Correlation of gingival crevicular fluid interleukin-18 and monocyte chemoattractant protein-1 levels in periodontal health and disease.

摘要

BACKGROUND: Interleukin (IL)-18 is a proinflammatory cytokine of the IL-1 superfamily and is unique, with the capacity to induce T-helper (Th)1 or Th2 differentiation depending on the immunologic context. Monocyte chemoattractant protein (MCP)-1 is a CC chemokine responsible for chemotaxis of monocytes. A previous study showed the induction of MCP-1 by IL-18 in mice macrophages. The present study was carried out to examine the gingival crevicular fluid (GCF) levels of IL-18 and MCP-1 in periodontal health and disease and to evaluate any correlation between IL-18 and MCP-1 GCF levels. METHODS: Sixty subjects (30 males and 30 females; age range: 26 to 49 years) participated in the study. The subjects were initially divided into three groups, consisting of 20 subjects in each group, based on the gingival index, probing depth (PD), clinical attachment loss (AL), and radiologic parameters (bone loss): healthy (group 1), gingivitis (group 2), and periodontitis (group 3), whereas patients in group 3 after treatment constituted group 4. GCF samples were collected from all of the groups to estimate the levels of IL-18 and MCP-1 using enzyme-linked immunosorbent assay. RESULTS: The mean IL-18 and MCP-1 concentrations in GCF were highest in group 3 (330.61 pg/microl and 73.3 pg/microl, respectively). The results suggest that IL-18 and MCP-1 levels increased in GCF from periodontal health to disease and decreased after periodontal therapy. Levels of IL-18 and MCP-1 positively correlated with PD and clinical AL in group 3. In addition, IL-18 and MCP-1 levels significantly correlated with each other in groups 2, 3, and 4. CONCLUSIONS: GCF IL-18 and MCP-1 concentrations increased in periodontal disease compared to health and correlated positively with the severity of disease. Further, based on the positive correlation of IL-18 and MCP-1 found in this study, it can be proposed that IL-18 may promote an inflammatory response by the induction of MCP-1 production and the subsequent recruitment and activation of circulating leukocytes at the inflammatory site.