Levels of interferon-gamma and transcription factor T-bet in progressive periodontal lesions in patients with chronic periodontitis.
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-gamma) 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-gamma levels in samples of gingival crevicular fluid (GCF) and to determine IFN-gamma 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 >or=5 mm, clinical attachment loss >or=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-gamma. Gingival biopsies were obtained from patients for real-time reverse transcription-polymerase chain reaction to determine IFN-gamma and T-bet expression. Statistical analysis was performed using statistical software. Data were expressed as subject means +/- SD. The chi(2) and Student t tests were used.


RESULTS
The total amount and concentration of cytokine IFN-gamma 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 Delta cycle threshold (Ct) of IFN-gamma than inactive sites (P = 0.04), whereas the expression of transcription factor T-bet was increased 1.42-fold in active sites compared to inactive sites.


CONCLUSIONS
The total amount and concentration of cytokine IFN-gamma in GCF samples and transcription factor T-bet expression were increased in progressive periodontal lesions in patients with chronic periodontitis.
Dutzan
Nicolas
N
Periodontal Biology Laboratory, Department of Conservative Dentistry, Dentistry Faculty, University of Chile, Santiago, Chile.
Vernal
Rolando
R
Hernandez
Marcela
M
Dezerega
Andrea
A
Rivera
Oriana
O
Silva
Nora
N
Aguillon
Juan Carlos
JC
Puente
Javier
J
Pozo
Patricia
P
Gamonal
Jorge
J
D000328:Adult; D055113:Chronic Periodontitis / Q000276:immunology* / Q000378:metabolism* / Q000473:pathology; D018076:DNA, Complementary / Q000032:analysis; D018450:Disease Progression; D005260:Female; D015870:Gene Expression; D005881:Gingiva / Q000378:metabolism; D005883:Gingival Crevicular Fluid / Q000737:chemistry; D006801:Humans; D007371:Interferon-gamma / Q000032:analysis / Q000096:biosynthesis*; D008297:Male; D008875:Middle Aged; D012335:RNA, Ribosomal / Q000032:analysis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D020825:T-Box Domain Proteins / Q000032:analysis / Q000096:biosynthesis*; D000098815:T-bet Transcription Factor
D018076:DNA, Complementary; D012335:RNA, Ribosomal; D020825:T-Box Domain Proteins; D000098815:T-bet Transcription Factor; D007371:Interferon-gamma