Over‐expression of forkhead box P3 and its association with receptor activator of nuclear factor‐κ B ligand, interleukin (IL) ‐17, IL‐10 and transforming growth factor‐β during the progression of chronic periodontitis

Abstract

AbstractAim: T regulatory (Treg) cells have been detected in periodontitis lesions, and forkhead box P3 (Foxp3) expression has been negatively correlated to receptor activator of nuclear factor‐κ B ligand (RANKL). The aim of this study was to correlate T‐helper type 1 (Th1), Th2, Th17 and Treg transcription factor expressions, in gingival tissues from patients undergoing active periodontal tissue destruction, with bone loss‐associated cytokines.Materials and Methods: In 10 chronic periodontitis patients undergoing disease progression, the mRNA expressions of T‐bet, GATA‐3, Foxp3, RORC2, interleukin (IL)‐1β, IL‐10, IL‐17, RANKL, interferon (IFN)‐γ and transforming growth factor (TGF)‐β1 were quantified using real‐time reverse transcription‐polymerase chain reaction. The levels of these markers were compared between active and inactive periodontal lesions.Results: In active periodontal lesions, Foxp3, T‐bet, RANKL, IL‐17, IL‐1β and IFN‐γ were significantly over‐expressed compared with inactive lesions. The expression of IFN‐γ was the highest within the active periodontal lesions, similar to that of TGF‐β1 within the inactive ones. There was a positive correlation between RANKL and IL‐17. Additionally, RANKL and IL‐17 were positively correlated with RORC2, but no correlation was detected with Foxp3.Conclusions: These results lead us to speculate that Foxp3+ cells that do not have a regulatory function might have a role in the pathogenesis of active periodontal lesions by down‐regulating TGF‐β1 and IL‐10 synthesis that lead to the over‐expression of Th17‐associated cytokines RANKL and IL‐17.