Osteoarthritis (OA) is a multifactorial disease characterized by degeneration of the articular cartilage due to genetic and epigenetic components. The pathogenesis of OA is complex and the mechanism of chondrocyte homeostatic regulation remains to be fully elucidated. Previous studies have demonstrated that microRNAs (miRNAs/miR) contribute to cartilage dysfunction. However, the functional role of miR-98 in interleukin-1 beta (IL-1 beta)-induced chondrocyte apoptosis in OA cartilage remains to be investigated. The present study aimed to identify and characterize the expression profile of miR-98 and apoptosis-associated proteins in healthy and OA chondrocytes, and western blot analysis and TUNEL staining were used to evaluate the role of miR-98 in the regulation of chondrocyte apoptosis. The present study demonstrated that miR-98 expression was increased in OA chondrocytes in response to IL-1 beta stimulation, and the expression levels of apoptosis-associated proteins, including Fas cell surface death receptor, caspase-3, caspase-8 and B-cell lymphoma-2 (Bcl-2) associated X protein, were also increased in IL-1 beta-stimulated chondrocytes. In addition, it was revealed that upregulation of miR-98 was accompanied by reduced expression of Bcl-2 following exposure to IL-1 beta. IL-1 beta-induced downregulation of Bcl-2 was associated with miR-98-mediated translational repression. Transfection of OA chondrocytes with a miR-98 inhibitor had an inhibitory effect on IL-1 beta-induced cell apoptosis, increased cell proliferation and upregulated Bcl-2 expression. It is possible that miR-98 inhibited IL-1 beta-induced chondrocyte apoptosis by modulating Bcl-2 expression levels. The findings of the present study indicated that the effects of miR-98 on chondrocyte apoptosis were induced by regulation of Bcl-2 expression. In addition, the present study confirmed that miR-98 targeted the 3'-untranslated region of Bcl-2. In conclusion, miRNA-coordinated regulation of apoptosis-associated protein expression has been identified in OA chondrocytes following IL-1 beta induction.