The articular cartilage layers coating the major synovial joints such as hips or knees are remarkable constructs. They not only support a wide range of stresses and impacts but, in particular, healthy cartilage surfaces sliding past each other exhibit extremely low levels of friction under physiologically-high pressures. This is a lubricity which no man-made surfaces can emulate. A detailed molecular-level understanding of this could benefit treatments of osteoarthritis (OA), as well as improved prosthetic joint implants, where low friction may suppress wear debris formation and the associated periprosthetic osteolysis. The relation of cartilage friction to OA development is especially intriguing: while traditionally OA was considered a 'wear and tear' disease, there is increasing evidence that protease production by chondrocytes within the cartilage in response to shear stresses may play an important role in the cartilage degradation and progress of OA. Since such shear stresses are a direct consequence of friction on the articulating cartilage surface, it is clear that insight into 'how nature does it' would be of considerable value in manipulating the friction. But despite decades of study, such understanding remains elusive. Any insight must, first and foremost, be able to account for the low friction (CoF down to ca. 0.001) at the high pressures (which can reach 100 atm or higher) of the joints. Hydrodynamic effects have been considered as a lubrication mechanism, but it is likely that a mixed regime including both fluid-film and boundary lubrication operates, and the crucial issue concerns the nature of the boundary layer at the cartilage surface. Three quite different components of articular cartilage and of the synovial fluid surrounding it have each, separately, been widely invoked as the boundary molecule responsible for the remarkable lubrication of joints: Hyaluronan (HA), a linear polysaccharide; lubricin a proteoglycan; and phospholipids. Direct measurements, however, indicate that none of these can, by itself, explain the low friction of the cartilage surface at the high pressures characteristic of the major joints. Over the past decade, hydration lubrication has emerged as a new paradigm for extreme lubrication in aqueous systems, which may underlie also the very efficient boundary lubrication of cartilage. According to this, the hydration shells formed by dipolar water molecules about charges in water (such as ions or zwitterions) may be very tenaciously attached, so that they resist being squeezed out even under large pressures. At the same time, these same hydration shells may behave very fluidly under shear. This resistance to pressure together with low-friction sliding makes them into excellent lubrication elements. Very recently, we discovered that HA which is attached to a surface - to resemble its configuration at the outer cartilage surface - may complex with phosphatidylcholines (PCs), lipids that are ubiquitous in synovial joints, to form robust boundary layers. These layers act synergistically to provide the very low friction (mz0.001) characteristic of cartilage, at the highest physiological pressures, and contrast with surface- attached HA on its own, which leads to considerably higher friction. The very low friction is ultimately due to the phosphocholine groups exposed by the HA/PC surface complexes; these groups are known to be strongly and highly-hydrated, and so they lubricate via the mechanism described above. Our results thus point to a scenario where HA, PCs and lubricin, each with a very different role, act together synergistically to reduce friction of cartilage in articulating joints. Hyaluronan, anchored at the outer surface of articular cartilage by lubricin molecules (which are known to be present in the outer superficial zone), complexes with joint phosphatidylcholines to provide the extreme boundary lubrication of synovial joints via the hydration-lubrication mechanism.
Klein, J. (2015). Joint lubrication: How does nature do it? Osteoarthritis and Cartilage, 23, A17. https://doi.org/10.1016/j.joca.2015.02.031