Osteoarthritis (OA) is a prevalent degenerative joint disease characterized by pain, limited movement, and joint stiffness, significantly impacting the quality of life and imposing substantial economic burdens. This review paper delves into the novel insights of ferroptosis, an iron-dependent form of cell death associated with lipid peroxidation, in the context of temporomandibular joint osteoarthritis (TMJ OA) and knee osteoarthritis (KOA). We explore the pathogenic characteristics of OA, including synovitis, chondrocyte death, and extracellular matrix (ECM) degradation, and discuss the limitations of current therapeutic interventions. Emerging evidence suggests a significant relationship between ferroptosis and OA, with iron accumulation and lipid peroxidation observed in osteoarthritic cartilage. This review highlights the role of ferroptosis in chondrocyte malfunction and apoptosis, inflammation, and extracellular matrix breakdown, which are central to OA pathogenesis. We also discuss potential therapeutic targets, such as Transient Receptor Potential Vanilloid 1 (TRPV1), Glutathione Peroxidase 4 (GPX4), and Nuclear Factor Erythroid 2-Related Factor 2 (NRF2), which modulate ferroptosis and OA progression. The paper consolidates studies on ferroptosis in OA, offering a comprehensive understanding of its role and the development of innovative therapies targeting this cell death mechanism to improve treatment outcomes for OA patients.