{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,28]],"date-time":"2026-02-28T04:34:00Z","timestamp":1772253240406,"version":"3.50.1"},"reference-count":41,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2006,9,1]],"date-time":"2006-09-01T00:00:00Z","timestamp":1157068800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Periodontology"],"published-print":{"date-parts":[[2006,9]]},"abstract":"<jats:p><jats:bold>Background:<\/jats:bold> The inflammatory response that is directed in large part by proinflammatory cytokine interleukin (IL)\u20101 is genetically determined, with some people having a more vigorous response than others to the same stimulus. The reason for this is speculated that the dysregulated production of IL\u20101 in some individuals overrides the feedback mechanisms that normally master the dose of inflammation to a level sufficient to fight microbial invasion without long\u2010lasting damage to the tissues involved. The aims of the present study were to determine the distribution of IL\u20101 gene polymorphism (IL\u20101A+4845 and IL\u20101B+3954) and their association with periodontal disease severity and to determine the significance of detecting the composite genotype (IL\u20101A allele2 + IL\u20101B allele2) versus detecting either of them alone.<\/jats:p><jats:p><jats:bold>Methods:<\/jats:bold> A total of 120 subjects were included and divided into four groups of 30 subjects each, namely, healthy, mild, moderate, and severe periodontitis groups. After a complete clinical examination, DNA was isolated from 0.5 ml blood. Specific primers were used to detect the presence of IL\u20101 gene polymorphism with the help of polymerase chain reaction (PCR) and subsequent allele detection with restriction fragment length polymorphism (RFLP) and separation by gel electrophoresis.<\/jats:p><jats:p><jats:bold>Results:<\/jats:bold> The distribution of the allele1 homozygous genotype was 3% in the severe periodontitis group, and the distribution for the allele2 genotype was 30%. A higly significant difference (Wilcoxon signed\u2010rank test; <jats:italic>P<\/jats:italic> &lt;0.001) was seen between subjects positive and negative for the composite genotype.<\/jats:p><jats:p><jats:bold>Conclusions:<\/jats:bold> Results of the present study reinforced the association of the IL\u20101 genotype as a risk factor for severe chronic periodontitis. Positivity for the composite genotype was found to be significantly associated with severe chronic periodontitis (odds ratio [OR] = 12.42).<\/jats:p>","DOI":"10.1902\/jop.2006.050427","type":"journal-article","created":{"date-parts":[[2006,8,31]],"date-time":"2006-08-31T22:23:31Z","timestamp":1157063011000},"page":"1515-1521","source":"Crossref","is-referenced-by-count":29,"title":["Assessment of Single Nucleotide Polymorphism at IL\u20101A+4845 and IL\u20101B+3954 as Genetic Susceptibility Test for Chronic Periodontitis in Maharashtrian Ethnicity"],"prefix":"10.1002","volume":"77","author":[{"given":"Amit A.","family":"Agrawal","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Atya","family":"Kapley","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ramreddy 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