Influence of type 2 diabetes on local production of inflammatory molecules in adults with and without chronic periodontitis: a cross-sectional study

BMC Oral Health. 2015 Jul 27:15:86. doi: 10.1186/s12903-015-0073-z.

Abstract

Background: Pathological changes in periodontal tissues are mediated by the interaction between microorganisms and the host immune-inflammatory response. Hyperglycemia may interfere with this process. The aim of this study was to compare the levels of 27 inflammatory molecules in the gingival crevicular fluid (GCF) of patients with type 2 diabetes, with and without chronic periodontitis, and of chronic periodontitis subjects without diabetes. A putative correlation between glycated haemoglobin (HbA1c) and levels of the inflammatory molecules was also investigated.

Methods: The study population comprised a total of 108 individuals, stratified into: 54 with type 2 diabetes and chronic periodontitis (DM + CP), 30 with chronic periodontitis (CP) and 24 with type 2 diabetes (DM). Participants were interviewed with the aid of structured questionnaire. Periodontal parameters (dental plaque, bleeding on probing and periodontal pocket depth) were recorded. The GCF levels of the 27 inflammatory molecules were measured using multiplex micro-bead immunoassay. A glycated haemoglobin (HbA1c) test was performed for patients with diabetes by boronate affinity chromatography.

Results: After adjustment for potential confounders, the DM + CP group had higher levels of IL-8 and MIP-1β, and lower levels of TNF-α, IL-4, INF-γ, RANTES and IL-7 compared to the CP group. Moreover, the DM + CP group had lower levels of IL-6, IL-7 and G-CSF compared to the DM group. The DM group had higher levels of IL-10, VEGF, and G-CSF compared to the CP group. The levels of MIP-1α and FGF were lower in diabetes patients (regardless of their periodontal status) than in chronic periodontitis subjects without diabetes. Diabetes patients (DM + CP and DM) had higher Th-2/Th-1 ratio compared to the CP group. HbA1c correlated positively with the pro-inflammatory cytokines (Pearson correlation coefficient = 0.27, P value: 0.02).

Conclusion: Type 2 diabetes and chronic periodontitis may influence the GCF levels of inflammatory molecules synergistically as well as independently. Type 2 diabetes was associated with high Th-2/Th-1 ratio, and modulated the local expression of molecules involved in the anti-inflammatory and healing processes.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Chemokine CCL3 / analysis
  • Chemokine CCL4 / analysis
  • Chemokine CCL5 / analysis
  • Chronic Periodontitis / blood
  • Chronic Periodontitis / immunology*
  • Cross-Sectional Studies
  • Dental Plaque Index
  • Diabetes Mellitus, Type 2 / blood
  • Diabetes Mellitus, Type 2 / immunology*
  • Female
  • Fibroblast Growth Factors / analysis
  • Gingival Crevicular Fluid / immunology*
  • Glycated Hemoglobin / analysis
  • Granulocyte Colony-Stimulating Factor / analysis
  • Humans
  • Inflammation Mediators / analysis*
  • Inflammation Mediators / blood
  • Interferon-gamma / analysis
  • Interleukin-10 / analysis
  • Interleukin-4 / analysis
  • Interleukin-6 / analysis
  • Interleukin-7 / analysis
  • Interleukin-8 / analysis
  • Male
  • Middle Aged
  • Periodontal Index
  • Th1 Cells / immunology
  • Th2 Cells / immunology
  • Tumor Necrosis Factor-alpha / analysis
  • Vascular Endothelial Growth Factor A / analysis
  • Young Adult

Substances

  • CCL3 protein, human
  • CCL4 protein, human
  • CCL5 protein, human
  • CXCL8 protein, human
  • Chemokine CCL3
  • Chemokine CCL4
  • Chemokine CCL5
  • Glycated Hemoglobin A
  • IL10 protein, human
  • IL4 protein, human
  • IL6 protein, human
  • IL7 protein, human
  • Inflammation Mediators
  • Interleukin-6
  • Interleukin-7
  • Interleukin-8
  • Tumor Necrosis Factor-alpha
  • VEGFA protein, human
  • Vascular Endothelial Growth Factor A
  • Interleukin-10
  • Granulocyte Colony-Stimulating Factor
  • Interleukin-4
  • Fibroblast Growth Factors
  • Interferon-gamma