Crosstalk between Venous Thromboembolism and Periodontal Diseases: A Bioinformatics Analysis

Abstract

Background. This current study applied bioinformatics analysis to reveal the crosstalk between venous thromboembolism (VTE) and periodontitis, as well as the potential role of immune-related genes in this context. Methods. Expression data were downloaded from the GEO database. Blood samples from venous thromboembolism (VTE) were used (GSE19151), while for periodontal disease, we used gingival tissue samples (GSE10334, GSE16134, and GSE23586). After batch correction, we used “limma” packages of R language for differential expression analysis ( p value < 0.05, ∣ logFC ∣ ≥ 0.5 ). We used Venn diagrams to extract the differentially expressed genes common to VTE and periodontitis as potential crosstalk genes and applied functional enrichment analysis (GO biological process and KEGG pathway). The protein-protein interaction (PPI) network of crosstalk genes was constructed by Cytoscape software. The immune-related genes were downloaded from the literature. The Wilcoxon test was used to test the scores of immune infiltrating cells. The crosstalk genes were further screened by LASSO Logistic Regression. Results. For periodontitis, 427 case and 136 control samples, and for VTE, 70 case and 63 control samples were included. The obtained PPI network had 1879 nodes and 2257 edges. Moreover, 782 immune genes and 28 cell types were included in the analysis. Over 90% of immune cells had different expressions in VTE and periodontitis. We obtained 12 significant pathways corresponding to crosstalk genes. CD3D, CSF3R, and CXCR4 acted as an immune gene and a crosstalk gene. We obtained a total of 12 shared biomarker crosstalk genes. Among those 12 biomarker crosstalk genes, 4 were immune genes (LGALS1, LSP1, SAMSN1, and WIPF1). Conclusion. Four biomarker crosstalk genes between periodontitis and VTE were also immune genes, i.e., LGALS1, LSP1, SAMSN1, and WIPF1. The findings of the current study need further validation and are a basis for development of biomarkers.

Is periodontal infection a risk factor for thromboembolic disease? A systematic review

“…Three possible mechanisms of interaction between VTE and periodontitis include (1) invasion of vascular system by periodontal pathogen, (2) effect of periodontitis-induced inflammation on platelet function and risk of thrombosis, and (3) effect of shared risk factors including diabetes and smoking. [ 40 ] Hence, periodontal disease can be suggested to be a modifiable risk factor associated with thromboembolic disease. Further controlled clinical studies are needed to validate specific mechanism underlying periodontal disease and thromboembolic events.…”

Suppression of SAMSN1 contributes to neuroprotection in neonatal rats suffering from hypoxic–ischemic encephalopathy injury

“…Meanwhile, the deletion of SAMSN1 significantly affected multiple cell types contributing to MM development 14 . In addition, recent research demonstrated that SAMSN1 is a biomarker crosstalk gene between periodontitis and venous thromboembolism 17 . Another study has found that platelet gene expression profiling can detect the early signal of impending acute myocardial infarction (AMI) before the occurrence of infarction, and SAMSN1 is one of the DEGs in platelet gene expression profiling 18 ; meanwhile, SAMSN1 is reported as a gene associated with coronary atherosclerosis and B‐cell activation 19 .…”

Investigating the Mechanism of Astragalus in the Treatment of Periodontitis through Bioinformatics Analysis

“…Target genes associated with periodontitis were searched using the GeneCards platform (https://www.genecards.org/)[18],, OMIM platform (https://www.omim.org/) [19], and DrugBank platform (https://www.drugbank.ca/) [20]. Two datasets, GSE10334 and GSE16134[8, 21,22], were obtained by searching the GEO database (https://www.ncbi.nlm.nih.gov/geo/) for periodontitis-related datasets using the keyword "periodontitis". The samples in both datasets were obtained from gingival tissue, with the experimental group consisting of samples from individuals with periodontitis and the control group consisting of samples from individuals with healthy gingiva.…”