Periodontitis, a chronic inflammatory disease caused by plaque biofilm, is characterized by the irreversible pathological destruction of periodontal supporting tissues, including gums, periodontal membranes, alveolar bone, and cementum, resulting in tooth loosening and dislocation in severe cases. Currently, research on the pathogenesis, early diagnosis, and treatment of periodontitis is limited. Circular RNAs (circRNAs), previously considered “splicing noise”, have gained increasing research attention with the development of high-throughput sequencing technologies and bioinformatics. CircRNAs are non-coding RNAs lacking a 5' cap and 3' poly(A) tail, with a unique covalently closed ring structure, high expression, long half-life, and resistance to nuclease degradation, which can regulate splicing, encode proteins, and act as microRNA and RNA-binding protein sponges. In recent years, circRNAs have been reported to be involved in the occurrence and development of periodontitis, suggesting its potential role as a therapeutic target for periodontitis treatment. In this study, we described the biological function of circRNAs and their role in the development of periodontitis and the regulation of periodontal homeostasis and immune microenvironment. We found that circRNAs affect periodontal homeostasis and immune microenvironment by regulating the apoptosis of periodontal tissue cells (such as periodontal ligament stem cells and gingival fibroblasts) and regulating immune cells or cytokines, respectively. This review article summarizes the latest research progress on the association between circRNAs and periodontitis to provide a scientific basis for the development of novel diagnostic, therapeutic, and prognostic strategies for periodontitis.

Periodontitis is a chronic inflammatory disease caused by plaque microorganisms, which is the main cause of tooth loss in adults in China. Due to the complexity of periodontitis, their pathogenesis is still unclear. Ferroptosis is a form of iron-dependent regulation of cell death, which affects the function of glutathione peroxidase (GPX4) in the cell through different signaling pathways, thus decreasing antioxidant capacity, accumulation of reactive oxygen species and lipid peroxidation, eventually causing cell and tissue damage. Recent studies have found that iron overload, oxidative stress and lipid peroxidation are closely related to the occurrence and development of periodontitis. This article reviews the characteristics of ferroptosis and the relationship between ferroptosis and inflammatory diseases, especially periodontitis, to provide new ideas for the diagnosis, treatment, and prognosis evaluation of periodontitis. ferroptosis is mainly manifested as the disruption of the body’s redox homeostasis, decreased antioxidant capacity, activation of damage related molecular patterns, release of pro-inflammatory mediators, and induction or exacerbation of inflammation. Iron dependent oxidative stress and lipid peroxidation are simultaneously involved in the regulation of ferroptosis and inflammatory diseases. Pathogenic bacteria of periodontitis can induce ferroptosis of periodontal ligament stem cells, thereby activating the release of inflammatory factors such as interleukin-17, tumor necrosis factor alpha, and hypoxia inducible factor-1 alpha, exacerbating periodontitis;In addition, inflammatory factors activated by ferroptosis play an important role in alveolar bone homeostasis, and ferroptosis is involved in the process of lipopolysaccharide induced inflammation of gingival fibroblasts. Future research can focus on exploring the molecular mechanisms and therapeutic targets of ferroptosis in periodontitis, providing new strategies for the prevention and treatment of periodontal disease.