Th1, Th2 and Th17 Cytokines in Progressive Periodontal Lesions

Objectives: Chronic periodontitis is an infection disease characterized by episodic destruction of tooth-supporting tissues, where short periods of tissue destruction are followed by long periods of remission of the tissue destruction and/or healing. The infiltrating inflammatory cells release a broad array of cytokines, which play an important role in that tissue destruction. The propose of this study was to quantify the protein levels and the mRNA expression of Th1, Th2 and Th17 cytokines (IFNγ, IL4, and IL17) in periodontal lesions showing active tooth-supporting tissues destruction and comparing them to those in inactive periodontal sites.

Methods: Periodontitis was characterized on at least 6 sites with probing depth ≥5mm, attachment loss ≥3mm, and radiographic bone loss. The active and inactive periodontal lesions were identified using the tolerance method. Gingival crevicular fluid and gingival biopsies were sampled according to the surgical therapy requirements. The protein synthesis and the mRNA expression of IFNγ, IL4 and IL17 were quantified by ELISA and quantitative real-time RT-PCR and expressed as pg and relative quantification (RQ), respectively. RQ was obtained using the 2^-ΔΔCt method, adjusting the mRNA cytokine expression to the expression of 18S rRNA. The unpaired Student t test was used to analyze differences between active and inactive sites.

Results: The progression of the chronic periodontitis was detected in 25 patients. In active and inactive sites, the levels of cytokine synthesis were: IFNγ, 90.90 ± 55.65 vs. 68.90±27.53 (p=0.03); IL4, 0.67±0.22 vs. 0.80±0.33 (p=0.48) and IL17, 7.60±4.21 vs. 5.02±2.88 (p=0.04), respectively. The mRNA expression of IFNγ and IL17 was higher in active periodontal lesions (7.28 and 2.31−fold change, respectively); however, the mRNA expression of IL4 was higher in inactive sites (1.24−fold change).

Conclusion: Th1 and Th17 cytokines would participate in the destructive processes associated to periodontal disease

This research was supported by project Fondecyt 1050518.