Ferroptosis and Cuproptosis in Periodontitis: Recent Biological Insights and Therapeutic Advances

Periodontitis is a significant global public health issue associated with the onset and progression of various systemic diseases, thereby requiring additional research and clinical attention. Although ferroptosis and cuproptosis have emerged as significant areas of research in the medical field, their precise roles in the pathogenesis of periodontitis remain unclear. We aim to systematically summarize the current research on ferroptosis and cuproptosis in periodontal disease and investigate the roles of glutathione pathway and autophagy pathway in connecting ferroptosis and cuproptosis during periodontitis. Further, we propose that a homeostatic imbalance of copper and iron, driven by periodontal pathogens, may contribute to elevated periodontal oxidative stress, representing a potential unifying link between ferroptosis and cuproptosis involved in periodontitis. This article presents a comprehensive overview of the molecular mechanisms underlying ferroptosis and cuproptosis in periodontitis, offering novel theoretical insights into its pathogenesis and potential therapeutic targets.牙周炎（Periodontitis）是一类全球重大公共卫生问题，与多种全身性疾病的发生及进展密切相关，因此亟需开展深入研究并获得临床关注。尽管铁死亡（ferroptosis）与铜死亡（cuproptosis）已成为医学领域的重要研究方向，但二者在牙周炎发病机制中的具体作用仍未明确。本研究旨在系统梳理当前牙周疾病领域中铁死亡与铜死亡的相关研究进展，并探究谷胱甘肽通路（glutathione pathway）与自噬通路（autophagy pathway）在牙周炎进程中连接铁死亡与铜死亡的调控作用。此外，本研究提出：由牙周致病菌介导的铜铁稳态失衡，可能会加剧牙周组织氧化应激，这或可作为连接牙周炎中铁死亡与铜死亡的潜在共同纽带。本文全面综述了牙周炎中铁死亡与铜死亡的分子机制，为阐明其发病机制及发掘潜在治疗靶点提供了全新的理论见解。