| Literature DB >> 30218097 |
Matthias Munz1,2, Gesa M Richter1, Bruno G Loos3, Søren Jepsen4, Kimon Divaris5,6, Steven Offenbacher7, Alexander Teumer8, Birte Holtfreter9, Thomas Kocher9, Corinna Bruckmann10, Yvonne Jockel-Schneider11, Christian Graetz12, Ilyas Ahmad2, Ingmar Staufenbiel13, Nathalie van der Velde14,15, André G Uitterlinden14, Lisette C P G M de Groot16, Jürgen Wellmann17, Klaus Berger17, Bastian Krone18, Per Hoffmann19,20, Matthias Laudes21, Wolfgang Lieb22, Andre Franke22, Jeanette Erdmann2,23,24, Henrik Dommisch1, Arne S Schaefer25.
Abstract
Periodontitis is one of the most common inflammatory diseases, with a prevalence of 11% worldwide for the severe forms and an estimated heritability of 50%. It is classified into the widespread moderate form chronic periodontitis (CP) and the rare early-onset and severe phenotype aggressive periodontitis (AgP). These different disease manifestations are thought to share risk alleles and predisposing environmental factors. To obtain novel insights into the shared genetic etiology and the underlying molecular mechanisms of both forms, we performed a two step-wise meta-analysis approach using genome-wide association studies of both phenotypes. Genotypes from imputed genome-wide association studies (GWAS) of AgP and CP comprising 5,095 cases and 9,908 controls of North-West European genetic background were included. Two loci were associated with periodontitis at a genome-wide significance level. They located within the pseudogene MTND1P5 on chromosome 8 (rs16870060-G, P = 3.69 × 10-9, OR = 1.36, 95% CI = [1.23-1.51]) and intronic of the long intergenic non-coding RNA LOC107984137 on chromosome 16, downstream of the gene SHISA9 (rs729876-T, P = 9.77 × 10-9, OR = 1.24, 95% CI = [1.15-1.34]). This study identified novel risk loci of periodontitis, adding to the genetic basis of AgP and CP.Entities:
Mesh:
Year: 2018 PMID: 30218097 PMCID: PMC6303247 DOI: 10.1038/s41431-018-0265-5
Source DB: PubMed Journal: Eur J Hum Genet ISSN: 1018-4813 Impact factor: 4.246