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Isolation, Characterization and Functional Examination of the Gingival Immune Cell Network
Published on: February 16, 2016
IL-17 in sera from patients with aggressive periodontitis
H A Schenkein1, T E Koertge, C N Brooks
1Department of Periodontics, School of Dentistry, Virginia Commonwealth University, Richmond, VA 23298-0566, USA. haschenk@vcu.edu
Journal of Dental Research
|April 20, 2010
Summary
Interleukin-17 (IL-17) levels are significantly elevated in patients with aggressive periodontitis compared to healthy individuals. This suggests IL-17 plays a role in the inflammatory processes underlying this severe gum disease.
Area of Science:
- Immunology
- Periodontology
- Oral Medicine
Background:
- Interleukin-17 (IL-17) is a key cytokine produced by Th17 cells, implicated in inflammatory, autoimmune, and antimicrobial responses.
- Aggressive periodontitis is a severe inflammatory oral disease.
- The role of IL-17 in aggressive periodontitis pathogenesis is not well understood.
Purpose of the Study:
- To investigate the presence and concentration of IL-17 in serum of patients with aggressive periodontitis.
- To determine if IL-17 serum levels correlate with the severity of aggressive periodontitis.
Main Methods:
- Serum samples were collected from periodontally healthy individuals (NP), patients with localized aggressive periodontitis (LAgP), and generalized aggressive periodontitis (GAgP).
- Enzyme-linked immunosorbent assay (ELISA) was employed to quantify IL-17 serum concentrations.
- Multivariate analyses were used to assess associations between IL-17 levels and clinical parameters.
Main Results:
- IL-17 was minimally detected in healthy individuals (1.9 pg/mL).
- Significantly higher IL-17 concentrations were found in patients with LAgP (7.6 pg/mL) and GAgP (17.1 pg/mL).
- IL-17 levels correlated with periodontal attachment loss but not with smoking status.
Conclusions:
- Elevated serum IL-17 levels are characteristic of aggressive periodontitis.
- The findings suggest that Th17 responses and IL-17 contribute to the pathogenesis of aggressive periodontitis.
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