Triamcinolone acetonide reduces viability, induces oxidative stress, and alters gene expressions of human chondrocytes.

OBJECTIVE: Patients with knee osteoarthritis (OA) are sometimes prescribed intra-articular injections of glucocorticoids (GCs), such as triamcinolone acetonide (TA). Whether GCs cause chondrotoxicity is not known. We wished to ascertain if TA induces toxicity by causing oxidative stress and alters expression of P21, growth differentiation factor (GDF)15, and cFos. PATIENTS AND METHODS: Primary chondrocytes isolated from 10 OA patients undergoing total knee replacement surgery were incubated with TA (0, 1, 5, 10 mg/ml), with or without 100 µM vitamin C for 7 and 14 days for viability assays and 48 h for oxidative stress and gene expression analyses.
RESULTS: TA significantly decreased chondrocyte viability and increased the ratio of oxidized glutathione to total glutathione suggesting an increase in oxidative stress. Vitamin C significantly increased the viability and decreased the oxidative stress of cells treated with 5 mg/ml TA. Expression of P21, GDF15, and cFos increased significantly when TA was added (5.17 ± 2.4-, 4.96 ± 3.1-fold for P21, 9.97 ± 2.9- and 4.2 ± 1.6-fold for GDF15, and 6.65 ± 4.8-, 12.96 ± 8.3-fold for cFos at 1, and 5 mg/ml TA, respectively).
CONCLUSIONS: TA induced chondrotoxicity by increasing oxidative stress and altering expressions of genes involved in cell death. The addition of vitamin C decreased oxidative stress and increased viability, suggesting that antioxidants might attenuate TA toxicity in cartilage.