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 beta 1 (TGF beta 1), interleukin-1 beta (IL-1 beta), 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 TGF beta 1, IL-1 beta, 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 (mu(0)), equilibrium friction coefficient (mu(eq)), and Young's modulus (E-Y) were determined from the temporal load data. Results. IL-1 beta and OSM decreased tissue glycosaminoglycan (GAG) content by similar to 20% over 48 hours and decreased E-Y to a similar extent (11-17%), but TGF beta did not alter GAG content or E-Y. Alterations in proteoglycan content corresponded to changes in mu(0), but endogenous lubricin decreased boundary mode mu(eq). The addition of exogenous lubricin, either localized at the tissue surface or in the lubricating solution, did not modulate mu(0), but it did lower mu(eq) 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.