Alteration of articular cartilage frictional properties by transforming growth factor β, interleukin-1β, and oncostatin M

Objective To evaluate the functional effects of transforming growth factor β1 (TGFβ1), interleukin-1β (IL-1β), and oncostatin M (OSM) on the frictional properties of articular cartilage and to determine the role of cytokine-mediated changes in cartilage frictional properties by extracting and redepositing lubricin on the surface of cartilage explants. Methods Neonatal bovine cartilage explants were cultured in the presence or absence of 10 ng/ml of TGFβ1, IL-1β, or OSM over 48 hours. Boundary lubrication tests were conducted to determine the effects of endogenously produced surface localized lubricin and of exogenous lubricin at the tissue surface and in the lubricant solution. The initial friction coefficient (μ0), equilibrium friction coefficient (μeq), and Young's modulus (EY) were determined from the temporal load data. Results IL-1β and OSM decreased tissue glycosaminoglycan (GAG) content by ∼20% over 48 hours and decreased EY to a similar extent (11–17%), but TGFβ did not alter GAG content or EY. Alterations in proteoglycan content corresponded to changes in μ0, but endogenous lubricin decreased boundary mode μeq. The addition of exogenous lubricin, either localized at the tissue surface or in the lubricating solution, did not modulate μ0, but it did lower μeq in cytokine-treated cartilage. Conclusion This study provides new insight into the functional consequences of cytokine-mediated changes in friction coefficient. In combination with established pathways of cytokine-mediated lubricin metabolism, these data provide evidence of distinct biochemical origins of boundary and biphasic pressure-mediated lubrication mechanisms in cartilage, with boundary lubrication regulated by surface accumulation of lubricants and biphasic lubrication controlled by factors such as GAG content that affect water movement through the tissue.