Protective effect of zoledronic acid on corticosteroid-induced chondrocyte apoptosis in rat articular cartilage

• Published in: Acta orthopaedica et traumatologica turcica Vol. 47; no. 6; p. 430
• Main Authors: Ozenci, Alpay Merter, Aslan, Tevfik, Sahin, Zeliha, Ozbey, Ozlem, Acar, Nuray, Ustünel, Ismail
• Format: Journal Article
• Language: English
• Published: Turkey 2013
• Subjects: Animals; Apoptosis - drug effects; Bone Density Conservation Agents - pharmacology; Cartilage, Articular - drug effects; Chondrocytes - drug effects; Diphosphonates - pharmacology; Disease Models, Animal; Imidazoles - pharmacology; Rats; Rats, Wistar
• ISSN: 1017-995X
• DOI: 10.3944/AOTT.2013.3136

The aim of this study was to assess the apoptotic effects of systemic corticosteroid application on the articular cartilage chondrocytes in vivo and to investigate the potential effects of zoledronic acid on corticosteroid-induced apoptosis. Twenty-four Wistar rats were randomly divided into 3 groups. In the control group, intramuscular isotonic salt solution was injected weekly. In the second group, a dose of 10 mg/kg intramuscular corticosteroid (methylprednisolone) injection was applied weekly for 8 weeks. In the third group, a dose of 10 mg/kg intramuscular corticosteroid (methylprednisolone) injection was applied weekly for 8 weeks and 0.1 mg/kg zoledronic acid was injected subcutaneously on days 0, 21 and 42. Femoral head specimens from each group were obtained at the end of the treatment and the TUNEL method was applied to detect apoptotic chondrocytes. Comparison analyses were performed using the ANOVA method and Tukey's test. There was a significant difference between the corticosteroid group and two other groups (control group: p=0.005; corticosteroid + zoledronic acid group: p=0.047). Zoledronic acid treatment significantly decreased the number of corticosteroid-induced apoptotic chondrocytes in the joint cartilage (p<0.05). Zoledronic acid may have the potential to prevent joint cartilage deterioration due to the corticosteroid-induced apoptosis of the chondrocytes.