Abstract
Objectives To investigate potential genetic biomarkers of peri-implantitis and target genes for the therapy of peri-implantitis by bioinformatics analysis of publicly available data. Methods The GSE33774 microarray dataset was downloaded from the Gene Expression Omnibus (GEO). The differentially expressed genes (DEGs) between peri-implantitis and healthy gingival tissues were identified using the GEO2R tool. GO enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were performed using the DAVID database and the Metascape tool, and the results were expressed as a bubble diagram. The protein-protein interaction network of DEGs was constructed using the Search Tool for the Retrieval of Interacting Genes (STRING) and visualized using Cytoscape. The hub genes were screened by the cytoHubba plugin of Cytoscape. The potential target genes associated with peri-implantitis were obtained from the DisGeNET database and the Open Targets Platform. The intersecting genes were identified using the Venn diagram web tool. Results Between the peri-implantitis group and the healthy group, 205 DEGs were investigated including 140 upregulated genes and 65 downregulated genes. These DEGs were mainly enriched in functions such as the immune response, inflammatory response, cell adhesion, receptor activity, and protease binding. The results of KEGG pathway enrichment analysis revealed that DEGs were mainly involved in the cytokine-cytokine receptor interaction, pathways in cancer, and the PI3K-Akt signaling pathway. The intersecting genes, including IL6, TLR4, FN1, IL1β, CXCL8, MMP9, and SPP1, were revealed as potential genetic biomarkers and target genes of peri-implantitis. Conclusions This study provides supportive evidence that IL6, TLR4, FN1, IL1β, CXCL8, MMP9, and SPP1 might be used as potential target biomarkers for peri-implantitis which may provide further therapeutic potentials for peri-implantitis.
Highlights
In recent decades, dental implants have been widely used for the restoration of missing teeth with high success rates [1]
The results showed that IL6, TLR4, FN1, IL1β, MMP9, CXCL8, CXCR4, CXCL1, PECAM1, and SPP1 were identified as hub genes (Table 2)
Our results showed that the proinflammatory cytokines IL-6, IL-1β, and CXCL8 were upregulated in peri-implantitis
Summary
Dental implants have been widely used for the restoration of missing teeth with high success rates [1]. Peri-implantitis can be defined as an inflammation of the peri-implant connective tissue and progressive loss of the supporting bone around the implants [2], and it is considered to be the leading cause of implant failure. Studies have shown that bacterial infection could be the cause of the peri-implantitis and subsequent implant failure, and the various gene polymorphisms may be associated with the occurrence of periimplantitis [2]. The underlying pathogenic mechanisms of peri-implantitis remain unclear, the excessive inflammatory response due to the microbial biofilms on implants and their toxins is believed to play an important role in the occurrence of peri-implantitis [5, 6]. The immune-inflammatory response elicited by the bacterial biofilm may be responsible for the gingival recession and alveolar bone loss associated with peri-implantitis. Lipopolysaccharide can induce the cells of gingival and osseous tissues
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