ArticleJournal of applied oral science : revista FOB2026
Notch2 is involved in regulating apical tissue repair following severe intrusive luxation.
Article in Journal of applied oral science : revista FOB, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
methodologyThis study aims to characterize apical repair dynamics in immature permanent teeth after severe intrusive luxation, and to explore Notch signaling pathway regulation in this process using a Sprague-Dawley rat model. In this study, a modified tool was utilized to establish an intrusive luxation model in SD rats. Tissue repair was assessed via micro-computed tomography (Micro-CT) and hematoxylin-eosin (H&E) staining. Differential gene expression analysis of stem cells from the apical papilla (SCAPs) was performed using the publicly available GEO dataset. Immunohistochemical detection of Notch2 receptor expression in the apical region of injured teeth was subsequently conducted, guided by bioinformatics screening. Finally, the Notch signaling pathway was pharmacologically inhibited using DAPT (γ-secretase inhibitor), and its impact on post-injury prognosis was evaluated.
resultsHistological analysis revealed prevalent pulp hypoplasia and apical tissue fibrosis after injury. Differential gene analysis suggested that the Notch signaling pathway, particularly Notch2, is involved in the regulation of angiogenesis-related pathways in SCAPs. Immunohistochemistry showed positive Notch2 expression in fibrotic apical regions. Notably, inhibition of Notch signaling significantly reduced aberrant fibrosis while enhancing vascular proliferation in the injury site.
conclusionsSevere intrusive luxation is primarily characterized by aberrant fibrous differentiation in the apical region. The Notch signaling pathway may negatively regulate angiogenesis in the damaged apical area, suggesting that targeted inhibition of this pathway could promote tissue repair following embedded dental injuries.
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