Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1261818 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR33525000_1.fastq.gz | Fastqsanger.gz | |||
| SRR33525000_2.fastq.gz | Fastqsanger.gz | |||
| SRR33525001_1.fastq.gz | Fastqsanger.gz | |||
| SRR33525001_2.fastq.gz | Fastqsanger.gz | |||
| SRR33525002_1.fastq.gz | Fastqsanger.gz |
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Project description:The peri-implant epithelium plays an important role in the prevention against initial stage of inflammation. In order to minimize the risk of peri-implantitis, it is necessary to understand the biological characteristics of the peri-implant epithelium. The aim of this study was to investigate the characteristic gene expression profile of peri-implant epithelium as compared to junctional epithelium using laser microdissection and microarray analysis.
2014-04-08 | GSE56533 | GEO
Project description:The peri-implant epithelium plays an important role in the prevention against initial stage of inflammation. In order to minimize the risk of peri-implantitis, it is necessary to understand the biological characteristics of the peri-implant epithelium. The aim of this study was to investigate the characteristic gene expression profile of peri-implant epithelium as compared to junctional epithelium using laser microdissection and microarray analysis. Left upper first molars of 4 week-old rat were extracted, and titanium alloy implants were placed. Four weeks after surgery, samples were harvested by laser microdissection, and total RNA samples were isolated. Comprehensive analyses of genes expressed in the junctional epithelium and peri-implant epithelium were performed using microarray analysis. Confirmation of the differential expression of selected genes was performed by quantitative real-time polymerase chain reaction and immunohistochemistry.
2014-04-08 | E-GEOD-56533 | biostudies-arrayexpress
Project description:Transcriptome analysis of oral tissue samples taken from peri-implantitis and healthy control patients Peri-implantitis is a condition resulting in destructive inflammation in the peri-implant soft tissue barrier. Clinically, it demonstrates vast clinical differences to periodontitis that suggests distinct inflammatory mechanisms. Implant-derived Titanium particles (i-TiPs) frequently found around diseased implants appear to alter the microenvironment and confer resistance to antibiotic treatments. Studies in orthopedic implants have demonstrated a strong inflammatory response to i-TiPs, involving a variety of cell types, in aseptic conditions. Nonetheless, the genetic programs of cells surveilling and supporting the peri-implant soft tissue barrier in response to the combined challenges of biomaterial degradation products and oral bacteria are poorly defined. Thus, we studied gene expression specific to oral peri-implant inflammatory disease. We found that certain cellular pathways were highly upregulated in diseased tissues. Upregulated pathways provided insight into important physiological pathways that might play a role in peri-implant pathology. These findings could potentially contribute to the production of more targeted and effective therapeutics for the disease.
2021-06-17 | GSE178351 | GEO
Project description:Oral health is associated with a symbiotic microbial community and host-microbe homeostasis is maintained by the controlled immune response. Various factors can disrupt this homeostasis. Dysbiosis, which is characterized by increased immune response and a shift in the microbiome, contributes the pathogenesis of peri-implantitis. Peri-implant mucosa and commensal bacteria play important roles in the maintenance of host-microbe homeostasis, but little is known about how they interact. We have therefore investigated the early host-microbe interaction between a commensal multispecies biofilm (Streptococcus oralis, Actinomyces naeslundii, Veillonella dispar, Porphyromonas gingivalis) and peri-implant mucosa at 24 and 48 h. Our in vitro peri-implant mucosa-biofilm model contained organotypic oral mucosa, implant material and biofilm. After 24 h, the biofilm induced a modest innate immune response in the peri-implant mucosa by the upregulation of 5 genes related to immune and inflammatory response and the increased secretion of IL-6 and CCL20. This controlled immune response protected tissue integrity and the peri-implant mucosa remained intact. The secreted antibacterial proteins human β-Defensins-1, -2, and CCL20 controlled the overgrowth of the biofilm by reducing its volume - without affecting the live/dead ratio or bacterial distribution. Thus, host-microbe homeostasis was established within the first 24 h. In contrast, host-microbe homeostasis was disrupted after 48 h. The mucosa was damaged and detached from the implant, due to the induced downregulation of cell adhesion related genes. The immune response was enhanced by upregulation of additional genes related to the immune and inflammatory response and increased secretion of IL-1β, TNF-α, and CCL20. Moreover, bacterial distribution was altered, with an increased proportion of V. dispar. The disrupted host-microbe homeostasis could lead to incipient dysbiosis. This deeper understanding of the early host-microbe interaction at the peri-implant site may provide the basis for new strategies to improve the prevention and therapy of peri-implant diseases.
2022-08-22 | GSE136274 | GEO
Project description:Purpose: The aim of this study was to explore whether differences exist and to what an extent of the immune-mediated inflammatory reactions between periodontitis and peri-implantitis at the transcriptional level in the same susceptible host. Methods: Ligature-induced experimental peri-implantitis and periodontitis in the same mice were established. Gingival tissues of healthy, periodontitis and peri-implantitis sites from the same oral cavity were collected and used for RNA-sequencing. Differentially expressed genes (DEGs) were screened between periodontitis/peri-implantitis sites and healthy sites. The enrichment analysis of DEGs were analyzed. Comprehensive immune landscape was annotated by seq-ImmuCC. Results: The results showed that 137 and 353 up-regulated DEGs as well as and 670 and 174 down-regulated DEGs were specifically expressed periodontitis/peri-implantitis group compared to the healthy control group, respectively. The pathways of complement and coagulation cascade and osteoclast differentiation were dominating in the peri-implantitis sites. Moreover, peri-implantitis sites exhibited elevated macrophage proportions and relatively enriched macrophage activation and bone loss compared with periodontitis. Conclusions: Results indicated that peri-implantitis and periodontitis exhibited significantly distinct transcriptional signatures. Additionally, the study suggests that the interplay between macrophages and bone resorption are comparatively more active in peri-implantitis compared with periodontitis. These biological processes may be factors contributing to the pathogenesis of peri-implantitis being distinct from that of periodontitis.
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Project description:To investigate the transcriptomic profile difference between LEPR cells in peri-implant fibrous tissue and peri-implant bone
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