Systemic Th17 response in the presence of periodontal inflammation

Abstract

Systemic Th17 response in the presence of periodontal inflammation The relationship between periodontitis and the pathogenesis of other inflammatory diseases, such as diabetes, rheumatoid arthritis and obesity has been an important topic of study in recent decades. The Th17 pathway plays a significant role in how local inflammation can influence systemic inflammation in the absence of systemic pathology. Objective: To determine Th17 biased-cells in systemically healthy patients in the presence of generalized chronic periodontitis. Methodology: A total of 28 patients were recruited without systemic inflammatory pathology, which was determined by clinical history, the Health Assessment Questionnaire (HAQ) and rheumatoid factor detection. Of these patients, 13 were diagnosed as healthy/gingivitis (H/G) and 15 as generalized chronic periodontitis (GCP). Th17 (CD4 + CD161 +) cells and Th17IL23R + (CD4 + CD161 + IL-23R +) cells were quantified by flow cytometry, based on the total cells and on the lymphocyte region, termed the "enriched population" (50,000 events for each). Results: The percentages of Th17 cells of the H/G and periodontitis groups were similar on total cells and enriched population (19 vs 21.8; p=4.134 and 19.6 vs 21.8; p=0.55). However, Th17IL23R+ cells differ significantly between periodontally healthy patients and generalized chronic periodontitis patients in both total cell (0.22% vs 0.65%; p=0.0004) and enriched populations (0.2% vs 0.75%; p=0.0266). Conclusions: GCP patients (otherwise systemically healthy) were characterized by increased Th17-proinflammatory cell phenotype positive for the IL-23 receptor in peripheral blood. The proportion of Th17 cells that are negative for the IL-23 receptor in the peripheral blood of systemically healthy patients seemed to be unaffected by the presence or absence of chronic periodontitis.

Effects of statins on cytokines levels in gingival crevicular fluid and saliva and on clinical periodontal parameters of middle-aged and elderly patients with type 2 diabetes mellitus

“…IL-23 can induce Th17 cell differentiation, thus producing IL-17 [55][56][57]. Although studies have observed changes in the immune response of Th17 cells and changes in Th17-related cytokines like IL-17 and IL-23 at sites of periodontitis and peri-implant inflammation [57][58][59], no research has been conducted on Th17 cell-related factors in gingivitis patients as of yet. The limitation of the present study is that only the changes of cytokines were observed, without identifying the number and activity of Th17 cells.…”

The Th17/Treg cell balance: crosstalk among the immune system, bone and microbes in periodontitis

“…IL‐23 is involved in the stabilization and maintenance of Th17s that induces these cells to become pathogenic 32,33 . It has been reported that periodontitis upregulates the expression of IL‐23 and IL‐23R and promotes an increase in pathogenic Th17IL‐23R + cells 34,35 . IL‐21, IL‐6 and IL‐17 can stimulate fibroblasts, periodontal ligament cells and dendritic cells (DCs) to express IL‐23 36‐38 .…”

Vascular Changes and Hypoxia in Periodontal Disease as a Link to Systemic Complications

“…There was a significant increase in B cells in the samples with periodontitis compared to the healthy group. In addition, Th17 cells were also detected in the samples of patients with chronic periodontitis [58,59].…”

“…Each response class plays a different protective role and contributes to immunopathology. Th1 cells interferon-γ, interleukin-2; Th2 cells are inter-leukin-4, interleukin-5, interleukin-6, interleukin-10, interleukin-13; Th17 cells interleukin-6, interleukin-21, and interleukin-23; Treg cells are characterized by the release of trans-forming growing factor-β, interleukin-2 cytokines [59]. The regulation of the response is determined by a complex cytokine network.…”