Programmed cell death: immune regulatory mechanisms in periodontitis and rheumatoid arthritis

Abstract

Periodontitis and rheumatoid arthritis, as chronic inflammatory diseases that share epidemiological associations and immunopathological characteristics, have various forms of programmed cell death (PCD) that play a core role in their pathogenesis, which form an important link between the two. The comorbidity of periodontitis and rheumatoid arthritis suggests that there might be a common immune regulatory mechanism, with PCD pathways playing a key role in regulating immune responses. Particularly, the Th17/Treg imbalance and apoptosis resistance in CD4+CD28− T cells emerge as shared T cell–centered mechanisms bridging periodontal infection to rheumatoid autoimmunity. Studying how PCD works in periodontitis and rheumatoid arthritis can help uncover the potential links between the two diseases, which provides new targets for clinical treatment and improves patient prognosis. In this article, we’ll review relevant research and discuss how PCD is important for immune regulation in periodontitis and rheumatoid arthritis, which provides a theoretical basis for future treatment strategies for both conditions, helping to control the progression of inflammation more effectively.