5.3
#159
NOVEL POLYMORPHISMS IN THE HUMAN INTERLEUKIN-7 GENE PROMOTER HAVE NOT ASSOCIATED WITH EARLY ONSET PERIODONTITIS (EOP).
Mohammad R. Bazrafshani, Dr , William E.R. Ollier, Dr , Martin H. Thornhill, Dr and Ali H. Hajeer, Dr . Manchester Lancashire, United Kingdom, University of Manchester, M13 9PL, The Centre for Integrated Genomic Medical Research and San Antonio TX, University of Texas Health Sciences Centre, 78229-3900, Department of Dental Diagnostic Sciences .
Objectives: Periodontal disease is a chronic inflammatory disease of the supporting tissues of the teeth. Early onset periodontitis (EOP) is characterised by a rapid rate of periodontal tissue destruction, in young individuals. There is now substantial evidence to suggest that genetic factors play a role in the pathogenesis of EOP. In human peripheral monocytes IL-7 induces the synthesis of some inflammatory mediators such as IL-1 and Il-6. We tried to examine the influence of a genetic polymorphism of the gene encoding Interleukin-7 (IL-7) on the development of early onset periodontitis.
Material and methods: In trying to analyse genetic polymorphism of the IL-7. The promoter region of the IL-7 gene was screened for polymorphisms using denaturing HPLC technique (wave analysis), single stranded conformation polymorphism (SSCP) analysis and direct PCR-sequencing on a set of UK healthy controls.
Results: Two novel single base nucleotide substitutions polymorphisms were identified both of which were rare. Allele and genotype frequencies were determined by polymerase chain reaction followed by restriction analysis with specific endonuclease for the T-316G polymorphism and a SNaPSHOT typing system was developed for the other polymorphism at T-822G on a larger set of EOP (n=77) and control (n=91) subjects. No Significant differences were observed in allele or genotype frequencies between the EOP patients and control group in this study.
Conclusions: IL-7 is considered as one of candidate genes for severity of EOP and identified polymorphism can be one of genetic determinants influencing the development of this inflammatory condition.