Role of Smoking and Type 2 Diabetes in the Immunobalance of Advanced Chronic Periodontitis

Abstract

Upregulation of IL-17(+), IL-15(+), and Foxp3(+) cells and increased amounts of fibrosis were observed in chronic periodontitis sites in subjects with type 2 diabetes, suggesting that periodontitis development in these subjects may be influenced by the T helper 17/T regulatory axis.

Expression of Immune‐Inflammatory Markers in Sites of Chronic Periodontitis in Patients With Type 2 Diabetes

“…Conversely, a recent study by our research group 44 using enzyme‐linked immunosorbent assay (ELISA) showed that the GCF of patients with type 2 DM presented higher levels of IFN‐γ, IL‐17, and IL‐23 and lower levels of IL‐4 when compared to patients without diabetes. Subsequently, we also demonstrated by immunohistochemical analysis that the number of Foxp3‐expressing and IL‐17‐expressing cells was higher in patients with type 2 diabetes compared to patients without diabetes 45 . Therefore, it seems that the process of mRNA transcription from a DNA template to the protein synthesis, activity, and detection in periodontitis is not essentially congruent among studies.…”

Interleukin (IL)-17A synergistically enhances CC chemokine ligand 20 production in IL-1β-stimulated human gingival fibroblasts

“…Recently, Duarte et al reported that Th17 cells are enhanced in the periodontal sites, especially in diabetic patients [24]. It has also been reported that high glucose induces CCL20 production in renal proximal tubule cells [25].…”

Interleukin-17A is involved in development of spontaneous pulmonary emphysema caused by Toll-like receptor 4 mutation

“…Inoue et al have reported that IL-17A can stimulate keratinocytes to produce vascular endothelial growth factor (VEGF), granulocyte-macrophage colony-stimulating factor (GM-CSF), TNF-α, IL-8, and CXCL10 and subsequently promote the growth and repair of airway epithelial cells [13] . Additionally, up-regulation of IL-17A has been demonstrated to induce the process of tissue fibrosis, which is opposite to the process of emphysema, in chronic periodontitis sites, heart, skin and lungs [28,29] . However, there have also been some reports that are opposed to the above-mentioned results regarding the association between IL-17A and emphysema.…”