Fig 1.
A classical Stribeck curve (dotted line) maps the transition of friction from high (boundary) friction to low (hydrodynamic) friction.
For soft, permeable contacts like articular cartilage, a divergence from the classical curve is described by an elastoviscous transition [26] where contact compliance and permeability hinder the transition to hydrodynamic lubrication.
Fig 2.
Presentation of friction coefficient as a function of the Sommerfeld number reveals viscous lubrication by HA.
(Top) Friction coefficient as a function of sliding speed for three different lubricants with a wide range of viscosities provided a range of friction coefficients that span almost an order of magnitude (n = 5). (Middle) When the friction coefficients from the top panel are presented as a function of the Sommerfeld number (Eq 1) instead of sliding speed, the mechanisms of lubrication become apparent and are fit to a model curve (Eq 2) to determine alterations of the elastoviscous transition. (Bottom) Serial dilutions of the HA solution provided overlapping data sets confirming HA had no influence on the boundary friction coefficient, and increased load (4.2, 5.2, and 6.2 N; all at 0.1 mm/s) and decreased concentration (2 mg/ml) tests with HYADD4 revealed convergence of HA and HYADD4 in the transition region (HYADD4 2 mg/ml and high load, n = 4, all others n = 5) (data points represent mean±SEM).
Fig 3.
(A) Altering the presence of lubricin at the articular surface and in the lubricant solution revealed distinct elastoviscous transition curves. (B-D) The curve fit parameters revealed the importance of lubricin in boundary lubrication and also its importance in facilitating the transition away from boundary mode lubrication when present with HA. (E-H) Replication of the HA curves by dextran revealed that both the viscous lubrication by HA and the synergy with lubricin are not specific to the chemistry of HA. (n = 5 for unaltered, n = 3 for lubricin removed and lubricin in solution; data points represent mean±SEM).
Fig 4.
In native cartilage, lubricin bound to the surface facilitates HA aggregation near the surface (A). Lubricin likely entraps HA through entanglements, causing a local increase in viscosity near the tissue surface (A, inset). When lubricin is removed from the surface, HA does not aggregate (B) and surface viscosity is likely similar to the bulk (B, inset). Boundary lubrication by lubricin shifts the boundary regime down and increased viscosity near the surface shifts the elastoviscous transition such that the low friction regime occurs at lower sliding speeds consistent with viscous boundary lubrication (C). These phenomena of lubricin and HA replicate the lubrication by synovial fluid which transition to low friction at low speeds. By treating synovial fluid with hyaluronidase, friction is shifted back towards the boundary mode plateau as the fluid viscosity decreases, and trypsin treatment disrupts the synergy between lubricin and HA by digesting lubricin (n = 4; data points represent mean±SEM).