Evidence map›Paper›PMID 42558958›Full record

ArticleNagoya journal of medical science2026

Effect of neurotrophin-3 on bone healing in distraction osteogenesis.

Masashi Wakasugi, Masahito Fujio, Makoto Tsuboi, Qi Chang, Huiting Bian, Yuqing Liu, Hideharu Hibi

Abstract read
In one paragraph

Article in Nagoya journal of medical science, 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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0citing papers 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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4 · The record

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5 · Who and what money

Authors and funding

7 authors.

Masashi WakasugiDepartment of Oral and Maxillofacial Surgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Masahito FujioDepartment of Oral and Maxillofacial Surgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Makoto TsuboiDepartment of Oral and Maxillofacial Surgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Qi ChangDepartment of Oral and Craniomaxillofacial Surgery, Shanghai Ninth People's Hospital, Shanghai, China.
Huiting BianDepartment of Oral and Maxillofacial Surgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Yuqing LiuDepartment of Oral and Maxillofacial Surgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Hideharu HibiDepartment of Oral and Maxillofacial Surgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Distraction osteogenesis (DO) is a surgical technique used to repair skeletal defects by promoting bone and soft tissue regeneration. However, prolonged use of external fixators often causes complications such as infections and joint contractures. Neurotrophin-3 (NT-3) enhances osteoblast differentiation via bone morphogenetic protein-2 (BMP-2) and Akt signaling and may also modulate the Wnt/β-catenin pathway. In this study, we investigated the role of NT-3 in bone regeneration during DO. A DO model was established in 9-week-old male ICR mice, in which tibiae were osteotomized and stabilized with external fixators under anesthesia. After a 5-day latency period, distraction was performed at 0.2 mm every 12 hours for 8 days. RNA was extracted at defined time points post-osteotomy for quantitative polymerase chain reaction (qPCR) analysis, and NT-3 was administered post-distraction. Bone regeneration was evaluated by radiographic, histological, and biomechanical analyses. The effects of NT-3 and Dickkopf-1 were further examined in ST2 bone marrow-derived mesenchymal stem cells. NT-3 significantly enhanced bone formation, increased bone mineral density within the DO gap, and improved the mechanical stiffness of regenerated bone. Histological examination revealed earlier bone continuity and greater callus formation in the NT-3 group. Gene expression analysis demonstrated upregulation of Wnt/β-catenin pathway components, including Wnt10b, β-catenin, and low-density lipoprotein receptor-related protein 5 (LRP5). In ST2 cells, NT3 increased the expression of LRP5, LRP6, β-catenin, and Runx2, while cotreatment with Dickkopf1 abolished these effects. These findings suggest that NT-3 promotes bone regeneration during DO by activating the Wnt/β-catenin signaling pathway, highlighting its therapeutic potential to improve DO outcomes.

Indexed as

Bone RegenerationNeurotrophin 3OsteogenesisOsteogenesis, DistractionAnimalsbeta CateninBone Morphogenetic Protein 2Cell DifferentiationIntercellular Signaling Peptides and ProteinsMaleMesenchymal Stem CellsMiceMice, Inbred ICROsteoblastsTibiaWnt Signaling Pathwaybeta CateninBone Morphogenetic Protein 2Dkk1 protein, mouseIntercellular Signaling Peptides and ProteinsNeurotrophin 3bone morphogenetic protein-2bone regenerationdistraction osteogenesis; neurotrophin-3Wnt/β-catenin signal pathway

Identifiers

PMID42558958
PMCPMC13438799

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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.