Evidence map›Paper›PMID 42310668›Full record

ArticleBMC oral health2026

Mechanical activation of Piezo1 promotes osteoclastogenesis in orthodontic tooth movement.

Fu Zheng, Tong Wu, Feifei Wang, Xinyu Cui, Hongyi Tang, Peng Chen, Cuiying Li, Jiuhui Jiang

Abstract read
In one paragraph

Article in BMC oral health, 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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1 · What the graph read from it

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.

2 · The registry

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3 · Its place in the literature

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0 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

8 authors.

Fu Zheng *Department of Orthodontics, Beijing Key Laboratory of Digital Stomatology, Peking University School and Hospital of StomatologyNational Clinical Research Center for Oral Diseases & National Engineering Laboratory for Digital and Material Technology of StomatologyHaidian District, No. 22 Zhongguancun Avenue South, Beijing, 100081, China.
Tong Wu *Department of Orthodontics, Beijing Key Laboratory of Digital Stomatology, Peking University School and Hospital of StomatologyNational Clinical Research Center for Oral Diseases & National Engineering Laboratory for Digital and Material Technology of StomatologyHaidian District, No. 22 Zhongguancun Avenue South, Beijing, 100081, China.
Feifei Wang *Center of Digital Dentistry, Beijing Key Laboratory of Digital Stomatology, Peking University School and Hospital of Stomatology, National Clinical Research Center for Oral Diseases & National Engineering Laboratory for Digital and Material Technology of Stomatology, Haidian District, Beijing, 100081, China.
Xinyu CuiDepartment of Orthodontics, Beijing Key Laboratory of Digital Stomatology, Peking University School and Hospital of StomatologyNational Clinical Research Center for Oral Diseases & National Engineering Laboratory for Digital and Material Technology of StomatologyHaidian District, No. 22 Zhongguancun Avenue South, Beijing, 100081, China.
Hongyi TangDepartment of Orthodontics, Beijing Key Laboratory of Digital Stomatology, Peking University School and Hospital of StomatologyNational Clinical Research Center for Oral Diseases & National Engineering Laboratory for Digital and Material Technology of StomatologyHaidian District, No. 22 Zhongguancun Avenue South, Beijing, 100081, China.
Peng ChenDepartment of Orthodontics, School of Stomatology Affiliated to Medical College, Zhejiang University, Hangzhou, 310005, China.
Cuiying LiCentral Laboratory, Beijing Key Laboratory of Digital Stomatology, Peking University School and Hospital of StomatologyNational Clinical Research Center for Oral Diseases & National Engineering Laboratory for Digital and Material Technology of StomatologyHaidian District, No. 22 Zhongguancun Avenue South, Beijing, 100081, China. kqlicuiying@bjmu.edu.cn.ORCID 0000-0002-5536-5432
Jiuhui JiangDepartment of Orthodontics, Beijing Key Laboratory of Digital Stomatology, Peking University School and Hospital of StomatologyNational Clinical Research Center for Oral Diseases & National Engineering Laboratory for Digital and Material Technology of StomatologyHaidian District, No. 22 Zhongguancun Avenue South, Beijing, 100081, China. kqjiangjiuhui@bjmu.edu.cn.ORCID 0000-0003-4881-5949

Funding

Beijing Natural Science Foundation 7232219
6 · The paper itself

Abstract

backgroundThe initiation of bone remodeling by periodontal ligament cells (PDLCs) in response to force is pivotal for mediating orthodontic tooth movement (OTM). Piezo1 plays a pivotal role in the process of bone remodeling under mechanical stimulation. Our objective was to elucidate the role and mechanism of Piezo1 in force-treated PDLCs, and its influence on orthodontic bone remodeling.

methodsHuman PDLCs (hPDLCs) were isolated and treated with compressive force, along with either si-PIEZO1 or Yoda1. The expression of Piezo1 and the receptor activator of NF-kB ligand/osteoprotegerin (RANKL/OPG) ratio were assessed by quantitative real-time polymerase chain reaction (qPCR) and Western blots. Intracellular calcium ion influx was assessed with Fluo4-AM staining. The effect of force-treated hPDLCs on the osteoclastic differentiation of RAW264.7 cells was analyzed by tartrate-resistant acid phosphatase (TRAP) staining, qPCR and Western blots. After constructing the OTM model, rats were injected with GsMTx4 or Yoda1. OTM distance, osteoclast differentiation, and the expression of RANKL and phosphorylated-ERK1/2 was analyzed with micro-computed tomography, hematoxylin and eosin, TRAP, immunofluorescence and immunohistochemistry staining.

resultsCompressive force-activated Piezo1 in hPDLCs mediated RANKL/OPG upregulation via ERK1/2 phosphorylation, thereby facilitating osteoclast differentiation. Yoda1 amplified this effect, while knocking down Piezo1 suppresses it in force-treated hPDLCs. In vivo, Yoda1 enhanced OTM and osteoclastogenesis in rats, while GsMTx4 inhibited these processes. The expression of phosphorylated-ERK1/2 in periodontal ligaments on the compressive side was enhanced by Yoda1 and attenuated by GsMTx4.

conclusionsCompressive force-activated Piezo1 in PDLCs triggers the osteoclast differentiation and orthodontic bone remodeling via ERK1/2 signal pathway.

Indexed as

Ion ChannelsOsteoclastsOsteogenesisPeriodontal LigamentTooth Movement TechniquesAnimalsBlotting, WesternBone RemodelingCell DifferentiationCells, CulturedHumansMaleMiceOsteoprotegerinRANK LigandRatsIon ChannelsOsteoprotegerinPIEZO1 protein, humanRANK LigandCompressive forceExtracellular signal-regulated kinasesOrthodontic tooth movementOsteoclastogenesisPeriodontal ligament cellsPiezo1

Identifiers

PMID42310668
PMCPMC13520292

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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.