title: Gingival crevicular fluid monocyte chemoattractant protein-1 and RANTES levels in patients with generalized aggressive periodontitis.
abstract: BACKGROUND
  Local and systemic inflammatory and immune mechanisms may be implicated in the pathogenesis of the aggressive forms of periodontal disease. Chemokines, monocyte chemoattractant protein-1 (MCP-1) and regulated on activation, normal T cells expressed and secreted RANTES (regulated on activation, normal T cells expressed and secreted), are involved in the activation and recruitment of inflammatory and immune cells to the infected sites and thereby mediating a variety of pathophysiological conditions. The aim of the present study was to examine the gingival crevicular fluid (GCF) levels of MCP-1 and RANTES in patients with generalized agressive periodontitis (G-AgP).
  
  
  METHODS
  MCP-1 and RANTES levels were investigated in GCF samples of 10 patients with G-AgP and 10 periodontally healthy subjects. Periodontal status was evaluated by measuring probing depth, clinical attachment loss, presence of bleeding on probing and plaque. In the G-AgP group, GCF samples were collected from the two approximal sites; from one single-rooted tooth and from one first molar tooth with > or =6 mm probing depth. In the healthy group, GCF samples were collected from one of the single-rooted teeth. GCF MCP-1 and RANTES levels were quantified by enzyme immunoassay.
  
  
  RESULTS
  The G-AgP patients had significantly higher GCF MCP-1 and RANTES levels compared to the healthy group (p<0.05). GCF MCP-1 and RANTES levels were positively correlated with both probing depth and clinical attachment loss (p<0.05). There was no correlation between GCF MCP-1 and RANTES levels and the percentage of sites with bleeding (p>0.05).
  
  
  CONCLUSIONS
  The results of the present study suggest that MCP-1 and RANTES could play key roles in both activation and recruitment of inflammatory and immune cells in periodontal environment of G-AgP patients. In conclusion, these CC chemokines may be considered in the biological mechanism underlying the pathogenesis and progression of G-AgP.
authors.affiliation: Department of Periodontology, School of Dentistry, Ege University, Izmir, Turkey. gemingil@yahoo.com
authors.forename: Gülnur
authors.initials: G
authors.lastname: Emingil
authors.forename: Gül
authors.initials: G
authors.lastname: Atilla
authors.forename: Afig
authors.initials: A
authors.lastname: Hüseyinov
mesh_terms: D000293:Adolescent; D000328:Adult; D016022:Case-Control Studies; D018932:Chemokine CCL2 / Q000032:analysis*; D018946:Chemokine CCL5 / Q000032:analysis*; D005260:Female; D005883:Gingival Crevicular Fluid / Q000737:chemistry* / Q000276:immunology; D006801:Humans; D008297:Male; D010518:Periodontitis / Q000276:immunology*; D018709:Statistics, Nonparametric
chemical_list: D018932:Chemokine CCL2; D018946:Chemokine CCL5