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Title: Epigenetic adaptations of the masticatory mucosa to periodontal inflammation
Authors: Richter, Gesa M
Kruppa, Jochen
Keceli, H Gencay
Ataman-Duruel, Emel Tuğba
Graetz, Christian
Pischon, Nicole
Wagner, Gunar
Rendenbach, Carsten
Jockel-Schneider, Yvonne
Martins, Orlando 
Bruckmann, Corinna
Staufenbiel, Ingmar
Franke, Andre
Nohutcu, Rahime M
Jepsen, Søren
Dommisch, Henrik
Schaefer, Arne S
Keywords: EWAS; Methylation; Periodontitis; Gingiva; Inflammation; Cell type deconvolution; ROBO2; PTP4A3
Issue Date: 3-Nov-2021
Publisher: Springer Nature
Project: Open Access funding enabled and organized by Projekt DEAL 
Deutsche Forschungsgemeinschaft (DFG), RI 2827/1-1 
Bundesministerium für Bildung und Forschung (01DL15002) 
grant of the DG PARO/CP GABA-Forschungsförderung 
Serial title, monograph or event: Clinical Epigenetics
Volume: 13
Issue: 1
Abstract: Background: In mucosal barrier interfaces, flexible responses of gene expression to long-term environmental changes allow adaptation and fine-tuning for the balance of host defense and uncontrolled not-resolving inflammation. Epigenetic modifications of the chromatin confer plasticity to the genetic information and give insight into how tissues use the genetic information to adapt to environmental factors. The oral mucosa is particularly exposed to environmental stressors such as a variable microbiota. Likewise, persistent oral inflammation is the most important intrinsic risk factor for the oral inflammatory disease periodontitis and has strong potential to alter DNA-methylation patterns. The aim of the current study was to identify epigenetic changes of the oral masticatory mucosa in response to long-term inflammation that resulted in periodontitis. Methods and results: Genome-wide CpG methylation of both inflamed and clinically uninflamed solid gingival tissue biopsies of 60 periodontitis cases was analyzed using the Infinium MethylationEPIC BeadChip. We validated and performed cell-type deconvolution for infiltrated immune cells using the EpiDish algorithm. Effect sizes of DMPs in gingival epithelial and fibroblast cells were estimated and adjusted for confounding factors using our recently developed “intercept-method”. In the current EWAS, we identified various genes that showed significantly different methylation between periodontitis-inflamed and uninflamed oral mucosa in periodontitis patients. The strongest differences were observed for genes with roles in wound healing (ROBO2, PTP4A3), cell adhesion (LPXN) and innate immune response (CCL26, DNAJC1, BPI). Enrichment analyses implied a role of epigenetic changes for vesicle trafficking gene sets. Conclusions: Our results imply specific adaptations of the oral mucosa to a persistent inflammatory environment that involve wound repair, barrier integrity, and innate immune defense.
ISSN: 1868-7075
DOI: 10.1186/s13148-021-01190-7
Rights: openAccess
Appears in Collections:FMUC Med. Dentária - Artigos em Revistas Internacionais

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