure subsides, and the friction force rises considerably, as all of the contact load becomes supported by collagen-against-collagen contact.

The second study showed that interstitial fluid pressurization can be up to 60 times more effective than boundary lubrication by synovial fluid at keeping the friction coefficient low in healthy and arthritic synovial joints. This result further validated the mathematical model where Pe is dependent on the product of aggregate modulus, which decreases in arthritic cartilage, and permeability, which increases in arthritic cartilage, possibly keeping the product constant.

In the third study, it was established that the effectiveness of a proprietary compound, meant to be injected intra-articularly to ease the effect of arthritis, was not effective in vivo since it could only maintain a low friction coefficient when the effect of fluid pressurization was not present.

The fourth study presented evidence that fluid pressurization and wear are inversely proportional. High pressurization of the interstitial fluid will maintain low friction and cause low wear;​ however, when the interstitial fluid pressure subsided and the friction was raised to higher values, the wear increased substantially.