Małgorzata Mazurek-Mochol1, Elżbieta Dembowska1, Damian Malinowski2, Krzysztof Safranow3, Andrzej Pawlik4. 1. Department of Periodontology, Pomeranian Medical University, Szczecin, Poland. 2. Department of Pharmacology, Pomeranian Medical University, Szczecin, Poland. 3. Department of Biochemistry and Medical Chemistry, Pomeranian Medical University, Szczecin, Poland. 4. Department of Physiology, Pomeranian Medical University, Powstancow Wlkp. 72, 70-111, Szczecin, Poland. Electronic address: pawand@poczta.onet.pl.
Abstract
BACKGROUND: Periodontal disease (PD) is a chronic inflammatory condition caused by pathogenic microflora in a biofilm, often leading to tooth loss. The inflammatory response of periodontal tissues to infection is influenced by both environmental and genetic factors. The interleukin (IL)-1 family of proinflammatory cytokines plays a role in the tissue destruction associated with PD due to their proinflammatory and bone-resorptive properties. In addition, recent studies have indicated that polymorphisms in the genes encoding IL-1 might be associated with greater PD severity. In this study, we examined the association between IL-1ß rs1143634 and rs16944 polymorphisms and PD in non-smoking and smoking patients. MATERIALS AND METHODS: This study included 200 patients with PD (130 non-smokers and 70 smokers) and 156 control subjects (124 non-smokers and 32 smokers). Periodontal evaluation included approximal plaque index, modified sulcus bleeding index, probing pocket depth and clinical attachment loss. Genotyping was utilized for all samples by using allelic discrimination assays with TaqMan® probes on a 7500Fast Real-Time PCR Detection System. RESULTS: There were no statistically significant differences in the distribution of rs1143634 and rs16944 genotypes and alleles between patients with PD and control subjects, between smoking patients with PD and smoking controls, or between non-smoking patients with PD and non-smoking controls. CONCLUSIONS: The results of this study suggest there is no association between IL-1ß rs1143634 and rs16944 polymorphisms and PD.
BACKGROUND:Periodontal disease (PD) is a chronic inflammatory condition caused by pathogenic microflora in a biofilm, often leading to tooth loss. The inflammatory response of periodontal tissues to infection is influenced by both environmental and genetic factors. The interleukin (IL)-1 family of proinflammatory cytokines plays a role in the tissue destruction associated with PD due to their proinflammatory and bone-resorptive properties. In addition, recent studies have indicated that polymorphisms in the genes encoding IL-1 might be associated with greater PD severity. In this study, we examined the association between IL-1ß rs1143634 and rs16944 polymorphisms and PD in non-smoking and smoking patients. MATERIALS AND METHODS: This study included 200 patients with PD (130 non-smokers and 70 smokers) and 156 control subjects (124 non-smokers and 32 smokers). Periodontal evaluation included approximal plaque index, modified sulcus bleeding index, probing pocket depth and clinical attachment loss. Genotyping was utilized for all samples by using allelic discrimination assays with TaqMan® probes on a 7500Fast Real-Time PCR Detection System. RESULTS: There were no statistically significant differences in the distribution of rs1143634 and rs16944 genotypes and alleles between patients with PD and control subjects, between smoking patients with PD and smoking controls, or between non-smoking patients with PD and non-smoking controls. CONCLUSIONS: The results of this study suggest there is no association between IL-1ß rs1143634 and rs16944 polymorphisms and PD.