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Oral inflammatory diseases encompass a wide range of conditions, such as periodontitis, pulpitis, and temporomandibular joint osteoarthritis. However, conventional pharmacological therapies often fail to achieve satisfactory clinical outcomes. Ferroptosis is an iron-dependent form of regulated cell death that has gained increasing attention in recent years. It is characterized by excessive production of reactive oxygen species, lipid peroxidation, iron overload, and depletion of glutathione.Impact StatementThis review systematically elucidates the core molecular mechanisms of ferroptosis and its involvement in the onset and progression of oral inflammatory diseases. In addition, we summarize the key regulatory genes and noncoding RNA networks associated with ferroptosis. We also discuss recent advances in ferroptosis-targeted therapeutic strategies, with the aim of offering new perspectives for the diagnosis and treatment of oral inflammatory diseases. Importantly, this review further emphasizes the potential integration of ferroptosis regulation with biomaterials, targeted delivery systems, and regenerative strategies for oral tissue repair. This underscores its significance in tissue engineering and regenerative medicine.
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Wang et al. (2026) studied this question.
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