Related Experiment Video
Updated: May 21, 2026

Isolation, Characterization and Functional Examination of the Gingival Immune Cell Network
Published on: February 16, 2016
Comparative analysis of TNF-α, TLR-2, and TLR-4 in GCF before and after periodontal therapy
Mithat Terzi1, Fatma Altiparmak2, Fatma Ucan Yarkac3
1Hisar Intercontinental Hospital, Istanbul, Turkey.
Abstract:
Periodontitis is a chronic inflammatory disease characterized by progressive destruction of tooth-supporting tissues, primarily driven by a dysregulated host immune response to subgingival biofilms. Toll-like receptors (TLR-2 and TLR-4) and tumor necrosis factor-alpha (TNF-α) are key mediators of immune signaling and tissue breakdown, making them potential biomarkers of periodontal disease activity. This prospective, non-randomized interventional study evaluated TLR-2, TLR-4, and TNF-α levels in gingival crevicular fluid (GCF) for periodontal disease monitoring and assessed the effects of nonsurgical periodontal therapy (NSPT) on clinical parameters. Forty systemically healthy individuals were enrolled and assigned to either periodontitis or healthy groups. Clinical indices-gingival index, plaque index, clinical attachment loss, and probing pocket depth-were recorded at baseline and 8 weeks after NSPT. GCF samples were analyzed using enzyme-linked immunosorbent assay to determine biomarker concentrations. At baseline, TNF-α and TLR-2 levels were significantly higher in periodontitis patients compared with healthy controls (p < 0.001). Following therapy, marked clinical improvements were observed, accompanied by significant reductions in TNF-α and TLR-4 levels (p < 0.05), while TLR-2 levels remained stable. receiver operating characteristic analysis demonstrated that TNF-α and TLR-2 reliably distinguished disease from health. In conclusion, NSPT effectively improved clinical outcomes and reduced TNF-α and TLR-4 levels in GCF, reflecting a decreased local inflammatory burden. The persistence of TLR-2 expression post-treatment suggests a stable role in immune surveillance rather than acute inflammatory response.