role of interleukin-1 beta gene polymorphism in aggressive periodontitis

The primary causal factor for periodontitis is bacteria, but the extent and severity of periodontal lesions can be influenced by environmental factors, acquired diseases, and genetic predisposition. Genetic polymorphisms for IL-1 beta have been proposed as potential genetic marker for periodontal disease susceptibility. To investigate the association of one of the IL-1 beta gene polymorphisms with aggressive periodontitis. The study was performed on a total of 50 individuals that were divided into 3 groups; healthy control group [HC] with clinically healthy periodontium, diseased control group suffering from chronic periodontitis [CP] and patients group suffering from aggressive periodontitis [AgP]. Patients and healthy controls received a full-mouth periodontal examination. Venous blood was taken by standard venipuncture and placed into EDTA-containing tube for DNA extraction and amplification by RFLP-PCR technique. The amplification products were subjected to digestion with Taq I restriction endonuclease enzyme. The resulting fragments were separated by agarose gel electrophoresis and visualized by ethidium bromide staining and UV light. The present study showed that the prevalence of the IL-1 beta positive genotype 1,1 at position+3953 was higher in AgP patients [75%] than in CP [40%] and HC [30%]. By estimating the OR for genotype 1, 1 of AgP and both CP and HC, it was found that it is more likely to develop AgP approximately 4.5 times than CP and approximately 7 times than HC. Thus, there was sufficient evidence to conclude that there is an association between the genotype 1,1 and AgP. These results suggested that this cytokine might predict and be associated with progressive inflammation and attachment loss as IL-1 plays a pivotal role in the inflammatory cascade of the immune response to microbial challenge and can induce several events associated with tissue destruction. From this we could support the association between IL-beta gene polymorphism and aggressive periodontitis. Hence IL-1 beta gene could be used as a genetic marker for early diagnosis of patients at risk

Assessment of the role of some haemostatic parameters in patients with cryptogenic stroke

Cryptogenic stroke [CS] is a stroke of unexplained aetiology, in 1/3 the of cases, the cause of stroke remains undetermined inspite of full investigations. Patient with CS are thought to have a state of hypercoagulablity. To unmask some of the pathogenic mechanisms underlying cryptogenic stroke through assessment of some genetic disorders including C6[77]T mutation methyl-enetetrahydrofolate reductase gene, activated protein C [APC] resistance and role of thrombin anti-thrombin complex concentration [TAT] in plasma as indicators of hypecoagulable state. The study was conducted on 20 Egyptian patients divided into 2 groups, group I included 10 patients [6 males and 4 females] with cryptogenic stroke aged less than 50 years and group II included 10 age and sex matched patients with non-cryptogenic stroke. All of the 20 cases studied were subjected to panel of investigations including routine laboratory tests and imaging studies in orders to exclude any risk factors for stroke in group I patients and to determine risk factor of stroke in group II. Both groups were investigated for C6[77]T mutation in methylenetetrahydrofolate reductase gene, activated protein C [APC] resistance and thrombin anti-thrombin complex concentration [TAT] in plasma. No statistical significant difference was found between the two groups as regard C6[77]T mutation in methylenetetrahydrofolate reductase gene, [APC] resistance and TAT concentration in plasma [p value >0.05]. However, TAT level was found to be positively correlated with the clinical severity in non-cryptogenic stroke [p value <0.05]. C6[77]T mutation in methylenetetrahydrofolate gene, [APC] resistance and TAT concentration in plasma are not independent risk factors for cryptogenic stroke. TAT could be used as indicator of clinical severity and prognosis in patient with non-cryptogenic stroke