Abstract:
:Pro-inflammatory cytokines, i.e., IL-1 mediate the inflammatory response and are genetically regulated in periodontal diseases. Strong association was found between the composite genotype allele 2 of IL-1β+3954 and IL-1α-889 and severe chronic periodontitis. The aim of this study is to determine the prevalence of IL-1β+3954 and IL-1α-889 polymorphism in a group of Lebanese individuals of homogeneous ethnicity and the possible association between genotype positive individuals and the severity of periodontal disease. One hundred and fifty-seven patients aged 53.29±13.13 years participated in the study. Subjects were classified as follows: 1) healthy subjects with no attachment loss >1mm and no clinical signs of gingival or periodontal inflammation; 2) diseased subjects with mild periodontitis (less than 15‰ of global periodontal bone loss); 3) subjects with moderate periodontitis (less than 4 interproximal sites with bone loss = or >50 percent and mean bone loss between 15 and 30%); 4) subjects with severe periodontitis (more than 7 interproximal sites with >50% bone loss and mean bone loss >35‰). Blood samples were taken and analyzed for polymorphism in the IL-1α gene at position +4845 and in the IL-1beta gene at position +3953. Statistical analysis was performed using chi-square test, Fisher Exact test, and ANOVA followed by Bonferroni multiple comparisons. The prevalence of genotype-positive subjects was 52.3‰ in the healthy control group and 42 ‰ in the diseased group. Positive genotype heterozygous of allele 1 and 2 for IL-1β+3954 and IL-1α-889 did not represent in this study a major risk for chronic periodontitis (p=0.590). Only subjects homozygous for allele2 of the IL-1β+3954 and IL-1α-889 were significantly more at risk for severe periodontitis with OR of 51.42.
journal_name
J Biol Regul Homeost Agentsjournal_title
Journal of biological regulators and homeostatic agentsauthors
Tawil G,Akl FA,Dagher MF,Karam W,Abdallah Hajj Hussein I,Leone A,Jurjus ARsubject
Has Abstractpub_date
2012-10-01 00:00:00pages
597-606issue
4eissn
0393-974Xissn
1724-6083pii
3journal_volume
26pub_type
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