{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,6,26]],"date-time":"2025-06-26T13:10:51Z","timestamp":1750943451067},"reference-count":44,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2009,5,18]],"date-time":"2009-05-18T00:00:00Z","timestamp":1242604800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Periodontal Research"],"published-print":{"date-parts":[[2009,10]]},"abstract":"<jats:p><jats:bold>Background and Objective:\u2002<\/jats:bold> As a pro\u2010inflammatory cytokine, interleukin\u20102 mediates the activation, growth and differentiation of T and B lymphocytes and natural killer cells. Promoter polymorphisms of the interleukin\u20102 gene have been associated with altered interleukin\u20102 production or identified as prognostic markers for various infectious diseases. Therefore, the aim of this study was to evaluate two polymorphisms at positions \u2212330 T\/G and 166 G\/T in patients with generalized chronic periodontitis (<jats:italic>n<\/jats:italic>\u2003=\u200358) or generalized aggressive periodontitis (<jats:italic>n<\/jats:italic>\u2003=\u200373) in comparison with periodontitis\u2010free controls (<jats:italic>n<\/jats:italic>\u2003=\u200369).<\/jats:p><jats:p><jats:bold>Material and Methods:\u2002<\/jats:bold> Both interleukin\u20102 polymorphisms were analyzed using the polymerase chain reaction with sequence\u2010specific primers. Distributions of single alleles, genotypes and haplotypes were calculated using the chi\u2010square test. Risk factor analyses were carried out by logistic regression with respect to established cofactors for periodontitis. The presence of subgingival bacteria in an individual were analyzed using a molecular biological method (the micro\u2010Ident<jats:sup>\u00ae<\/jats:sup> test).<\/jats:p><jats:p><jats:bold>Results:\u2002<\/jats:bold> The interleukin\u20102 genotype \u2212330 TG occurred less frequently in patients with chronic periodontitis (25.9% vs. 49.3%). Moreover, this genotype decreased the adjusted odds ratio for chronic periodontitis (odds ratio\u2003=\u20030.394), whereas the interleukin\u20102 genotype 166 TT and the haplotype combination interleukin\u20102 \u2212330,166 TT\u2003:\u2003TT were associated with an increased adjusted odds ratio (odds ratio\u2003=\u20032.82 or 2.97). For the latter interleukin\u20102 combination, a positive association for the subgingival presence of <jats:italic>Porphyromonas gingivalis<\/jats:italic> (81.3% vs. 59.5%) and bacteria of the \u2018red complex\u2019 (78.1% vs. 56.0%) was shown.<\/jats:p><jats:p><jats:bold>Conclusion:\u2002<\/jats:bold> The interleukin\u20102 genotypes \u2212330 TG and 166 TT, as well as the combination genotype interleukin\u20102 TT\u2003:\u2003TT, could be putative prognostic factors for chronic periodontitis.<\/jats:p>","DOI":"10.1111\/j.1600-0765.2008.01173.x","type":"journal-article","created":{"date-parts":[[2009,5,18]],"date-time":"2009-05-18T16:00:49Z","timestamp":1242662449000},"page":"628-635","source":"Crossref","is-referenced-by-count":16,"title":["Interleukin\u20102 \u2212330 and 166 gene polymorphisms in relation to aggressive or chronic periodontitis and the presence of periodontopathic bacteria"],"prefix":"10.1111","volume":"44","author":[{"given":"S.","family":"Reichert","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"H. 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