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:Traumatic occlusion exacerbates bone resorption by modifying gene expression in the bone tissue of ligature-induced periodontitis in mice
Project description:Traumatic occlusion exacerbates bone resorption by modifying gene expression in the bone tissue of ligature-induced periodontitis in 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