الفهرس 
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Abstract
Periodontal disease is a chronic multifactorial disease
which initiated and sustained by bacterial plaque. Cytokines has a
leading role at all stages of the immune response in periodontal
disease. Components of the cell wall of pathogenic bacteria
stimulate the production of proinflammatory cytokines release
from the host immune cells. Most blamed proinflammatory
cytokines are interleukin-1beta (IL-1β) and tumor necrosis factoralpha (TNF-α).
There are several risk factors for periodontal disease
including endocrine disorders like diabetes mellitus, hematologic
disorder and immune deficiencies, genetic disorders, stress,
nutrition, medications and other systemic conditions. Genetics is
an important risk factor for periodontal diseases and individual
susceptibility to periodontal disease is determined in part by a
genetic predisposition.
Polymorphism arises as a result of gene mutation and has
different types. The simplest and most frequent type resulted from
a single base mutation is termed a single nucleotide
polymorphism (SNP). IL-1 single nucleotide genetic
polymorphisms were the most common SNP studied in both chronic and aggressive periodontitis. These SNPs were IL-1A -
889, IL-1A +4845, IL1B-511, IL-1B -31, IL-1B +3954 and
IL1RN (VNTR). Significant differences were reported in the
distribution of interleukin-1B gene polymorphism in different
ethnic populations.
This case-control study included 83 Egyptian patients that
were recruited from the outpatient clinic of Oral Medicine,
Periodontology, Oral Diagnosis and Radiology Department, AinShams University, Cairo, Egypt in the period from November
2014 to November 2015. The study subjects were divided into
four groups: group 1 (control group) consisted of 20 patients,
group 2 (chronic periodontitis) consisted of 23 patients, group 3
(localized aggressive periodontitis) consisted of 20 patients, and
group 4 (generalized aggressive periodontitis) consisted of 20
patients.
Patients’ genotype and allele frequencies (C vs T) were
compared to controls to have an idea whether their genetic
background was a predisposing factor for the disease. We have
found that cases of chronic periodontitis were not statistically
different from controls regarding their IL-1B +3954 polymorphic
genotypes. On the other hand, cases with localized aggressive
periodontitis had a positive association. The T allele frequency
among these cases was about 3.5 times that of controls. Similarly,