Abstract
Hypocellularity after joint infection has been attributed to the cytotoxic effects of pus, which can cause necrosis of chondrocytes. In this study, primary cultures of human chondrocytes lost their viability and underwent necrosis rapidly with high inocula of Staphylococcus aureus infection. Chondrocytes were shown to undergo apoptosis with low inocula of Staphylococcus aureus or their culture ultrafiltrate. These findings further support the hypothesis that residual bacterial toxins or triggered apoptotic processes in chondrocytes participate in the pathogenesis of post-infectious arthropathy.