Abstract
Abstract
Periodontitis is a chronic inflammatory disease initiated by a dysbiotic microbiome, yet tissue destruction is primarily driven by an exaggerated host immune response. CD4⁺ T helper (Th) cell subsets play important roles in regulating periodontal inflammation and osteoclast-mediated bone resorption through distinct cytokine networks. Th1 and Th17 responses are closely associated with pro-inflammatory signaling and alveolar bone loss, whereas Th2 and regulatory T (Treg) cells exert context-dependent immunomodulatory functions. Beyond these subsets, Th9 and Th22 cells further expand the complexity of T cell-mediated regulation in periodontal lesions. Importantly, accumulating evidence supports T helper cell plasticity, exemplified by the emergence of IL-17⁺ Treg, suggesting that periodontal disease reflects immune imbalance and functional instability rather than the dominance of a single lineage. Clarifying these mechanisms may support the development of targeted immunomodulatory strategies aimed at restoring oral mucosal immune homeostasis. This review shifts the focus from static T cell subsets to their dynamic phenotypic flexibility, highlighting how maladaptive transitions drive chronic tissue destruction.