Project description:Aim: To clarify the molecular mechanisms of occlusal trauma in bone loss through periodontal tissue transcriptome analysis in mice with periodontitis and traumatic occlusion. Materials and Methods: Ligature-induced periodontitis (Li) and composite resin-induced traumatic occlusion (Tra) mouse models were established: control (Co), Li, Tra, and LiTra. Bone resorption was evaluated using micro-computed tomography (micro-CT). RNA sequencing (RNA-seq) was conducted on gingiva, bone, and periodontal ligament from all groups 3 days post-induction. For long-term evaluation, the Co and Tra groups were maintained for 8 weeks, then analyzed using micro-CT and qRT-PCR. Results: Traumatic occlusion alone, sustained for 8 weeks, did not directly induce bone resorption; however, it significantly exacerbated bone resorption in mice with periodontitis. Cytokine–cytokine receptor interactions and Toll-like receptor signaling pathways were upregulated in LiTra bone tissue. Il11, Il1rl1, and Mmp3, associated with inflammation and bone metabolism, were more highly expressed in the LiTra group than in the Li group. TNF-α signaling via NFκB and inflammatory response gene sets were enriched in the bone tissue of LiTra group. Conclusions: Traumatic occlusion accelerates bone resorption in ligature-induced periodontitis but does not independently cause significant bone loss. Occlusal trauma enhances the expression of inflammation-related genes especially in bone with periodontitis.
Project description:The purpose of this study was to elucidate the molecular mechanisms of occlusal trauma using transcriptome analysis of periodontal tissues of periodontitis and traumatic occlusion mice.
Project description:To identify gene expression profiles in those periodontitis-associated fibroblasts (PAFs) versus normal gingival fibroblasts to determine their molecular repertoire, and exploit it for therapeutic intervention. We collected RNA from 4 paired PAF and non PAF from patients with periodontitis
Project description:This study evaluated the transcriptome of healthy gingival tissue in patients with a history of generalized aggressive periodontitis (GAgP) and chronic periodontitis (CP) and in subjects with no history of periodontitis (H), using microarray analysis.
Project description:Gene expressions relate to the pathogenesis of periodontitis and have a crucial role in local tissue destruction and susceptibility to the disease. The aims of the present study were to explore comprehensive gene expressions/transcriptomes in periodontitis-affected gingival tissues, and to identify specific biological processes. The purpose of the present study was 1) to compare comprehensive gene expression/transcriptomes of periodontitis-affected gingival tissues with those of healthy tissues by using microarray and data mining technologies, and 2) to analyze significantly differentially expressed genes which belong to pathological pathways in periodontitis by qRT-PCR. Two distinct gingival samples including healthy and periodontal-affected gingiva were taken from 3 patients with severe chronic periodontitis. Total RNAs from 6 gingival tissue samples were used for microarray and data-mining analyses. Comparisons, gene ontology, and pathway frequency analyses were performed and identified significant biological pathways in periodontitis. Quantitative reverse transcription real-time polymerase chain reaction (qRT-PCR) analyse using 14 chronic periodontitis patients including 3 patients listed above and 14 healthy individuals showed 9 differentially expressed genes in leukocyte migration and cell communication pathways.
Project description:Transcriptome analysis of periodontitis-associated fibroblasts by CAGE sequencing identified DLX5 and RUNX2 long variant as novel regulators involved in periodontitis
Project description:Redondoviridae is a recently identified family of DNA viruses associated with periodontitis. Circular RNAs (circRNAs) emerged as a novel endogenous, conserved noncoding RNAs, which contributed to the virus related immune‐inflammatory response. However, the characteristics and function of circRNAs in Redondoviridae related periodontal inflammation are not yet understood. The present study aimed to analyze the expression profiles of circRNAs in gingival tissues in periodontitis patients with and without Redondoviridae-infection and healthy controls using high-throughput RNA sequencing combined with experimental validation. Out of 17819 circRNAs, 175 circRNAs were dysregulated. Functional annotation and enrichment analysis of the differential circRNAs host genes demonstrated the potential alteration in the molecular and cellular components and metabolism in individuals suffering from periodontitis with Redondoviridae infection. Moreover, “axon guidance” (PATH:04360), “lysine biosynthesis” (PATH:00300) and “vascular endothelial growth factor signaling pathways” (PATH:04370) were significantly enriched in Redondoviridae infected gingivitis tissues. Furthermore, the key circRNAs (circCOL1A1, circAASS, circPTK2, circATP2B4, circDOCK1, circTTBK2, and circMCTP2) associated with the pathobiology of Redondoviridae related periodontitis were revealed by constructing circRNA-miRNA-mRNA networks. The bioinformatic analyses demonstrated that several abnormal expression circRNAs may contribute to the etiopathogenesis and development of Redondoviridae-related periodontitis. The findings of the present study have enhanced the current understanding of the mechanism of Redondoviridae-related periodontitis process and provide an insight into further applications for diagnostic markers and therapeutic uses.
Project description:The progression of periodontitis is closely associated with Th17 cells, yet the functional differences of Th17 cells under periodontitis conditions remain poorly understood. Therefore, we established an experimental periodontitis model using IL-17GFP/+ transgenic mice, isolated Th17 cells via flow cytometry, and performed RNA sequencing. Results showed that periodontitis induced significant changes in Th17 cells, including a marked increase in cell proportion, as well as upregulated expression of Th17-associated immunoinflammatory signaling pathways and inflammatory cytokines (IL-17, IL-23, and GM-CSF). Within Th17 differentiation-related pathways, Zap70 expression was significantly upregulated and exhibited a positive correlation with IL-17. Local silencing of Zap70 via AAV-sh-Zap70 significantly reduced the expression of IL-17, IL-23/IL-23r, and GM-CSF, while alleviating alveolar bone resorption. In conclusion, periodontitis significantly enhances the proinflammatory capacity of Th17 cells, and this change is associated with Zap70, which indicates that Zap70 holds promise as a potential therapeutic target for periodontitis.