Effects of Anti-Inflammatory Agents on Expression of Early Responsive Inflammatory and Catabolic Genes in Ex Vivo Porcine Model of Acute Knee Cartilage Injury.

Objective Early intervention therapies targeting inflammation and cell death during the acute phase of cartilage injury have the potential to prevent posttraumatic osteoarthritis. The objective of this study was to investigate the effects of interleukin receptor antagonist protein (IRAP), hyaluronan (HA), dexamethasone (DEX), and mesenchymal stem cell (MSC) treatment on the expression of established genetic markers for matrix degradation, apoptosis, and inflammation in articular cartilage during the acute phase of injury. Design A custom impact device was used to create replicable injury ex vivo to intact porcine knee joint.

Inflammatory cytokines induce specific time- and concentration-dependent MicroRNA release by chondrocytes, synoviocytes, and meniscus cells.

In knee osteoarthritis (OA), concentrations of interleukin (IL)-1β and tumor necrosis factor (TNF)-α increase in joint tissues and synovial fluid which incite a catabolic cascade and further the progression of OA. Several microRNAs (miRNA) have been associated with apoptosis (miR-16), inflammation (miR-22, miR-146a), and matrix degradation (miR-140, miR-27b) in developed OA or its symptoms. In this study, the time- and concentration-dependent nature of cellular and extracellular miRNAs in synoviocytes, meniscus cells, and chondrocytes as influenced by inflammatory cytokines was investigated.