The Role of Hyaluronic Acid in Cartilage Boundary Lubrication.

Weifeng Lin,Jacob Klein,Nir Kampf,Zhang Liu

doi:10.3390/cells9071606

Weifeng Lin, Jacob Klein + Show 2 more

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https://doi.org/10.3390/cells9071606

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Abstract

Hydration lubrication has emerged as a new paradigm for lubrication in aqueous and biological media, accounting especially for the extremely low friction (friction coefficients down to 0.001) of articular cartilage lubrication in joints. Among the ensemble of molecules acting in the joint, phosphatidylcholine (PC) lipids have been proposed as the key molecules forming, in a complex with other molecules including hyaluronic acid (HA), a robust layer on the outer surface of the cartilage. HA, ubiquitous in synovial joints, is not in itself a good boundary lubricant, but binds the PC lipids at the cartilage surface; these, in turn, massively reduce the friction via hydration lubrication at their exposed, highly hydrated phosphocholine headgroups. An important unresolved issue in this scenario is why the free HA molecules in the synovial fluid do not suppress the lubricity by adsorbing simultaneously to the opposing lipid layers, i.e., forming an adhesive, dissipative bridge between them, as they slide past each other during joint articulation. To address this question, we directly examined the friction between two hydrogenated soy PC (HSPC) lipid layers (in the form of liposomes) immersed in HA solution or two palmitoyl–oleoyl PC (POPC) lipid layers across HA–POPC solution using a surface force balance (SFB). The results show, clearly and surprisingly, that HA addition does not affect the outstanding lubrication provided by the PC lipid layers. A possible mechanism indicated by our data that may account for this is that multiple lipid layers form on each cartilage surface, so that the slip plane may move from the midplane between the opposing surfaces, which is bridged by the HA, to an HA-free interface within a multilayer, where hydration lubrication is freely active. Another possibility suggested by our model experiments is that lipids in synovial fluid may complex with HA, thereby inhibiting the HA molecules from adhering to the lipids on the cartilage surfaces.

Highlights

IntroductionThe articular cartilage coating bone ends in the major joints exhibits extremely low sliding friction (friction coefficient μ ≈ 0.001 [1,2,3]) under physiologically high pressures (up to 1 × 107 Pa or more [4,5])
The articular cartilage coating bone ends in the major joints exhibits extremely low sliding friction under physiologically high pressures.Both cartilage fluid pressurization [1,6,7] and boundary lubrication [3,8,9,10,11] are responsible for this superior lubricity
We examined the effect on the lubrication by surface-attached PC lipids, in the form of either vesicles or bilayers, of introducing Hyaluronic acid (HA), which is known to interact via charge–dipole forces with such lipids, and so might be expected to form friction-enhancing bridges between the lipid-coated surfaces

Summary

Introduction

The articular cartilage coating bone ends in the major joints exhibits extremely low sliding friction (friction coefficient μ ≈ 0.001 [1,2,3]) under physiologically high pressures (up to 1 × 107 Pa or more [4,5]) Both cartilage fluid pressurization [1,6,7] and boundary lubrication [3,8,9,10,11] are responsible for this superior lubricity. Layers at lipids, thefluids most common in our and abundantgood in cartilage andlubrication synovial fluids [17,18],PC may act as sliding interfaces exhibit extremely efficient lubrication properties

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