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Genomewide association study on chronic periodontitis in Korean population: results from the Yangpyeong health cohort
Author(s) -
Hong KyungWon,
Shin MyungSeop,
Ahn YooBeen,
Lee HyunJin,
Kim HyunDuck
Publication year - 2015
Publication title -
journal of clinical periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.456
H-Index - 151
eISSN - 1600-051X
pISSN - 0303-6979
DOI - 10.1111/jcpe.12437
Subject(s) - periodontitis , single nucleotide polymorphism , chronic periodontitis , odds ratio , medicine , genome wide association study , cohort , population , confounding , genetics , biology , genotype , gene , environmental health
Abstract Aim This study aims to locate the genes related to periodontitis through genome‐wide association study ( GWAS ) in Korean population. Methods Total of 677 adults aged 44–88 years were recruited from the Yangpyeong cohort in Korea. The participants did not have self‐reported metabolic diseases, cardiovascular diseases or cancer. Periodontitis was assessed using alveolar bone loss from a digital panoramic radiograph and classified into three groups: normal to mild, moderate and severe periodontitis. DNA from blood samples were genotyped using the Illumina Human 1M‐duo Beadchip. Multivariable logistic regression analysis in PLINK was applied to examine the single‐nucleotide polymorphisms ( SNP s) related to periodontitis after controlling for various confounders. Results Associations of three SNP s suggested TENM 2 (rs4242220) and LDLRAD 4 (rs12969041, rs2027756) as putative risk genes of chronic periodontitis ( p ‐values <1 × 10 −5 ). The odds ratio [95% confidence interval ( CI )] of TENM 2 was 0.53 (0.40–0.70) for moderate periodontitis and that of LDLRAD 4 was 2.86 (1.92–4.27) for severe periodontitis. Two nonsynonymous SNP s of protein coding region and seven SNP s selected from previous reports showed nominal association. Conclusion Our GWAS supports a previously reported gene of TENM 2 and newly suggests LDLRAD 4 . These two genes’ role on lipid metabolism may play a part in the molecular aetiology of periodontitis.