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Title: 0074 - Single Nucleotide Polymorphisms and Inflammatory Response in Localized Aggressive Periodontitis

Authors:

Luciana Shaddox (Presenter)
University of Florida

Theodore Harris, University of Florida
Yan Gong, University of Florida
Hong Huang, University of Florida
Ikramuddin Aukhil, University of Florida
Peter Harrison, University of Florida
Theodora Kompotiati, University of Florida
Margaret Wallace, University of Florida

Abstract:

Objectives: Although it is known there is a genetic predisposition and a hyper- inflammatory response in localized aggressive periodontitis (LAP), current literature is limited regarding the role of specific single nucleotide polymorphisms (SNPs) in LAP or its inflammatory response. The objective of this study is to evaluate specific SNPs in relationship to phenotype and the hyper-responsiveness seen in LAP.

Methods: A total of 220 African-Americans between the ages of 5-25, who were either diagnosed with LAP (103) or healthy unrelated controls (117), were included. Peripheral blood from all the patients was stimulated with lipopolysaccharide (LPS) from E. coli (Ec). Twenty-four SNPs in 13 different genes were evaluated. SNPs frequencies were compared between LAP and controls as well as correlated with the levels of LPS stimulated cyto/chemokines.

Results: Genotype frequencies for IL-1β (rs1143627 and rs16944), IL6 (rs2069849), CXCL2 (rs9131), CXCL5 (rs425535), and LTF (rs1126478) were significantly associated with LAP (p< 0.05). In addition, correlations were found between all TNFα genes (rs 1800683, rs2229094 and 1800629), IL1β (rs16944 and 1143634), TLR2 (rs3804100), CXCL2 (rs9131), and CXCL5 (rs425535) and Ec LPS stimulated levels of several cyto/chemokines (P<0.05).

Conclusions: Based on these findings, specific SNPs seem to be associated with LAP and also correlated with the inflammatory response to LPS in these individuals. By narrowing down the SNPs that are contributing to LAP risk, we can hopefully find mechanisms to slow down, if not prevent, this disease process in the future.

This abstract is based on research that was funded entirely or partially by an outside source:
NIH/NIDCR R01DE019456

Disclosure Statement:
The submitter must disclose the names of the organizations with which any author have a relationship, the nature of the relationship, and the clinical or research area involved. The following is submitted: NONE

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