BACKGROUND: The inflammatory response that is directed in large part by proinflammatory cytokine interleukin (IL)-1 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-1 in some individuals overrides the feedback mechanisms that normally master the dose of inflammation to a level sufficient to fight microbial invasion without long-lasting damage to the tissues involved. The aims of the present study were to determine the distribution of IL-1 gene polymorphism (IL-1A+4845 and IL-1B+3954) and their association with periodontal disease severity and to determine the significance of detecting the composite genotype (IL-1A allele2+IL-1B allele2) versus detecting either of them alone. METHODS: 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-1 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. RESULTS: 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-rank test; P<0.001) was seen between subjects positive and negative for the composite genotype. CONCLUSIONS: Results of the present study reinforced the association of the IL-1 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).
BACKGROUND: The inflammatory response that is directed in large part by proinflammatory cytokine interleukin (IL)-1 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-1 in some individuals overrides the feedback mechanisms that normally master the dose of inflammation to a level sufficient to fight microbial invasion without long-lasting damage to the tissues involved. The aims of the present study were to determine the distribution of IL-1 gene polymorphism (IL-1A+4845 and IL-1B+3954) and their association with periodontal disease severity and to determine the significance of detecting the composite genotype (IL-1A allele2+IL-1B allele2) versus detecting either of them alone. METHODS: 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-1 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. RESULTS: 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-rank test; P<0.001) was seen between subjects positive and negative for the composite genotype. CONCLUSIONS: Results of the present study reinforced the association of the IL-1 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).