Adaptive mechanically controlled lubrication mechanism found in articular joints

Abstract

Articular cartilage is a highly efficacious water-based tribological system that is optimized to provide low friction and wear protection at both low and high loads (pressures) and sliding velocities that must last over a lifetime. Although many different lubrication mechanisms have been proposed, it is becoming increasingly apparent that the tribological performance of cartilage cannot be attributed to a single mechanism acting alone but on the synergistic action of multiple "modes" of lubrication that are adapted to provide optimum lubrication as the normal loads, shear stresses, and rates change. Hyaluronic acid (HA) is abundant in cartilage and synovial fluid and widely thought to play a principal role in joint lubrication although this role remains unclear. HA is also known to complex readily with the glycoprotein lubricin (LUB) to form a cross-linked network that has also been shown to be critical to the wear prevention mechanism of joints. Friction experiments on porcine cartilage using the surface forces apparatus, and enzymatic digestion, reveal an "adaptive" role for an HA-LUB complex whereby, under compression, nominally free HA diffusing out of the cartilage becomes mechanically, i.e., physically, trapped at the interface by the increasingly constricted collagen pore network. The mechanically trapped HA-LUB complex now acts as an effective (chemically bound) "boundary lubricant"--reducing the friction force slightly but, more importantly, eliminating wear damage to the rubbing/shearing surfaces. This paper focuses on the contribution of HA in cartilage lubrication; however, the system as a whole requires both HA and LUB to function optimally under all conditions.

Fig. 1.

The effect of HA digestion on the friction force between cartilage and glass in PBS. Step-load experiment showing how the friction force, F, and the friction coefficient, μ, changes with time, t, and following the in situ digestion of HA under a normal load of 170 mN, sliding velocity of approximately 50 μm/s, and peak-to-peak sliding amplitude of approximately 500 μm. The solid line at the top is the average friction coefficient of grafted HA gel on mica surfaces under similar load and shear conditions reported in ref. , shown for comparison. Solid lines indicate equilibrium values.

Fig. 2.

Normal load, L, and friction force, F, as a function of time, t, for cartilage samples measured before and after digestion of HA under low (A) and high (B) dynamically applied normal loads.

Fig. 3.

(A) The effect of the load on the change in friction force, ΔF = (F_{max ,undigested-}F_{max ,digested})/F_{max ,undigested}, and observed sliding behavior. (A, Inset) The sliding behavior of the cartilage before digestion. (B, Inset) Normal load, L, and friction force, F, before and after HA digestion in a cartilage sample under a normal load of approximately 12 mN. Before digestion, the cartilage exhibits stick–slip behavior and high friction force but little evidence of surface wear or damage. After HA digestion, stick–slip behavior disappears and the friction force decreases, but frequent “wear spikes” (darts) indicate significant wear and damage.

Fig. 4.

Schematic illustration of the HA “mechanical trapping? mechanism. (A) The pore structure of cartilage is formed by counter spiraling collagen fibril coils (blue and green). When undeformed, the lateral pores (void space between fibril “coils”) are open and the entangled HA molecules (yellow), with attached Aggrecans (red) are nominally “free.” (B) In compression, fibril realignment mechanically traps (white arrows) the HA/Aggrecan complexes in the collapsing lateral pores, maintaining a layer of immobilized HA between the collagen and top surface. (C and D) Schematic representation of HA trapping mechanism in the cartilage contact during physiological sliding under low (C) and high (D) loads. For clarity, only the HA-LUB layer from the lower surface was shown.