Th17/treg immune imbalance in smoking-associated periodontitis: A flow cytometric and gene expression analysis

Introduction: Periodontitis involves chronic immune dysregulation, with Th17/Treg imbalance contributing to disease progression. Smoking further disrupts immune homeostasis, exacerbating inflammatory pathways. Methods: Forty-five participants were divided into three groups: healthy controls, non-smokers with periodontitis, and smokers with periodontitis. Flow cytometry quantified Th17 (CD4 + IL-17A + ) and Treg (CD4 + CD25 + FOXP3 + ) cells. qRT-PCR assessed IL-17, FOXP3, IL-12A, and hEIB3 gene expression in gingival tissues. Results: Th17 cells were markedly increased in smokers (1.31%) versus non-smokers (0.93%) and controls (0.26%). Treg cells increased in disease groups but were functionally unstable in smokers. hEIB3 expression was lowest in smokers, indicating impaired IL-35–mediated regulation. Conclusions: Smoking amplifies immune dysregulation in periodontitis by increasing Th17 activity and diminishing Treg stability. Immunomodulatory and cessation strategies may enhance periodontal outcomes.