DNA methylation profiles of immune response‐related genes in apical periodontitis. (3rd July 2018)

• Record Type: Journal Article
• Authors: Wichnieski, C.; Maheshwari, K.; Souza, L. C.; Nieves, F.; Tartari, T.; Garlet, G. P.; Carneiro, E.; Letra, A.; Silva, R. M.
• Is Part Of: International endontic journal. Volume 52:Number 1(2019)
• Page Start: 5
• Page End: 12
• Publication Date: 2018-07-03
• Subjects: apical periodontitis -- DNA methylation -- gene -- inflammation -- promoter; Endodontics -- Periodicals; 617.6342
• DOI: 10.1111/iej.12966
• Languages: English
• ISSNs: 0143-2885

Abstract

Abstract: Aim: To investigate the DNA methylation profiles of immune response‐related genes in apical periodontitis (AP) lesions. Methodology: The methylation profiles on the cytosine‐phosphate‐guanine (CpG) regions of 22 gene promoters involved in inflammation and autoimmunity were assessed in 60 human AP lesions and 24 healthy periodontal ligaments (controls) using a pathway‐specific real‐time polymerase chain reaction array (EpiTect® Methyl Signature PCR Array Human Inflammatory Response). Differentially methylated genes were subsequently assessed for their mRNA expression. Data analyses (One‐wayanova, Tukey's multiple comparisons tests and Mann–Whitney tests) were performed using GraphPad Prism 6 software. P values ≤ 0.05 were considered statistically significant. Results: Significant DNA hypermethylation was observed for CXCL3 and FADD gene promoters in AP lesions when compared to control tissues ( P < 0.001) and among other genes ( P < 0.05). In contrast, IL12B and IL4R were associated with significant hypomethylation in comparison to other genes ( P < 0.05). IL12B, IL4R, CXCL3 and FADD had differential mRNA expression in AP lesions and controls ( P < 0.001). Conclusions: Differential methylation profiles of immune response‐related genes, such as FADD, CXCL3, IL12B and IL4R, may have an influence on individual AP susceptibility and patient treatment outcomes, through their potential contributions to altered expression of disease‐relevant genes. Methylation and/or genetic variations in additional genes may also contribute to the dynamics of AP development and should be considered in future studies.