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

Aim: 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)‐1 β, IL‐10, IL‐17, RANKL, interferon (IFN)‐γ and transforming growth factor (TGF)‐β 1 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‐1 β 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‐β 1 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‐β 1 and IL‐10 synthesis that lead to the over‐expression of Th17‐associated cytokines RANKL and IL‐17.