Abstract
BackgroundDespite of numerous studies on periodontitis, the mechanism underlying the progression of periodontitis still remains largely unknown. This study aimed to have an expression profiling comparison between periodontitis and normal control and to identify more candidate genes involved in periodontitis and to gain more insights into the molecular mechanisms of periodontitis progression.MethodsThe gene expression profile of GSE16134, comprising 241 gingival tissue specimens and 69 healthy samples as control which were obtained from 120 systemically healthy patients with periodontitis (65 with chronic and 55 with aggressive periodontitis), was downloaded from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) in periodontitis samples were screened using the limma package in R compared with control samples. Gene Ontology (GO) and pathway enrichment analysis upon the DEGs were carried out using Hypergeometric Distribution test. Protein-protein interaction (PPI) network of the DEGs was constructed using Cytoscape, followed by module selection from the PPI network using MCODE plugin. Moreover, transcription factors (TFs) of these DEGs were identified based on TRANSFAC database and then a regulatory network was constructed.ResultsTotally, 762 DEGs (507 up- and 255 down-regulated) in periodontitis samples were identified. DEGs were enriched in different GO terms and pathways, such as immune system process, cell activation biological processes, cytokine-cytokine receptor interaction, and metabolic pathways. Cathepsin S (CTSS) and pleckstrin (PLEK) were the hub proteins in the PPI network and 3 significant modules were selected. Moreover, 19 TFs were identified including interferon regulatory factor 8 (IRF8), and FBJ murine osteosarcoma viral oncogene homolog B (FOSB).ConclusionThis study identified genes (CTSS, PLEK, IRF-8, PTGS2, and FOSB) that may be involved in the development and progression of periodontitis.Electronic supplementary materialThe online version of this article (doi:10.1186/s12903-015-0086-7) contains supplementary material, which is available to authorized users.
Highlights
Despite of numerous studies on periodontitis, the mechanism underlying the progression of periodontitis still remains largely unknown
Data preprocessing and Differentially expressed genes (DEGs) screening In the original analysis of Kebschull et al [12], a total of 248 differentially regulated probes were identified at an absolute fold change of ≥1.19, and 30 overexpressed only one under-expressed probe by an absolute change of >1.5 fold were identified in aggressive periodontitis lesions compared with chronic periodontitis lesions
Gene Ontology (GO) and pathway enrichment analysis of DEGs Functional and pathway enrichment analysis indicated that up-regulated DEGs and down-regulated DEGs in the periodontitis samples were significantly enriched in different GO terms and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways (Tables 1 and 2)
Summary
Despite of numerous studies on periodontitis, the mechanism underlying the progression of periodontitis still remains largely unknown. Periodontitis is a chronic inflammatory disease involving interactions between complex microbial biofilms, many cell populations and inflammatory mediators, leading to the destruction of the tooth-supporting structures like the periodontal ligament and the alveolar bone [1]. Inflammation and bone loss are hallmarks of periodontal disease [7] and accumulated evidence demonstrates that a number of mediators are involved in these processes [8]. Cochran et al had reported that the reduction of inflammation and attenuation of the host’s immune reaction to the microbial plaque could lead to a decrease in the ratio of nuclear factor-kappa B ligand (RANKL)/osteoprotegerin (OPG) and a decrease in associated bone loss [7]. Despite of numerous investigations on periodontitis, the mechanism still remains largely unknown
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