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Background: Recurrent aphthous stomatitis (RAS) is one of the most common chronic oral diseases with morbidity ranging from 5% to 20%. The pathogenesis is still not fully understood though immune dysregulation and local trauma have been implicated and the curative effect that can be achieved through current therapy is mainly to alleviate the pain. So, the understanding of its molecular mechanisms can allow the prevention and treatment of RAS at the molecular level.
Methods: 14 normal tissues and 14 ulcerated tissues were subjected to Affymetrix Human Genome U133 Plus 2.0 Array transcriptome analysis. Then, Gene Set Expression Analysis and Gene Pattern tools were carried out to determine the gene expression differences between normal and ulcerated tissues. qRT-PCR was used to validate the expression level of identified genes in 10 normal and 10 ulcerated tissues.
Results: We obtained a total of 1379 DEGs with adjPval < 0.05 and |logFC| > 1 including 1052 up-regulated genes and 327 down-regulated genes. 4 GO terms and 4 KEGG pathways were screened out by comparing the genomewide gene set expression patterns of normal and ulcerated tissues. 7 genes involved in RAS were identified from the VEGF signaling pathway.
Conclusions: Present findings demonstrated that several immune processes have a deep impact on RAS and a number of genes involved in the VEGF signaling pathway may be critical mediators or participators in the pathogenesis of RAS.
DOI: 10.7754/Clin.Lab.2016.160721
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