Human oral metagenome
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA548277 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9280570.fastq.gz | Fastqsanger.gz | |||
| SRR9280580.fastq.gz | Fastqsanger.gz | |||
| SRR9280590.fastq.gz | Fastqsanger.gz | |||
| SRR9280600.fastq.gz | Fastqsanger.gz | |||
| SRR9280610.fastq.gz | Fastqsanger.gz |
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Project description:The goal of this study was to compare the gene expression profiles of chronically inflamed human peri-implant and chronically inflamed human periodontal tissues in order to elucidate potential changes at the molecular level. Cells out of the pocket depth of the inflamed peri-implant and periodontal ligament as well as from the middle third of healthy periodontal ligament were applied. Genome-wide gene expression was compared with the help of microarray analysis, and the data were validated by real-time RT-PCR. The expression rates of 14,239 genes were investigated and 2,079 of them were found differentially expressed by at least two-fold; the expression rates of 1,093 genes were significantly up-regulated and the expression rates of 986 genes were significantly down-regulated in inflamed peri-implant cells compared to inflamed periodontal cells. We focused on genes coding for extracellular matrix components and those that degrade them. Only genes of non-fibril-forming collagens (types IV, VI, VII, and XVII) were increased in inflamed peri-implant tissue, whereas only the genes of two fibril-forming collagens (types III and XVII) were decreased, suggesting that peri-implant tissue re-models faster than periodontal tissue. Furthermore, cathepsin D and cathepsin S might participate to a greater extent in connective tissue destruction of peri-implant tissue. The present investigation demonstrated that, despite their clinical similarities, periimplantitis and periodontitis are two different diseases at the genetic level. Keywords: inflammation, peri-implant, periodontal ligament cells The peri-implant tissue was scraped of the implant and the periodontal tissue was scraped off the roots of the teeth. Both tissue probes were treated with the RNeasy mini Kit (Qiagen, Hilden, Germany) to isolate total RNA from chronically inflamed peri-implant and chronically inflamed PDL cells, according to the manufacturer’s instructions. Healthy PDL cells were taken from the middle third of the root clearly avoiding sampling the gingiva. The chronically inflamed peri-implant and periodontal cells were taken directly out of the depth of the pocket again avoiding the ingrown gingiva. Quality control and quantitation of total RNA samples were determined prior to the microarray experiments (Agilent 2100 Bioanalyzer, Agilent Technologies, Palo Alto, CA, USA). Equal amounts of total RNA were pooled into an inflamed peri-implant and an inflamed and healthy periodontal cell pool. To monitor the relative abundance of mRNA for full-length human genes, the Affymetrix GeneChip HG_U133A was used, representing 22,283 probe sets (14,239 unique human genes). Labelled cRNA, fragmented to an average size of 100–150 bases, was hybridized to the GeneChips. For each pool of cRNA, two GeneChips were hybridized. Chronically inflamed peri-implant as well as healthy and chronically inflamed periodontal tissue was collected from 48 patients at the Dental Medical School of the University of Goettingen (21 men, 27 women, aged between 18 and 72 years) from March 2005 to August 2006, as already described by Gersdorff et al. (2007). The peri-implant tissue probes were taken from endosteal implants (Astra Tech®, ITI Bonefit®, or Brånemark®) with chronic peri-implant lesions (Schwarz et al. 2007). The periodontal tissue probes were taken from teeth, either extracted for orthodontic reasons or due to carious lesions (healthy periodontium) or from teeth with generalized chronic periodontitis (Armitage 2004). Teeth with healthy PDL had no clinical signs of inflammation (no bleeding on probing), exhibited a probing depth of ?3,5 mm and had no radiographic detectable bone loss. In contrast, implants and teeth with generalized chronic inflammation exhibited obvious clinical signals of inflammation (bleeding on probing), exhibited a probing depth of >4 mm and had radiographic evidence of bone loss (1 to 7 mm). A detailed anamnesis of each patient was explored. All patients were without a medical history, i.e. heart diseases or diabetes, and were not on medication. In addition, the tissue samples used in our study were only taken from non-smokers. The explanted implants and extracted teeth were immediately frozen and stored at -80 °C. All patients who participated in the study were informed about the nature and aim of this project and gave their written informed consent. The study was approved according to the regulations of the Ethics Committee of the Medical Faculty of the University of Goettingen.
2009-08-30 | E-GEOD-8908 | biostudies-arrayexpress
Project description:The goal of this study was to compare the gene expression profiles of chronically inflamed human peri-implant and chronically inflamed human periodontal tissues in order to elucidate potential changes at the molecular level. Cells out of the pocket depth of the inflamed peri-implant and periodontal ligament as well as from the middle third of healthy periodontal ligament were applied. Genome-wide gene expression was compared with the help of microarray analysis, and the data were validated by real-time RT-PCR. The expression rates of 14,239 genes were investigated and 2,079 of them were found differentially expressed by at least two-fold; the expression rates of 1,093 genes were significantly up-regulated and the expression rates of 986 genes were significantly down-regulated in inflamed peri-implant cells compared to inflamed periodontal cells. We focused on genes coding for extracellular matrix components and those that degrade them. Only genes of non-fibril-forming collagens (types IV, VI, VII, and XVII) were increased in inflamed peri-implant tissue, whereas only the genes of two fibril-forming collagens (types III and XVII) were decreased, suggesting that peri-implant tissue re-models faster than periodontal tissue. Furthermore, cathepsin D and cathepsin S might participate to a greater extent in connective tissue destruction of peri-implant tissue. The present investigation demonstrated that, despite their clinical similarities, periimplantitis and periodontitis are two different diseases at the genetic level. Keywords: inflammation, peri-implant, periodontal ligament cells
2009-08-30 | GSE8908 | GEO
Project description:In this study we want to ascertain the differences and similarities of infected and inflammated peri implant tissue versus healthy peri implant tissue at the mRNA level.
2014-05-14 | GSE57631 | GEO
Project description:In this study we want to ascertain the differences and similarities of infected and inflammated peri implant tissue versus healthy peri implant tissue at the mRNA level. Six of the patients where affected by periimplantitis. In situ dental implants where explanted because of inflammation and non-integration. From two patients, implants were explanted because of wrong placement. They where classified as implants with healthy periimplant tissue.
2014-05-14 | E-GEOD-57631 | biostudies-arrayexpress
Project description:The mucosal penetration area formed by implant placement is critical problems of dental implant treatment, because epithelial barrier is broken and it can become a source of inflammation. To clarify the influence and risk caused by dental implant treatment in peri-implant soft tissue, we compared to gene expression profile of peri-implant soft tissue and oral mucosal tissue with microarray analysis. Both side upper first molars of 4 week-old rat were extracted, and titanium alloy implants were placed only in the left extraction socket. Four weeks after surgery, samples were harvested from left side of peri-implant soft tissue and right side of oral mucosal tissue.
2013-01-24 | E-GEOD-43744 | biostudies-arrayexpress
Project description:The mucosal penetration area formed by implant placement is critical problems of dental implant treatment, because epithelial barrier is broken and it can become a source of inflammation. To clarify the influence and risk caused by dental implant treatment in peri-implant soft tissue, we compared to gene expression profile of peri-implant soft tissue and oral mucosal tissue with microarray analysis.
2013-01-24 | GSE43744 | GEO
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.
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Project description:Subgingival plaque and peri-implant biofilm
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