Project description:We used a nonhuman primate (NHP) model of ligature-induced periodontitis to identify gingival transcriptome changes associated with aging during the phases of periodontitis lesions (initiation, progression, and resolution). Four age groups of nonhuman primate were studied: Young (<3 years of age); Adolescent (3 to 7 years), Adult (12 to 15 years), and Aged (17-23 years)
Project description:Purpose: The goal of this study was to characterize the gingival oral barrier immunity of mouse periodontitis gingiva. Method: A silk thread (ligature) was tied wround the mouse maxillary molar. Mouse palatal gingiva was harvested at 1 days after the ligature placement. Gingival cells were harvested and subjected to 10X Genomix scRNA-seq. Cell Ranger processed data were analysed.
Project description:Purpose: The goal of this study was to characterize the gingival oral barrier immunity of mouse early periodontitis gingiva. Method: A silk thread (ligature) was tied wround the mouse maxillary molar. Mouse palatal gingiva was harvested at 1 days after the ligature placement. Gingival cells were harvested and subjected to 10X Genomix scRNA-seq. Cell Ranger processed data were analysed.
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:We examined the molecular and cellular mechanism for chronic periodontitis in patients' gingival tissue by whole transcriptome sequencing.
Project description:The onset of periodontitis involves the response of gingival stroma to inflammatory stimulus. The cell constitution of gingival stroma, however, has never been mapped at the resolution of single cell. In this study, we used single-cell mRNA sequencing to establish cell atlas in mouse gingival stroma. Epithelial, mesenchymal, pericyte and neuronal clusters were successfully identified and their subpopulation and response to ligature-induced inflammation were also examined. While shifts in epithelial cell gene profile and proportion recapitulated the epithelium breakdown during periodontitis, mesenchymal cluster maintained its proportion and gene expression patterns.
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:We investigated the association between subgingival bacterial profiles and gene expression patterns in gingival tissues of patients with periodontitis. A total of 120 patients undergoing periodontal surgery contributed with a minimum of two interproximal gingival papillae (range 2-4) from a maxillary posterior. Prior to tissue harvesting, subgingival plaque samples were collected from the mesial and distal aspects of each papilla. Gingival tissue RNA was extracted, reverse-transcribed, labeled, and hybridized with whole-genome microarrays (310 in total)
Project description:We profiled miRNAs in gingival crevicular fluid (GCF) by a PCR-based method that yielded quantitative measures of more than 600 miRNAs. We found that miRNA profiles in GCF of periodontitis patients are distinct from those of healthy controls.
Project description:<p><strong>AIM:</strong> The role of lipids in periodontitis has not been well studied. Thus, this study aimed to explore periodontitis-associated lipid profile changes and identify differentially expressed lipid metabolites in gingival tissues.</p><p><strong>MATERIALS AND METHODS:</strong> Gingival tissues from 38 patients with periodontitis (periodontitis group) and 38 periodontally healthy individuals (control group) were collected. A UHPLC-QTOF-MS-based non-targeted metabolomics platform was used to identify and compare the lipid profiles of the two groups. The distribution and expression of related proteins were subsequently analyzed via immunohistochemistry to further validate the identified lipids.</p><p><strong>RESULTS:</strong> Lipid profiles significantly differed between the two groups, and 20 differentially expressed lipid species were identified. Lysophosphatidylcholines (lysoPCs), diacylglycerols (DGs) and phosphatidylethanolamines (PEs) were significantly upregulated, while triacylglycerols (TGs) were downregulated in the periodontitis group. Moreover, the staining intensity of ABHD5/CGI-58, secretory phospholipase A2 (sPLA2), and sPLA2-IIA was significantly stronger in the gingival tissues of patients with periodontitis than in those of healthy controls.</p><p><strong>CONCLUSIONS:</strong> LysoPCs, DGs, and PEs were significantly upregulated, whereas TGs were downregulated in gingival tissues of patients with periodontitis. Correspondingly, the immunohistochemical staining of ABHD5/CGI-58, sPLA2 and sPLA2-IIA in gingival tissues was consistent with the downstream production of lipid classes (lysoPCs, TGs and DGs).</p>