Poster 387, Sprache: EnglischEngl-Schmuecker, Jennifer/Gassmann, Georg/Petrie, Judith/Grimm, Wolf-Dieter
Background: The formation of AGEs (Advanced Glycosylation Endproducts) has previously been shown to alter basement membranemacromolecules. Published findings (Lalla et al. 2003) demonstrate that theblockade of RAGEs (Receptor for AGEs) results in suppression of bothalveolar bone loss and markers of cellular activation/tissue-destructiveproperties. These data indicate that AGEs stimulate increased production ofprostaglandins by monocytes following LPS exposure. To test the hypothesisthat activation of RAGEs contributes to the pathogenesis ofdiabetes-associated periodontitis we used gingival biopsy samples forimmunohistochemical analysis in a clinical-controlled case study with 20periodontitis patients associated with diabetes and without systemicimplications.
Material and methods: The biopsy samples wereexamined immunohistochemically with a monoclonal antibody specific for AGEs,6D12. Quantifications of immunohistochemistry were then performed usingIMAGES J. For the two group comparison a 2-tailed student's t test was used.Additionally analysis of GCF samples (PGE2, IL-1 ß) and measurement ofserum PGE2, IL-1 ß were performed.
Results: Gingival tissuefrom periodontitis patients with diabetes type II demonstrated enhancedaccumulation of AGEs compared with non-diabetic periodontitis patients,especially surrounding epithelial and connective tissues (17% inexperimental group to 13% in controls).
Conclusions: Our data indicate thatan increased concentration of glycated proteins present in diabetics mayhave the potential to increase the monocytic secretion of PGE2 and IL-1ß in periodontitis patients with diabetes type II.
Schlagwörter: periodontitis, diabetes, advanced glycosylation end products, receptor for advanced glycosylation end products, biopsy, immunohistochemistry