| 1782 Periodontal Inflammatory Mediator Levels Before and After Full Mouth Extraction | ||
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M.J. MADSEN, L.L. CUNNINGHAM, J.L. EBERSOLE, M.J. NOVAK, and B. ABADI, University of Kentucky, Lexington, USA Objectives: This longitudinal investigation evaluated systemic inflammatory biomarkers in generalized severe periodontal disease patients who elected to become edentate. The hypothesis proposed the removal of the chronic infection of periodontitis would result in a significant decrease in systemic inflammation. Materials and Methods: 12 subjects needing full mouth extraction were recruited from the University of Kentucky College of Dentistry. Blood was collected at surgery, 1, 3, 6, and 12 months to quantitate an array of antibodies, cytokines, acute phase proteins, and inflammatory mediators. Serum was examined using Luminex technology and ELISA for a battery of analytes: IgG antibody to periodontal microorganisms, acute phase reactants [haptoglobin (HG), fibrinogen, CRP, serum amyloid A, serum amyloid P (SAP), bactericidal permeability-inducing factor, lipopolysaccharide binding protein and mannose binding lectin, plasminogen activator inhibitor-1, adiponectin, myeloperoxidase, and MMP-9], inflammatory cytokines/chemokines/mediators (Rantes, IP-10, MCP-1, IL-8,PGE2), and biomarkers of vascular activities (ICAM-1, VCAM-1, E-Selectin). Results: Levels of selected analytes demonstrated noticeable trends following tooth extraction and elimination of periodontitis. IgG antibody to all 7 of the periodontal pathogens decreased over time with lowest levels by 12 months. Acute phase markers CRP (30%), SAP (35%) and HG (32%) markers also decreased. Rantes (30%) and IP-10 (35%), markers of T cells, decreased post-extraction. No significant changes occurred in the other analytes. Conclusions: This prospective longitudinal study examined the contribution of severe oral disease on systemic inflammatory responses. This investigation developed a unique approach to eliminating the chronic oral infection of periodontitis, focusing on patients that become edentate. The results support previous data suggesting that chronic periodontal disease may contribute to elevations in systemic inflammatory mediators. Evidence also suggests that successful treatment of periodontitis may decrease these systemic biomolecules. Study sponsored by NIH General Clinical Research Center (GCRC), University of Kentucky, M01 RR02602 and the Center for Biomedical Research Excellence, P20 RR01245 | ||
| Seq #207 - Clinical Science 2:00 PM-3:00 PM, Saturday, 11 March 2006 Dolphin Hotel Pacific Hall | ||
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