Interactions Between Bilayers of Phospholipids Mixture Extracted from Human Osteoarthritic Synovial Fluid

TL;DR

This study investigates how lipid bilayers derived from osteoarthritic synovial fluid interact and influence joint lubrication, revealing effects of lipid heterogeneity and calcium ions on friction and potential cartilage wear.

Contribution

It provides new insights into the behavior of boundary lipid layers from osteoarthritic fluid and their role in joint lubrication and degradation.

Findings

Lipid vesicles spontaneously rupture to form bilayers on negatively charged surfaces.

Friction coefficients are approximately 0.03 for hemi-fused bilayers, indicating residual hydration lubrication.

Calcium ions increase friction to about 0.2, possibly due to calcium-bridging effects.

Abstract

Duncan Dowson, whom this issue commemorates, was a world leader in the field of biotribology, with prolific contributions both in fluid-based and boundary lubrication of biological tissues, in particular articular cartilage, a central issue in biotribology due to its importance for joint homeostasis. Here we explore further the issue of cartilage boundary lubrication, which has been attributed to phospholipid (PL)-exposing layers at the cartilage surface in part. A surface force balance (SFB) with unique sensitivity is used to investigate the normal and frictional interactions of the boundary layers formed by PLs extracted from osteoarthritic (OA) human synovial fluid (hSF). Our results reveal that vesicles of the OA-hSF lipids rupture spontaneously to form bilayers on the mica substrate (which, like the in-vivo articular cartilage surface in synovial joints, is negatively-charged) which then undergo hemifusion at quite low pressures in the SFB, attributed to the large heterogeneity of the hSF lipids. Nanometric friction measurements reveal friction coefficients mu = ca. 0.03 across the hemi-fused bilayer of these lipids, indicating residual hydration lubrication at the lipid-headgroup vs. substrate interface. Addition of calcium ions causes an increase in friction to mu = ca. 0.2, attributed either to calcium-bridging attraction of lipid headgroups to the negatively-charged substrate, or a shift of the slip plane to the more dissipative hydrophobic-tail vs. hydrophobic-tail interface. Our results suggest that the heterogeneity and composition of the OA-hSF lipids may be associated with higher friction at the cartilage boundary layers, and thus a connection with greater wear and degradation, due to hemifusion of the exposed lipid bilayers.