Epigenetic findings in periodontitis in UK twins: a cross-sectional study.
作者： Yuko Kurushima , Pei-Chien Tsai , Juan Castillo-Fernandez , Alexessander Couto Alves , Julia Sarah El-Sayed Moustafa
DOI: 10.1186/S13148-019-0614-4
关键词:
摘要: Genetic and environmental risk factors contribute to periodontal disease, but the underlying susceptibility pathways are not fully understood. Epigenetic mechanisms malleable regulators of gene function that can change in response genetic stimuli, thereby providing a potential mechanism for mediating effects periodontitis. The aim this study is identify epigenetic changes across tissues associated with disease. Self-reported gingival bleeding history gum or tooth mobility, were used as indicators DNA methylation profiles generated using Infinium HumanMethylation450 BeadChip whole blood, buccal, adipose tissue samples from predominantly older female twins (mean age 58) TwinsUK cohort. Epigenome-wide association scans (EWAS) mobility conducted blood 528 492 twins, respectively. Subsequently, targeted candidate analysis at 28 genomic regions was carried out testing phenotype-methylation associations 41 (tooth mobility) 43 (gingival bleeding) 501 556 samples. analyses identified one CpG-site (cg21245277 ZNF804A) (FDR = 0.03, nominal p value = 7.17e−8) 58 sites (FDR < 0.05) top signals IQCE XKR6. variation (247 CpG-sites) chronic periodontitis showed an enrichment traits, eight genes (VDR, IL6ST, TMCO6, IL1RN, CD44, IL1B, WHAMM, CXCL1) significant both traits. methylation-phenotype validated buccal samples, subset (25%) also tissue. adult specific linked self-reported Future work will explore basis functional impact these results infer strategic personalized treatments prevention
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