ArticleBMC oral health2024
Endo 180 participates in collagen remodeling of the periodontal ligament during orthodontic tooth movement.
Article in BMC oral health, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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.
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Who cites it
2 citing papers in PubMed.
- Type 2 diabetes mellitus impairs tooth supraeruption by disrupting periapical alveolar bone remodeling.BMC oral health · 2026Article
- Integrative multi-omics and causal inference reveal periodontal ligament cell-macrophage crosstalk under orthodontic force.Progress in orthodontics · 2025Article
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Authors and funding
11 authors.
Funding
Abstract
backgroundOrthodontic tooth movement (OTM) relies on the remodeling of periodontal tissues, including the periodontal ligament (PDL) and alveolar bone. Collagen remodeling plays a crucial role during this process, allowing for the necessary changes in the PDL's structure and function. Endo180, an urokinase plasminogen activator receptor-associated protein, is a transmembrane receptor regulated collagen remodeling. This study aims to investigate whether and how Endo180 participates in collagen remodeling within the PDL during OTM. MATERIALS AND
methodsA mechanical force-induced OTM rat model was established using a closed coiled spring to mesially move the right maxillary first molar. The distance of OTM was examined by micro-computed tomography (micro-CT). The collagen remodeling within the PDL was assessed using atomic force microscope (AFM), Hematoxylin-Eosin (HE) staining and Masson staining. Protein expressions of Endo180, collagen I (COL I) and collagen III (COL III) were analyzed via immunofluorescence staining. Additionally, the mRNA expressions of Endo180, COL I, and COL III in force-induced PDL cells were examined by RT-qPCR in vitro. To further illustrate the role of Endo180 in regulating COL I and COL III expressions, Endo180 siRNA (siEndo) was applied to force-stimulated PDL cells.
resultsForce application increased OTM distance and disrupted collagen fiber organization, with a greater decrease in collagen elastic modulus on the mesial side than on the distal side of the PDL. After 7 days of force application, Endo180 and COL III expressions significantly increased in PDL tissues, while COL I expression decreased in PDL tissues. Compressive force loading in vitro upregulated the mRNA expressions of Endo180 and COL III, but downregulated COL I mRNA expression. Notably, Endo180 knockdown using siRNA suppressed force-induced COL III expression while restoring the downregulated COL I expression under compressive force stimuli.
conclusionForce-induced Endo180 expression modulates collagen remodeling in PDL during OTM by upregulating COL III and downregulating COL I. This collagen reorganization facilitates efficient tooth movement, highlighting Endo180 as a potential therapeutic target to optimize orthodontic treatment outcomes.
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