Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1050775 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR27255103_1.fastq.gz | Fastqsanger.gz | |||
| SRR27255103_2.fastq.gz | Fastqsanger.gz | |||
| SRR27255104_1.fastq.gz | Fastqsanger.gz | |||
| SRR27255104_2.fastq.gz | Fastqsanger.gz | |||
| SRR27255105_1.fastq.gz | Fastqsanger.gz |
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Project description:Peri-implantitis (PI) is a pathological condition occurring in tissues around dental implants, resulting in a high risk of treatment failure, which lack of efficacious treatment. The prevention and treatment of peri-implant mucositis is considered an effective and economical measure to prevent the occurrence of PI because oral mucosa provides the first line of defense against deleterious stimuli. Importantly, though there are similar morphological structure in the epithelium barrier between dental implant and natural teeth, the one around the implant having a lower capacity to seal tightly than it does around a natural tooth. Meanwhile, the immune system of peri-implant tissue is inferior in defense to periodontal tissue. Compared by natural teeth, the specific molecules and cell types involved in the pathogenesis of PI is still unclear. This study collected clinical patient gingival tissue samples and used single-cell RNA sequencing to analyze multiple aspects, discovering significant heterogeneity in the epithelial barriers and surrounding immune defenses of periodontitis and peri-implantitis, as well as related response molecules. It provided strong evidence for clinical strategies for the treatment of peri-implantitis.
2026-08-12 | GSE272774 | 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.
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:Peri-implant fibrosis is one of the most common reasons for implant failure and surgical revision after prosthetic joint replacement. This type of surgical revisionis associated with substantial additional morbidity and healthcare costs. However, the cellular and molecular mediators of peri-implant fibrosis remain unclear. Here, we show that peri-implant fibrotic tissue in mice and humans is largely composed of a specific population of leptin receptor-expressing(LEPR+) cells and that these LEPR+cells are necessary and sufficient to both generate and maintain peri-implant fibrotic tissue. Genetic ablation of LEPR+cells prevents peri-implant fibrosis, and implantation of LEPR+cells from peri-implant fibrotic tissue is sufficient to induce fibrosis in secondary hosts. We further identify adhesion G protein-coupled receptorF5 (ADGRF5) as a crucial mediator of the fibrotic response by LEPR+cells, as conditional deletion of ADGRF5 in LEPR+cells attenuates peri-implant fibrosis while augmenting peri-implant bone formation. Finally, we demonstrate that inhibition of ADGRF5 by intra articular or systemic administration of neutralizing anti-ADGRF5prevents and reverses peri-implant fibrosis. Thus, pharmaceutical agents that inhibit the ADGRF5 pathway inLEPR+cells may represent a new approach to prevent and treat peri-implant fibrosis.
2024-03-10 | GSE227128 | 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:Peri-implantitis is a common complication characterized by chronic inflammation of the periodontal tissue. This disease is marked by irreversible and progressive degradation of the gingiva and alveolar bone, ultimately leading to tooth loss.Most current research has focused on the entire periodontal tissue, which restricts a comprehensive understanding of the heterogeneity between gingiva and bone tissues, and hinders the development of targeted host therapies for peri-implantitis. To uncover the pathogenic mechanisms of peri-implantitis, our study employed a tissue-specific approach to investigate the interactions between stromal and immune cells in gingiva and bone tissues separately, using single-cell sequencing techniques. This strategy aims to develop the insights of the pathogenesis of peri-implantitis, providing a scientific basis for the treatment of peri-implantitis.
2024-11-11 | GSE281266 | GEO
Project description:Oral inflammatory diseases affect nearly half of all humans, yet mechanisms underlying rapidly-destructive inflammation remain poorly understood. We compared peri-implantitis with moderate- and high-grade periodontitis using integrated microbial and single-cell sequencing (>967,169-cells; single-cell RNA-seq, spatial proteotranscriptomics). Laser capture microdissection with compartmental microbiome analysis revealed reduced bacterial load and diversity in peri-implantitis. Expansion of the Human Periodontal Atlas with peri-implantitis single-cell RNA-seq data (36-samples; 121,395 cells) identified CD34+ vascular endothelial cell (VEC) rarefaction and oxidative stress, hypoxia, and NAD⁺ metabolism-associated transcriptional programs enriched in a TNFRSF6B⁺/ICAM1⁺ post-capillary venule (PC-VEC) subpopulation. NAD⁺-consuming ectoenzyme CD38 was selectively enriched and orthogonally confirmed by spatial transcriptomics (6-samples; 283,377-cells) and proteomics (23-samples; 562,397-cells). Spatial neighborhood analyses demonstrated CD38⁺-high PC-VEC expansion, closer proximity, and higher IL16–CD4 T cell signaling in peri-implantitis. Matched high-grade periodontitis biopsies confirmed spatially restricted CD38⁺-VECs despite similar microbial burden, identifying endothelial vasculopathy underlying rapidly advancing oral inflammation and a potential therapeutic axis.
2026-05-08 | GSE310110 | GEO
Project description:Systemic antibiotics in the surgical treatment of peri-implantitis: Impact on the salivary microbiome
| PRJEB102458 | ENA
Project description:Peri-implantitis prevention remains a significant challenge in implant dentistry. This study evaluated the dual functionality of a curcumin-carbon dot (Cur-CD) complex in enhancing the osteogenic differentiation of rat bone marrow mesenchymal stem cells (rBMSCs) and exerting antibacterial effects. Primary rBMSCs were isolated and divided into control and Cur-CD-treated groups. After 21 days of osteogenic induction, total RNA was extracted for transcriptome sequencing analysis to investigate the molecular mechanisms underlying Cur-CD-promoted osteogenesis. The results demonstrated that Cur-CD significantly enhanced mineralized nodule formation and up-regulated expression of key osteogenic markers (Runx2, OPN, Osterix, OCN), providing evidence for its potential as a bioactive agent for preventing peri-implantitis.
2026-08-12 | GSE343587 | GEO