Archives of oral biology · 2026
Smoking and systemic Th17/Treg immune alterations in periodontitis: A cross-sectional study.
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Sidharthan Sangamithra, Gopalakrishnan Dharmarajan, Kheur Supriya, Suryavanshi Poonam, Sanap Avinash
Аннотация
OBJECTIVE: To investigate the impact of smoking on systemic and local immune responses in periodontitis, focusing on Th17 and regulatory T (Treg) cell frequencies and their associated cytokine expression.
DESIGN: Forty-five participants were categorized into healthy controls (n = 15), non-smokers with periodontitis (n = 15), and smokers with periodontitis (n = 15). Clinical periodontal parameters were recorded. Peripheral blood mononuclear cells were analyzed by flow cytometry to quantify CD4⁺ T cells, Th17 (CD4⁺IL-17A⁺), and Treg (CD4⁺CD25⁺FOXP3⁺) populations. Gingival biopsies from a subset of participants (n = 24) were assessed by qRT-PCR for IL-17A, FOXP3, IL-12(p35), and hEBI3 expression. Group comparisons and correlation analyses were performed using appropriate parametric or non-parametric tests.
RESULTS: Smokers with periodontitis exhibited greater probing depth and clinical attachment loss than non-smokers and healthy controls (p < 0.001). Both periodontitis groups showed elevated circulating CD4⁺ T cells and Tregs, with Th17 frequencies highest in smokers. These systemic differences remained significant after false discovery rate (FDR) correction, with moderate effect sizes (η² = 0.25-0.44). Gingival expression of IL-17A, FOXP3, IL-12(p35), and hEBI3 did not differ significantly between groups after FDR adjustment, with small effect sizes (η² ≤ 0.09). No significant correlations were observed between smoking exposure and systemic or local immune markers.
CONCLUSION: Periodontitis is associated with marked systemic immune alterations, whereas local transcriptional changes are subtle. Smoking modestly enhances systemic Th17 responses without robust changes in gingival cytokine expression, highlighting the need for adequately powered and longitudinal studies to clarify immune mechanisms in periodontitis.
DESIGN: Forty-five participants were categorized into healthy controls (n = 15), non-smokers with periodontitis (n = 15), and smokers with periodontitis (n = 15). Clinical periodontal parameters were recorded. Peripheral blood mononuclear cells were analyzed by flow cytometry to quantify CD4⁺ T cells, Th17 (CD4⁺IL-17A⁺), and Treg (CD4⁺CD25⁺FOXP3⁺) populations. Gingival biopsies from a subset of participants (n = 24) were assessed by qRT-PCR for IL-17A, FOXP3, IL-12(p35), and hEBI3 expression. Group comparisons and correlation analyses were performed using appropriate parametric or non-parametric tests.
RESULTS: Smokers with periodontitis exhibited greater probing depth and clinical attachment loss than non-smokers and healthy controls (p < 0.001). Both periodontitis groups showed elevated circulating CD4⁺ T cells and Tregs, with Th17 frequencies highest in smokers. These systemic differences remained significant after false discovery rate (FDR) correction, with moderate effect sizes (η² = 0.25-0.44). Gingival expression of IL-17A, FOXP3, IL-12(p35), and hEBI3 did not differ significantly between groups after FDR adjustment, with small effect sizes (η² ≤ 0.09). No significant correlations were observed between smoking exposure and systemic or local immune markers.
CONCLUSION: Periodontitis is associated with marked systemic immune alterations, whereas local transcriptional changes are subtle. Smoking modestly enhances systemic Th17 responses without robust changes in gingival cytokine expression, highlighting the need for adequately powered and longitudinal studies to clarify immune mechanisms in periodontitis.