An in vitro study of cartilage-meniscus tribology to understand the changes caused by a meniscus implant.

Active lifestyles increase the risk of meniscal injury. A permanent meniscus implant of polycarbonate urethane (PCU) is a promising treatment to postpone/prevent total knee arthroplasty. Study of the changes in articular cartilage tribology in the presence of PCU is essential in developing the optimum meniscus implant. Therefore, a cartilage-meniscus reciprocating, sliding model was developed in vitro, mimicking the stance and swing phases of the gait cycle. The meniscus was further replaced with PCU and surface-modified PCUs (with C18 chains, mono-functional polydimethylsiloxane groups and mono-functional polytetrafluoroethylene groups) to study the changes. The coefficient of friction (COF) was calculated, and cartilage wear was determined and quantified histologically. The cartilage-meniscus sliding resulted in low COF during both stance and swing (0.01< COF <0.12) and low wear of cartilage (scores <1). The cartilage-PCU sliding, during stance, revealed similar low COFs. But during swing, the COFs were high (average ∼1, maximum 1.6), indicating a breakdown in interstitial fluid pressurization lubrication and non-effective activation of the boundary lubrication. This may lead to wear of cartilage in long term. However, under the tested conditions the wear of cartilage against PCUs was not higher than its wear against meniscus, and the cartilage was occasionally damaged. The COF decreased with increasing the contact pressure (as-per a power equation) up to 1MPa. The changes in the surface modification of PCU did not affect PCU's tribological performance.

Both hyaluronan and collagen type II keep proteoglycan 4 (lubricin) at the cartilage surface in a condition that provides low friction during boundary lubrication.

Wear resistant and ultralow friction in synovial joints is the outcome of a sophisticated synergy between the major macromolecules of the synovial fluid, e.g., hyaluronan (HA) and proteoglycan 4 (PRG4), with collagen type II fibrils and other non-collagenous macromolecules of the cartilage superficial zone (SZ). This study aimed at better understanding the mechanism of PRG4 localization at the cartilage surface. We show direct interactions between surface bound HA and freely floating PRG4 using the quartz crystal microbalance with dissipation (QCM-D). Freely floating PRG4 was also shown to bind with surface bound collagen type II fibrils. Albumin, the most abundant protein of the synovial fluid, effectively blocked the adsorption of PRG4 with HA, through interaction with C and N terminals on PRG4, but not that of PRG4 with collagen type II fibrils. The above results indicate that collagen type II fibrils strongly contribute in keeping PRG4 in the SZ during cartilage articulation in situ. Furthermore, PRG4 molecules adsorbed very well on mimicked SZ of absorbed HA molecules with entangled collagen type II fibrils and albumin was not able to block this interaction. In this last condition PRG4 adsorption resulted in a coefficient of friction (COF) of the same order of magnitude as the COF of natural cartilage, measured with an atomic force microscope in lateral mode.