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1 Introduction Periodontitis is a globally prevalent chronic inflammatory disease triggered by dysregulation of oral biofilm and host immune responses, serving as the primary cause of adult tooth loss ( A multi-platform analysis of human gingival crevicular fluid reveals that ferroptosis is an associated regulated cell death mechanism during the clinical progression of periodontitis ( Porphyromonas gingivalis can actively induce ferroptosis through multiple pathways ( This review systematically summarizes the molecular mechanisms of ferroptosis in periodontitis, with a focus on how dysregulated iron metabolism, reprogrammed lipid metabolism, and suppressed antioxidant defenses in the periodontal microenvironment regulate ferroptosis

Their proposed mechanisms of action include the promotion of angiogenesis, modulation of inflammatory cascades, and enhancement of tissue repair through multiple cellular pathways

GPX4, a glutathione peroxidase, plays a key role in attenuating the inflammatory response and preventing ferroptosis [39]