Purpose

The molecular inflammation hypothesis of ageing implies that the molecular activation of proinflammatory genes by altered redox-sensitive cellular signal pathway might serve as a bridge between normal ageing and age-related diseases such as osteoarthritis (OA). We studied the effect that dysfunction of the mitochondrial respiratory chain (MRC), the main cellular source of reactive oxygen species (ROS), could induce on the inflammatory response in cultured normal human chondrocytes, specifically in interleukin 8 (IL8) and cyclooxygenase 2 (COX-2) expression.