Circulating interleukin-6 and high-sensitivity C-reactive protein decrease after periodontal therapy in otherwise healthy subjects

• Published in: Journal of periodontology (1970) Vol. 80; no. 4; p. 594
• Main Authors: Marcaccini, Andrea M, Meschiari, César A, Sorgi, Carlos A, Saraiva, Maria C P, de Souza, Ana M, Faccioli, Lúcia H, Tanus-Santos, José E, Novaes, Arthur B, Gerlach, Raquel F
• Format: Journal Article
• Language: English
• Published: United States 01.04.2009
• Subjects: Adult; C-Reactive Protein - analysis; Case-Control Studies; CD40 Ligand - blood; Chemokine CCL2 - blood; Chronic Periodontitis - blood; Chronic Periodontitis - therapy; Dental Scaling; Female; Humans; Inflammation Mediators - blood; Intercellular Adhesion Molecule-1 - blood; Interleukin-6 - blood; Male; Middle Aged; P-Selectin - blood; Vascular Cell Adhesion Molecule-1 - blood
• ISSN: 0022-3492
• DOI: 10.1902/jop.2009.080561

Periodontal disease has been associated with many chronic inflammatory systemic diseases, and a common chronic inflammation pathway has been suggested for these conditions. However, few studies have evaluated whether periodontal disease, in the absence of other known inflammatory conditions and smoking, affects circulating markers of chronic inflammation. This study compared chronic inflammation markers in control individuals and patients with periodontal disease and observed whether non-surgical periodontal therapy affected inflammatory disease markers after 3 months. Plasma and serum of 20 controls and 25 patients with periodontal disease were obtained prior to and 3 months after non-surgical periodontal therapy. All patients were non-smokers, they did not use any medication, and they had no history or detectable signs and symptoms of systemic diseases. Periodontal and systemic parameters included probing depth, bleeding on probing, clinical attachment level, hematologic parameters, as well as the following inflammatory markers: interleukin (IL)-6, high-sensitivity C-reactive protein (hs-CRP), CD40 ligand, monocyte chemoattractant protein (MCP)-1, soluble P-selectin (sP-selectin), soluble vascular adhesion molecule (sVCAM)-1, and soluble intercellular adhesion molecule (sICAM)-1. There were no differences in the hematologic parameters of the patients in the control and periodontal disease groups. Among the tested inflammatory markers, IL-6 concentrations were higher in the periodontal disease group at baseline compared to the controls (P = 0.006). Therapy was highly effective (P <0.001 for all the analyzed clinical parameters), and a decrease in circulating IL-6 and hs-CRP concentrations was observed 3 months after therapy (P = 0.001 and P = 0.006, respectively). Our results also suggest that the CD40 ligand marker may have been different in the control and periodontal disease groups prior to the therapy (P = 0.009). In apparently otherwise healthy patients, periodontal disease is associated with increased circulating concentrations of IL-6 and hs-CRP, which decreased 3 months after non-surgical periodontal therapy. With regard to the CD40 ligand, MCP-1, sP-selectin, sVCAM-1, and sICAM-1, no changes were seen in the periodontal disease group between baseline and 3 months after therapy.