The degenerative joint disease osteoarthritis (OA) is the most prevalent form of chronic musculoskeletal disease worldwide, and it commonly afflicts the elderly population. OA-induced impairment of joint function can debilitate normal physical activity, and in more severe cases, it can lead to complete joint destruction and loss of independence or even mobility. The pathophysiology of OA remains to be fully elucidated, despite the extensive research efforts into this complex disease. Studies have revealed that reactive oxygen species (ROS) can contribute to the onset and progression of OA by inducing indispensable chondrocyte death and matrix degradation. However, ROS are also key components of many normal physiological processes, and at moderate levels, they act as indispensable second messengers. This review focuses on the dual role of ROS in cartilage, with the aim of gaining insights into how ROS can be regulated such that its beneficial effects are maintained and its detrimental effects are eliminated.