Association of interleukin-1 receptor antagonist gene polymorphisms with generalized aggressive periodontitis in an Iranian population.

BACKGROUND: Periodontitis is a multifactorial disease that occurs in the presence of bacteria, environmental factors, and genetic predispositions. It is suggested that polymorphisms in the interleukin-1 (IL1) receptor antagonist gene have an important role in the susceptibility of the host to periodontitis. This study investigates the association of a variable number of tandem repeat polymorphism in the IL1RN gene with generalized aggressive periodontitis (GAgP). METHODS: Sixty-six subjects with GAgP and 56 periodontally healthy subjects took part in the study. All subjects were of Iranian Khorasanian (north-east province of Iran) descent. Subjects were identified through clinical examinations and radiographs at the Mashad Dental School and Dental Research Center. DNA was extracted from peripheral blood cells, and different genotypes were detected using polymerase chain reaction amplification and fragment-size analysis. Data were analyzed using the chi(2) test. RESULTS: The frequencies of the IL1RN genotype A1A2 (chi(2) test; P = 0.001) and allele A2 (chi(2) test; P = 0.006) were found to be significantly increased in patients with GAgP compared to normal subjects. CONCLUSION: These findings suggest that the polymorphic IL1RN gene is a risk determinant for generalized aggressive periodontitis in the Iranian Khorasanian population.

Analysis of -1082 IL-10 gene polymorphism in Iranian patients with generalized aggressive periodontitis.

BACKGROUND: Periodontitis is a multifactorial disease and its severe forms, such as aggressive periodontitis, are suggested to have a genetic basis. Among the genetic factors, polymorphisms in cytokine genes have recently been described in susceptibility to periodontitis. IL-10 is a multi-functional cytokine thought to play a role in the pathogenesis of periodontitis. A substitution G/A polymorphism in the promoter region of the IL-10 gene at position -1082 has been associated with different amounts of IL-10 production. The aim of the present study was to investigate the possible links between -1082(G/A) polymorphism of the IL-10 gene and the generalized form of aggressive periodontitis. MATERIAL/METHODS: This study included 52 Iranian Khorasanian (north-east province of Iran) subjects suffering from generalized aggressive periodontitis referred to the Periodontology Department of Mashhad Dental School. They were compared to 61 age and sex-matched healthy controls of the same race. DNA was isolated from peripheral blood cells and genotyping was performed by means of the amplification refractory mutation system polymerase chain reaction (ARMS-PCR) method. Data were analyzed using the chi-squared test. RESULTS: There was no marked difference in genotype frequencies between the controls and generalized aggressive periodontitis patients (p=0.585). Moreover, no association between patients and normal subjects was found in their allele frequency (p=0.329). CONCLUSIONS: We conclude that the polymorphic nucleotide A at position -1082 of the IL-10 gene is not associated with generalized aggressive periodontitis in the Iranian population.

Interleukin-6 production by cultured peripheral blood monocytes before and after stimulation by E. coli lipopolysaccharide in Iranian patients with aggressive periodontitis.

BACKGROUND: It has been suggested that hyper-responsiveness of monocytes to the products of dental plaque, especially the endotoxin of Gram-negative bacteria and the secretion of high levels of pro-inflammatory cytokines, may have a role in the pathogenesis of aggressive periodontitis (AP). To investigate this possibility, IL-6 production by cultured peripheral blood monocytes before and after stimulation by E. coli lipopolysaccharide (LPS) in AP patients was evaluated. MATERIAL/METHODS: Fifteen patients with AP were compared with 15 periodontally healthy controls in a case control study. Monocytes were obtained from peripheral blood samples and cultured. The reaction of monocytes was studied by their IL-6 production using ELISA before and six hours after stimulation by 0.1 microg/ml E. col. LPS. The Wilcoxon and Mann-Whitney U tests were used to compare the groups. RESULTS: There was no significant difference in IL-6 production levels before LPS stimulation between patients and controls. Upon LPS stimulation, IL-6 levels increased in both the patient and control groups compared with their IL-6 levels before stimulation. IL-6 production after LPS stimulation in the patients was higher than controls, but this was not statistically significant. However, the increase in IL-6 production as a result of LPS stimulation was significantly higher in patients than in controls. CONCLUSIONS: Increased monocyte responsiveness may play a potential role in the pathogenesis of AP. However, whether this is an intrinsic characteristic of the monocyte/macrophage cells of AP patients or just a priming effect as a result of the periodontal disease remains to be investigated.