Influence of Compressive Force and IL-1β on Metabolism of the Extracellular Matrix in Human Chondrocytes

Both mechanical stress and inflammatory cytokines play key roles in amplifying and perpetuating inflammation of the temporomandibular joint (TMJ), although the relationship between these conditions and arthritis at this site is unclear. The present study examined the effects of compressive force and interleukin-1 beta (IL-1 beta) on the metabolism of extracellular matrix (ECM) cartilage. Chondrocytes derived from human normal femoral cartilage were treated with or without different magnitudes of compressive force and/or 100 (U) units/mL IL-1 beta. The expression of chondrocyte-related genes and proteins (type II collagen, type X collagen, aggrecan core, and link protein), matrix metalloproteinases (MMPs), and tissue inhibitor of metalloproteinases (TIMPs) were estimated at the mRNA level using real-time polymerase chain reaction (PCR) and at the protein level using enzyme-linked immunosorbent assay (ELISA). The gene and protein expression levels of MMPs and ECM proteins were significantly higher in compressive force-treated cells than in control cells. MMP gene expression in compressive force-plus IL-1 beta-treated cells was markedly higher than that in compressive forcetreated cells. By contrast, gene expression of ECM proteins in compressive force-plus IL-1 beta-treated cells was significantly lower than that in compressive force treated-cells. These results suggest that compressive force stimulates metabolism of ECM proteins and enhances protein degradation in the presence of IL-1 beta.