Levels of Interferon-Gamma and Transcription Factor T-Bet in Progressive Periodontal Lesions in Patients With Chronic Periodontitis
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Background: Periodontitis is an infection with an episodic pattern of tissue-support destruction. During the generation of a primary CD4+ T helper 1 (Th1) response, interferon-gamma (IFN-g) acts as a positive regulator by selectively inducing Th1 differentiation through increased transcription of T-bet. The aims of this work were to determine IFN-g levels in samples of gingival crevicular fluid (GCF) and to determine IFN-g and transcription factor T-bet expression in gingival tissue from patients undergoing the progression of chronic periodontitis. Methods: One hundred six patients with moderate or advanced chronic periodontitis were selected. Periodontitis was characterized by at least six sites with probing depth ‡5 mm, clinical attachment loss ‡3 mm, and radiographic bone loss. Periodontitis progression was determined by the tolerance method. GCF was collected using a paper strip, and enzyme-linked immunosorbent assay was performed to determine the total amount of IFN-g. Gingival biopsies were obtained from patients for real-time reverse transcription-polymerase chain reaction to determine IFN-g and T-bet expression. Statistical analysis was performed using statistical software. Data were expressed as subject means – SD. The x2 and Student t tests were used. Results: The totalamount and concentration of cytokine IFN-g were significantly higher in active sites than in inactive sites (99.90 versus 68.90 pg; P = 0.03; 106.62 pg/mg versus 75.64 pg/mg, P = 0.04, respectively).Active sites showed a significantly lower D cycle threshold (Ct) of IFN-g than inactive sites (P = 0.04),whereas the expression of transcription factor T-betwas increased 1.42-fold in active sites compared to inactive sites. Conclusion: The total amount and concentration of cytokine IFN-g in GCF samples and transcription factor T-bet expression were increased in progressive periodontal lesions in patients with chronic periodontitis.
DOI: doi: 10.1902/jop.2009.080287