Evidence map›Paper›PMID 34047890›Full record

ArticleBiomechanics and modeling in mechanobiology2021

Bone morphogenetic protein 2-induced cellular chemotaxis drives tissue patterning during critical-sized bone defect healing: an in silico study.

Edoardo Borgiani, Georg N Duda, Bettina M Willie, Sara Checa

Open access · hybridAbstract read
In one paragraph

Article in Biomechanics and modeling in mechanobiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.3field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

12 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Observational
  3. Review
  4. Article
  5. Article
  6. Trabecular bone remodeling in the aging mouse: A micro-multiphysics agent-basedFrontiers in bioengineering and biotechnology · 2023
    Article
  7. Article
  8. AnFrontiers in bioengineering and biotechnology · 2023
    Article
  9. Article
  10. Article
  11. Article
  12. TowardsFrontiers in bioengineering and biotechnology · 2021
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 2 countries.

Edoardo BorgianiJulius Wolff Institute, Berlin Institute of Health, Charité - Universitätsmedizin Berlin, Campus Virchow Klinikum, Institutsgebäude Süd/ Südstraße 2, Augustenburger Platz 1, 13353, Berlin, Germany.ORCID http://orcid.org/0000-0002-9645-2524
Georg N DudaJulius Wolff Institute, Berlin Institute of Health, Charité - Universitätsmedizin Berlin, Campus Virchow Klinikum, Institutsgebäude Süd/ Südstraße 2, Augustenburger Platz 1, 13353, Berlin, Germany.
Bettina M WillieResearch Centre, Department of Pediatric Surgery, Shriners Hospital for Children-Canada, McGill University, 1003 Decarie Blvd, Montreal, QC, H4A 0A9, Canada.ORCID http://orcid.org/0000-0003-2907-3580
Sara ChecaJulius Wolff Institute, Berlin Institute of Health, Charité - Universitätsmedizin Berlin, Campus Virchow Klinikum, Institutsgebäude Süd/ Südstraße 2, Augustenburger Platz 1, 13353, Berlin, Germany. sara.checa@charite.de.ORCID http://orcid.org/0000-0002-1444-5858
Berlin Institute of Health at Charité - Universitätsmedizin Berlin · DEMontreal Children's Hospital · CA

Funding

Deutsche Forschungsgemeinschaft WI 3761/4-1, DU298/14-1; CH 1123/4-1
6 · The paper itself

Abstract

Critical-sized bone defects are critical healing conditions that, if left untreated, often lead to non-unions. To reduce the risk, critical-sized bone defects are often treated with recombinant human BMP-2. Although enhanced bone tissue formation is observed when BMP-2 is administered locally to the defect, spatial and temporal distribution of callus tissue often differs from that found during regular bone healing or in defects treated differently. How this altered tissue patterning due to BMP-2 treatment is linked to mechano-biological principles at the cellular scale remains largely unknown. In this study, the mechano-biological regulation of BMP-2-treated critical-sized bone defect healing was investigated using a multiphysics multiscale in silico approach. Finite element and agent-based modeling techniques were combined to simulate healing within a critical-sized bone defect (5 mm) in a rat femur. Computer model predictions were compared to in vivo microCT data outcome of bone tissue patterning at 2, 4, and 6 weeks postoperation. In vivo, BMP-2 treatment led to complete healing through periosteal bone bridging already after 2 weeks postoperation. Computer model simulations showed that the BMP-2 specific tissue patterning can be explained by the migration of mesenchymal stromal cells to regions with a specific concentration of BMP-2 (chemotaxis). This study shows how computational modeling can help us to further understand the mechanisms behind treatment effects on compromised healing conditions as well as to optimize future treatment strategies.

Indexed as

AnimalsBone Morphogenetic Protein 2Bone RegenerationBony CallusCell DifferentiationChemotaxisCollagenComputer SimulationFemurFinite Element AnalysisHumansIn Vitro TechniquesMesenchymal Stem CellsOsteogenesisRatsRecombinant ProteinsBMP2 protein, humanBone Morphogenetic Protein 2Collagenrecombinant human bone morphogenetic protein-2Recombinant ProteinsTransforming Growth Factor betaAgent-based modelBone defect healingBone morphogenetic protein 2Finite element analysisMechanobiology

Identifiers

PMID34047890
PMCPMC8298257
OpenAlexW3165635859

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.