Traumatic occlusion exacerbates bone resorption by modifying gene expression in the bone tissue of ligature-induced periodontitis in mice
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE292710 | GEO | 2026/05/20
REPOSITORIES: GEO
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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.
2026-05-20 | GSE316444 | GEO
Project description:We performed single-cell RNA-sequencing analysis on mouse periodontal lesions to analyze the detailed mechanism underlying immune–bone cell interactions in periodontitis.
2024-03-06 | GSE254766 | GEO
Project description:Treatment of periodontitis in people with diabetes remains challenging. Diabetes-enhanced oxidative stress is a primary cause of aggravation of periodontitis. The present study aimed to investigate the therapeutic potential of thioredoxin-1 (TRX1), an essential endogenous antioxidant protein, in the management of periodontitis with diabetes, as well as its role in modulating osteogenic differentiation. Our findings indicated that the production of reactive oxygen species (ROS) was elevated, while the expression of TRX1 was significantly reduced in the periodontal tissues of periodontitis mice with diabetes. Furthermore, knockdown of TRX1 in periodontal ligament stem cells (PDLSCs) resulted in the inhibition of osteogenic differentiation through disrupting Wnt/β-catenin signal pathway. However, this inhibition was restored upon administration of recombinant human TRX1 (rhTRX1). Importantly, rhTRX1 treatment decreased ROS generation, activated Wnt/β-catenin signal pathway and considerably promoted the alveolar bone repair of periodontitis mice with diabetes. These findings highlighted the crucial protective role of TRX1 in periodontitis with diabetes and suggested that it may serve as a potential therapeutic target for refractory periodontitis associated with oxidative stress.
2023-09-06 | GSE235930 | GEO
Project description:Ligature-induced periodontitis (LIP) induces rapid alveolar bone loss followed by gingival immunosuppressive conditions
2026-03-04 | GSE298066 | GEO
Project description:Periodontitis induces myeloid lineage skewing of the bone marrow progenitor cells. In this study, we performed single cell RNA-sequencing in LSK (Lin—Sca-1+cKit+ ) cells to determine whether the periodontitis-induced myeloid lineage bias persists after the resolution of periodontal inflammation.
2022-04-27 | GSE196808 | GEO
Project description:Neutrophil recruitment and activation are hallmarks of the prevalent inflammatory disease, periodontitis. However, the mechanisms by which neutrophils contribute to in inflammatory bone destruction remain unclear. Herein, we document that neutrophil extracellular traps (NETs) have a direct role in mediating inflammatory pathology. In an established animal model of periodontitis, we demonstrate that genetic or pharmacologic inhibition of NETs formation, or removal of NETs by DNase-Ⅰ, alleviates inflammatory bone loss in vivo. Investigating the mechanisms by which NETs drive periodontal inflammation, we find that extracellular histones have a direct role in disease progression. Consistent with findings in animal models, histones bearing classic NET-associated post-translational modifications are correlated with disease severity and are significantly elevated in local lesions and systemic circulation of patients with periodontitis. Our work reveals NETs-associated components as pathogenic mediators, potential biomarkers, and therapeutic targets for periodontitis.
