Transforming growth factor‐β, interleukin‐17, and IL‐23 gene expression profiles associated with human peri‐implantitis

Abstract

Data presented in this report demonstrated a predominant Th17 response in peri-implantitis subjects based on the higher levels of IL-23 and lower levels of TGF-β detected.

CyPA and Emmprin play a role in peri‐implantitis

“…If Th17 signaling is activated, then differentiation into Treg and Th2 cells is suppressed, and TGF‐β is decreased . In a study by Gustavo Pereira Mardegan and colleagues, a predominant Th17 response was demonstrated in subject with peri‐implantitis, and a lower level of TGF‐β was also observed . Therefore, the tendency of TGF‐β is a result of the CyPA concentration and Th17 cell activation.…”

“…In addition, Th17 cells emerge parallel to Th1 cells, and they may interact in the inflammatory process . If Th17 signaling is activated, then differentiation into Treg and Th2 cells is suppressed, and TGF‐β is decreased . In a study by Gustavo Pereira Mardegan and colleagues, a predominant Th17 response was demonstrated in subject with peri‐implantitis, and a lower level of TGF‐β was also observed .…”

“…TIMP‐1 has been found at higher levels in peri‐implant crest fluid (PICF) than in GCF . Transforming growth factor (TGF)‐β is an inhibitor secreted by Treg cells that decreases during the rapid progression of inflammation . IL‐1β, MMP‐9, TIMP‐1, and TGF‐β, as the positive and negative factors of the immune response, indicate the progress of inflammation to some extent.…”

“…23,27 Transforming growth factor (TGF)-b is an inhibitor secreted by Treg cells 28 that decreases during the rapid progression of inflammation. 29,30 IL-1b, MMP-9, TIMP-1, and TGF-b, as the positive and negative factors of the immune response, indicate the progress of inflammation to some extent. They can serve as references for the expression and effects of other factors and are possibly correlated with inflammation.…”

Host response and peri-implantitis

“…45 Interestingly, a recent study investigating the IL-17, IL-23, and TGF-β gene expression levels in healthy and diseased peri-implant tissues showed a predominant Th17 response and a diminution of Treg response in the presence of peri-implantitis when compared to peri-implant healthy condition, especially caused by the up-regulation of IL-23 and down-regulation of TGF-β observed in peri-implantitis tissues. 46 Importantly, a systematic review of Duarte et al, 47 aimed to define if cytokine levels in the fluid around implants could be employed to differentiate healthy implants and those with peri-implantitis, pointed-out that most of studies include in the review described statistically significantly augmented concentration of pro-inflammatory mediators in the peri-implant fluid of dental implants with peri-implantitis than in the peri-implant crevicular fluid of healthy implants, whereas many investigations did not find any significant differences in the peri-implant crevicular fluid levels of anti-inflammatory cytokines.…”