ArticleMolecular medicine (Cambridge, Mass.)2012
Inhibition of GSK3 abolishes bacterial-induced periodontal bone loss in mice.
Article in Molecular medicine (Cambridge, Mass.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed, 42 citations in OpenAlex.
- Combined application of a GSK3 inhibitor and injectable platelet rich fibrin with deproteinized bovine bone improves bone regeneration.Scientific reports · 2026Article
- Tobacco-enhanced biofilm formation by Porphyromonas gingivalis and other oral microbes.Molecular oral microbiology · 2024Review
- AR-A014418, a glycogen synthase kinase-3β inhibitor, mitigates lipopolysaccharide-induced inflammation in rat dental pulp stem cells via NLR family pyrin domain containing 3 inflammasome impairment.Journal of dental sciences · 2023Article
- SGK1 negatively regulates inflammatory immune responses and protects against alveolar bone loss through modulation of TRAF3 activity.The Journal of biological chemistry · 2022Article
- Porphyromonas gingivalis infection alters Nrf2-phase II enzymes and nitric oxide in primary human aortic endothelial cells.Journal of periodontology · 2021Article
- Article
- Glycogen Synthase Kinase 3β Modulates the Inflammatory Response Activated by Bacteria, Viruses, and Parasites.Frontiers in immunology · 2021Review
- Review
- GSK3 inhibitor-loaded osteotropic Pluronic hydrogel effectively mitigates periodontal tissue damage associated with experimental periodontitis.Biomaterials · 2020Article
- JAK3 restrains inflammatory responses and protects against periodontal disease through Wnt3a signaling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Bacterial Manipulation of Wnt Signaling: A Host-Pathogen Tug-of-Wnt.Frontiers in immunology · 2019Review
- Marijuana-Derived Cannabinoids Trigger a CB2/PI3K Axis of Suppression of the Innate Response to Oral Pathogens.Frontiers in immunology · 2019Article
- Tobacco-induced suppression of the vascular response to dental plaque.Molecular oral microbiology · 2018Review
- Manipulation of Neutrophils byFrontiers in cellular and infection microbiology · 2017Review
- Does Oxidative Stress Induced by Alcohol Consumption Affect Orthodontic Treatment Outcome?Frontiers in physiology · 2017Review
- Wnt/β-Catenin Regulates the Activity of Epiprofin/Sp6, SHH, FGF, and BMP to Coordinate the Stages of Odontogenesis.Frontiers in cell and developmental biology · 2016Article
- GSK3β and the control of infectious bacterial diseases.Trends in microbiology · 2014Review
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- Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
Abstract
The tissue destruction that characterizes periodontitis is driven by the host response to bacterial pathogens. Inhibition of glycogen synthase kinase 3β (GSK3β) in innate cells leads to suppression of Toll-like receptor (TLR)-initiated proinflammatory cytokines under nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) p65 transcriptional control and promotion of cyclic adenosine monophosphate response element-binding (CREB)-dependent gene activation. Therefore, we hypothesized that the cell permeable GSK3-specific inhibitor, SB216763, would protect against alveolar bone loss induced by the key periodontal pathogen, Porphyromonas gingivalis (P. gingivalis), in a murine model. B6129SF2/J mice either were infected orally with P. gingivalis ATCC 33277; or treated with SB216763 and infected with P. gingivalis; sham infected; or exposed to vehicle only (dimethyl sulfoxide [DMSO]); or to GSK3 inhibitor only (SB216763). Alveolar bone loss and local (neutrophil infiltration and interleukin [IL]-17) and systemic (tumor necrosis factor [TNF], IL-6, Il-1β and IL-12/IL-23 p40) inflammatory indices also were monitored. SB216763 unequivocally abrogated mean P. gingivalis-induced bone resorption, measured at 14 predetermined points on the molars of defleshed maxillae as the distance from the cementoenamel junction to the alveolar bone crest (p < 0.05). The systemic cytokine response, the local neutrophil infiltration and the IL-17 expression were suppressed (p < 0.001). These data confirm the relevance of prior in vitro phenomena and establish GSK3 as a novel, efficacious therapeutic preventing periodontal disease progression in a susceptible host. These findings also may have relevance to other chronic inflammatory diseases and the systemic sequelae associated with periodontal infections.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.