2023-05-23 | GSE228021 | GEO
Project description:Periodontitis (PD) as a chronic inflammatory disease instigated by periodontal pathogenic bacteria and mediated by the host immune response, resulting in the destruction of supporting periodontal tissue and tooth loss in adults. Constructing an injectable delivery system that allows for sustained drug release within periodontal pockets to continuously eliminate pathogenic bacteria, reduce periodontal inflammation, and promote periodontal tissue regeneration is an effective strategy for periodontitis treatment. Here, we explore the therapeutic potential and underlying mechanisms of curcumin-loaded Pickering emulsion (PE-CUR) in periodontitis treatment. The Pickering emulsion formulation offers an effective delivery system, enhancing curcumin's bioavailability and therapeutic efficacy. In vitro studies, we demonstrate that the PE-CUR exhibit excellent biocompatibility and anti-inflammatory property by elimination of reactive oxygen species (ROS). In addition, PE-CUR significantly eliminate key periodontal pathogens, including Porphyromonas gingivalis (P. gingivalis) and Staphylococcus aureus (S. aureus). In a rat model of periodontitis, PE-CUR significantly attenuates periodontal tissue inflammation and alveolar bone loss, indicating a protective effect against periodontal tissue destruction. Mechanistically, PE-CUR promotes the expression of anti-inflammatory factors and inhibits the release of pro-inflammatory factors by regulating macrophage polarization from M1 to M2 and modulating the MAPK and PI3K-AKT signaling pathway. Furthermore, PE-CUR decreases the formation of osteoclasts as well as stimulates the activation and differentiation of osteoblasts successively, thereby ameliorating the periodontal inflammation and promoting the alveolar bone regeneration. Overall, our findings elucidate the therapeutic mechanisms of PE-CUR in periodontitis, suggesting its potential as a promising treatment strategy warranting further clinical investigation.
2024-08-16 | GSE274645 | GEO
Project description:Hypoxia has a significant impact on periodontal homeostasis and is a contributing factor to periodontal pathogenicity. This study aimed to investigate the role and mechanism of hypoxia in periodontitis.
2024-04-28 | GSE262663 | GEO
Project description:Periodontitis is an inflammatory condition affecting periodontal tissues, such as the gingiva and alveolar bone, surrounding the teeth. However, previous research has focused on analyzing a single sample type, such as tissue, blood, or gingival crevicular fluid (GCF), which may limit the comprehensive understanding of the complex pathology of periodontitis. We conducted a proteomic analysis using liquid chromatography-mass spectrometry (LC-MS) on the periodontal tissues and GCF from patients with periodontitis. This analysis distinguished distinct proteomic signatures between the two sample types, with 3,803 proteins being identified in periodontal tissue and 910 proteins in GCF, underscoring the significant variances pertinent to periodontal health. Proteins such as S100A12, MPO, APOA1, CTSG, and PSMA1 were markedly upregulated in GCF, suggesting their potential as key markers of neutrophil activity and systemic inflammation. These findings provide profound insights into both the local and systemic pathophysiological processes underlying periodontitis, emphasizing the utility of GCF as a non-invasive medium for reflecting comprehensive disease states.
2026-04-06 | PXD054953 | Pride
Project description:Background/purpose Periodontal diseases exacerbate hepatic inflammation and diseases like non-alcoholic fatty liver disease via circulating pathogenic factors from periodontal tissue. Long-term pre-symptomatic state eventually leads to the development of such hepatic diseases. However, it is uncertain if periodontitis contributes in the onset of hepatic pre-symptomatic state. Herein, we conducted a hepatic whole transcription analysis of periodontitis-affected mice and healthy mice to understand the early functional changes in the hepatic system in periodontitis-affected mice. Materials and methods Silk ligatures were tied around mice second maxillary molars for 14 days to develop periodontitis. RNA-seq samples were collected from periodontal tissues and liver tissues of mice with periodontitis and healthy mice. Lipidomic analysis of hepatic omega-3 fatty acids in periodontitis-affected and healthy mice was conducted. The anti-inflammatory effects of omega-3 fatty acids and their metabolites were elucidated using hepatocytes HepG2 cells. Results In the liver of mice with periodontitis, genes coding for cytochrome P450 such as Cyp4a12a and Cyp4a12b were identified as significantly down-regulated genes. Lipidomic analyses identified that epoxidation and subsequent hydrolysis of hepatic omega-3 fatty acids were inhibited in periodontitis-affected mice. Eicosapentaenoic acid metabolites, epoxy eicosatetraenoic acid and dihydroxyeicosatetraenoic acid, inhibited inflammatory responses of HepG2 cells. Conclusion These results suggest that, in the liver of periodontitis-affected mice, due to the reduced activity of omega-3 fatty acid epoxidation, pre-symptomatic state with pro-inflammatory status develop. Therefore, early intervention of periodontitis might contribute to the prevention of the onset of hepatic diseases.
2024-05-03 | GSE264546 | GEO