Background: Monocyte chemoattractant protein-1 (MCP-1) is a well-known chemotactic cytokine that regulates mononuclear inflammatory cell recruitment. This recruitment has particular importance in the oral cavity because inflammatory cells will be challenged with periodontopathogenic bacteria during infections. Tumor necrosis factor-alpha (TNF-α) is a cytokine that induces bone resorption by stimulating proliferation and differentiation of osteoclasts’ progenitors and also stimulates MCP-1 expression. The aims of this study were to investigate the presence of MCP-1 in gingival crevicular fluid (GCF) samples from patients with chronic periodontitis (CP) and aggressive periodontitis (AgP) and to examine the possible correlations between the GCF levels of MCP-1 and TNF-α.

Methods: Twenty-five CP, 20 AgP, and 20 healthy control (C) patients were selected for the study. Plaque index (PI), gingival index (GI), probing depth (PD), and clinical attachment level (CAL) measurements were recorded from each sampling area. Assays for GCF MCP-1 and TNF-α were carried out by an enzyme-linked immunosorbent assay (ELISA) method.

Results: The concentration (nanograms per microliters) and total MCP-1 and TNF-α (nanograms per site) were not statistically significant between CP and AgP groups, but total MCP-1 and TNF-α was statistically different between CP and C and between AgP and C groups (P <0.001). All clinical parameters were statistically different between CP and C and between AgP and C groups (P <0.001). A positive statistical correlation was detected between the levels of MCP-1 and TNF-α, and there was also a positive correlation between all clinical parameters and total MCP-1 and TNF-α levels.

Conclusions: These results suggest that MCP-1 could have an important role in the activation and recruitment of inflammatory and immune cells in periodontal diseases, and both AgP and CP patients may have the same pattern of MCP-1 expression. A strong positive correlation between the GCF levels of MCP-1 and TNF-α may account for the mechanism of amplification of inflammatory events in gingival inflammation.