Ferroptosis in the pathogenesis and therapeutic target of oral infectious diseases: A narrative review.

OBJECTIVE

This review summarizes the major metabolic processes underlying ferroptosis, elucidates its interaction mechanisms with oral infectious diseases, and outlines potential therapeutic targets for ferroptosis in oral infections, aiming to inform future treatment approaches.

DESIGN

An electronic literature search was conducted in PubMed, Scopus, EBSCO, ProQuest, ScienceDirect, and Springer for studies on ferroptosis, periodontitis, pulpitis, periapical periodontitis, hand, foot, and mouth disease, Porphyromonas gingivalis, Fusobacterium nucleatum, Candida albicans and Enterovirus A71 published between 2010 and 2025.

RESULTS

Ferroptosis is a newly discovered iron-dependent form of programmed cell death closely associated with a range of oral infectious diseases, including periodontitis, pulpitis, and apical periodontitis. It influences disease progression by regulating iron metabolism, lipid peroxidation, and the antioxidant defense system. Within the oral microenvironment, interactions among microorganisms, host cells, and immune modulators create an inflammatory milieu that further modulates ferroptosis. Crosstalk between ferroptosis regulatory pathways and other inflammatory regulatory pathways also occurs in this setting, playing a pivotal role in the induction of infectious diseases. Advances in mechanistic research are beginning to inform therapeutic strategies, and investigations into ferroptosis-targeted interventions for oral infection diseases are emerging.

CONCLUSIONS

Ferroptosis is an important factor in the pathogenesis of oral infectious diseases and is a promising therapeutic target. Targeting ferroptosis pathway may provide a new approach for the treatment of oral infectious diseases. Further studies are needed to fully understand the mechanisms of ferroptosis in oral infectious diseases and to develop targeted therapies for clinical use.