PurposeDigital image technology and a real-time fluorescent quantitative polymerase chain reaction (RQ-PCR) were used to determine the changes in dental plaque caused by different toothbrushing tools.MethodsA total of 120 subjects were selected and divided into four groups: a manual toothbrush group, a manual toothbrush combined with an oral irrigator group, an electric toothbrush combined with an oral irrigator group, and an electric toothbrush group. We compared the changes in plaque count, plaque area, and colony colonization of the four groups after different cleaning tools had been used for a period of time.ResultsDental plaque count and plaque area decreased in all four groups. The decreases in plaque count and Streptococcus mutans in the electric toothbrush combined with an oral irrigator group were significantly higher than those in other groups.ConclusionElectric toothbrush combined with an oral irrigator shows a good result for plaque removal effect. Digital image analysis combined with biological methods can be used to evaluate dental plaque.
BACKGROUND: DNA methylation plays a vital role as an epigenetic change that contributes to chronic periodontitis. OBJECTIVE: This study aimed to integrate two methylation datasets (GSE173081 and GSE59962) and two gene expression datasets (GSE10334 and GES16134) to identify abnormally methylated differentially expressed genes related to chronic periodontitis. METHODS: Differentially methylated genes were obtained. Functional enrichment analysis of DMGs was performed. The protein-protein interaction (PPI) network was constructed using STRING and Cytoscape software. Finally, the hub genes were selected from the PPI network by using CytoHubba. RESULTS: In total, 122 hypomethylated and highly expressed genes were enriched in the biological mechanisms that are involved in the differentiation of extracellular matrix organization, extracellular structure organization, and cell chemotaxis. The three selected hub genes of the PPI network were IL1B, KDR, and MMP9. A total of 122 hypermethylated and lowly expressed genes were identified, and biological processes, such as cornification, epidermis development, skin development, and keratinocyte differentiation were enriched. CDSN DSG1, and KRT2 were identified as the top 3 hub genes of the PPI network. CONCLUSION: Based on the comprehensive bioinformatics analysis, six hub genes (IL1B, KDR, MMP9, CDSN DSG1, and KRT2) were associated with chronic periodontitis. Our findings provide novel insights into the mechanisms underlying epigenetic changes in chronic periodontitis.
Objective Chronic periodontitis is an incurable infectious disease characterized by complex inflammatory immune response. This study aimed was to screen and identify effective biomarkers correlated with macrophage in chronic periodontitis. Materials and methods Periodontitis datasets obtained from the gene expression omnibus (GEO) were analyzed to identify differentially expressed genes (DEGs). Functional enrichment analysis of DEGs by GO and KEGG revealed multiple biological processes and signaling pathways related to immune response. Further analysis was performed on two immune-related gene databases, ImmPort and innateDB, to identify DEGs related to immune cells infiltration in chronic periodontitis. Subsequently, Protein-protein interaction (PPI) network were established to reveal hub genes with MCC algorithm using CytoHubba tool. Enrichment analysis in DisGeNet showed that immune-related DEGs were enriched in periodontitis. Next, CIBERSORTx tool was analyzed to investigate immune cells infiltration in GSE10334 dataset. Results The results demonstrated differential macrophage infiltration in periodontitis. Notably, RAC2 and CXCR4 were identified as biomarkers correlated with M2 macrophages in chronic periodontitis. Finally, receiver operating curve (ROC) was plotted to determine the diagnostic value of identified hub genes which was then validated using relevant datasets of macrophages. Conclusion RAC2 and CXCR4 are potential biomarker of chronic periodontitis correlated with M2 macrophages infiltration. Further experiments are needed to more deeply explore the roles of CXCR4 and RAC2 in the molecular mechanism of M2 macrophages in periodontitis microenvironment.
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