RGD Reference Report - Tension force-induced bone formation in orthodontic tooth movement via modulation of the GSK-3ß/ß-catenin signaling pathway. - Rat Genome Database

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Tension force-induced bone formation in orthodontic tooth movement via modulation of the GSK-3ß/ß-catenin signaling pathway.

Authors: Mao, Yelin  Wang, Liangliang  Zhu, Ye  Liu, Yu  Dai, Hongwei  Zhou, Jianping  Geng, Dechun  Wang, Lin  Ji, Yong 
Citation: Mao Y, etal., J Mol Histol. 2018 Feb;49(1):75-84. doi: 10.1007/s10735-017-9748-x. Epub 2017 Dec 9.
RGD ID: 13792728
Pubmed: PMID:29224185   (View Abstract at PubMed)
PMCID: PMC5750339   (View Article at PubMed Central)
DOI: DOI:10.1007/s10735-017-9748-x   (Journal Full-text)

Orthodontic force-induced osteogenic differentiation and bone formation at tension sites play a critical role in orthodontic tooth movement. However, the molecular mechanism underlying this phenomenon is poorly understood. In the current study, we investigated the involvement of the GSK-3ß/ß-catenin signaling pathway, which is critical for bone formation during tooth movement. We established a rat tooth movement model to test the hypothesis that orthodontic force may stimulate bone formation at the tension site of the moved tooth and promote the rate of tooth movement via regulation of the GSK-3ß/ß-catenin signaling pathway. Our results showed that continued mechanical loading increased the distance between the first and second molar in rats. In addition, the loading force increased bone formation at the tension site, and also increased phospho-Ser9-GSK-3ß expression and ß-catenin signaling pathway activity. Downregulation of GSK-3ß activity further increased bone parameters, including bone mineral density, bone volume to tissue volume and trabecular thickness, as well as ALP- and osterix-positive cells at tension sites during tooth movement. However, ICG-001, the ß-catenin selective inhibitor, reversed the positive effects of GSK-3ß inhibition. In addition, pharmaceutical inhibition of GSK-3ß or local treatment with ß-catenin inhibitor did not influence the rate of tooth movement. Based on these results, we concluded that GSK-3ß/ß-catenin signaling contributes to the bone remodeling induced by orthodontic forces, and can be used as a potential therapeutic target in clinical dentistry.



Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
Ctnnb1Ratbone remodeling  IEP  RGD 
Gsk3bRatbone remodeling  IDA  RGD 

Objects Annotated

Genes (Rattus norvegicus)
Ctnnb1  (catenin beta 1)
Gsk3b  (glycogen synthase kinase 3 beta)


Additional Information