Evidence map›Paper›PMID 32424558›Full record

ArticleJournal of molecular medicine (Berlin, Germany)2020

Local Wnt3a treatment restores bone regeneration in large osseous defects after surgical debridement of osteomyelitis.

Johannes Maximilian Wagner, Felix Reinkemeier, Mehran Dadras, Christoph Wallner, Julika Huber, Alexander Sogorski, Maxi Sacher, Sonja Schmidt, Marius Drysch, Stephanie Dittfeld and 5 more

Erratum issuedAbstract read
In one paragraph

Article in Journal of molecular medicine (Berlin, Germany), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
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

9 citing papers in PubMed.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors.

Johannes Maximilian Wagner *University Hospital BG Bergmannsheil Bochum, Bürkle-de-la-Camp Platz 1, 44789, Bochum, Germany.
Felix Reinkemeier *University Hospital BG Bergmannsheil Bochum, Bürkle-de-la-Camp Platz 1, 44789, Bochum, Germany.
Mehran DadrasUniversity Hospital BG Bergmannsheil Bochum, Bürkle-de-la-Camp Platz 1, 44789, Bochum, Germany.
Christoph WallnerUniversity Hospital BG Bergmannsheil Bochum, Bürkle-de-la-Camp Platz 1, 44789, Bochum, Germany.
Julika HuberUniversity Hospital BG Bergmannsheil Bochum, Bürkle-de-la-Camp Platz 1, 44789, Bochum, Germany.
Alexander SogorskiUniversity Hospital BG Bergmannsheil Bochum, Bürkle-de-la-Camp Platz 1, 44789, Bochum, Germany.
Maxi SacherUniversity Hospital BG Bergmannsheil Bochum, Bürkle-de-la-Camp Platz 1, 44789, Bochum, Germany.
Sonja SchmidtUniversity Hospital BG Bergmannsheil Bochum, Bürkle-de-la-Camp Platz 1, 44789, Bochum, Germany.
Marius DryschUniversity Hospital BG Bergmannsheil Bochum, Bürkle-de-la-Camp Platz 1, 44789, Bochum, Germany.
Stephanie DittfeldUniversity Hospital BG Bergmannsheil Bochum, Bürkle-de-la-Camp Platz 1, 44789, Bochum, Germany.
Mustafa BecerikliUniversity Hospital BG Bergmannsheil Bochum, Bürkle-de-la-Camp Platz 1, 44789, Bochum, Germany.
Kathrin BeckerPoliklinik für Kieferorthopädie, University Hospital Düsseldorf, Düsseldorf, Germany.
Nicole RauchPoliklinik für Kieferorthopädie, University Hospital Düsseldorf, Düsseldorf, Germany.
Marcus LehnhardtUniversity Hospital BG Bergmannsheil Bochum, Bürkle-de-la-Camp Platz 1, 44789, Bochum, Germany.
Björn BehrUniversity Hospital BG Bergmannsheil Bochum, Bürkle-de-la-Camp Platz 1, 44789, Bochum, Germany. bjorn.behr@rub.de.ORCID http://orcid.org/0000-0001-6890-4290

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Impaired bone homeostasis caused by osteomyelitis provokes serious variations in the bone remodeling process, thereby involving multiple inflammatory cytokines to activate bone healing. We have previously established a mouse model for post-traumatic osteomyelitis and studied bone regeneration after sufficient debridement. Moreover, we could further characterize the postinfectious inflammatory state of bony defects after debridement with elevated osteoclasts and decreased bone formation despite the absence of bacteria. In this study, we investigated the positive effects of Wnt-pathway modulation on bone regeneration in our previous established mouse model. This was achieved by local application of Wnt3a, a recombinant activator of the canonical Wnt-pathway. Application of Wnt3a could enhance new bone formation, which was verified by histological and μ-CT analysis. Moreover, histology and western blots revealed enhanced osteoblastogenesis and downregulated osteoclasts in a RANKL-dependent manner. Further analysis of Wnt-pathway showed downregulation after bone infections were reconstituted by application of Wnt3a. Interestingly, Wnt-inhibitory proteins Dickkopf 1 (DKK1), sclerostin, and secreted frizzled protein 1 (sFRP1) were upregulated simultaneously to Wnt-pathway activation, indicating a negative feedback for active form of Beta-catenin. In this study, we could demonstrate enhanced bone formation in defects caused by post-traumatic osteomyelitis after Wnt3a application. KEY MESSAGES: Osteomyelitis decreases bone regeneration Wnt3a restores bone healing after infection Canonical Wnt-pathway activation with negative feedback.

Indexed as

Animalsbeta CateninBone RegenerationDebridementDisease ManagementDisease Models, AnimalDisease SusceptibilityFemaleFluorescent Antibody TechniqueGlycogen Synthase Kinase 3 betaImage Processing, Computer-AssistedMaleMiceOsteoclastsOsteogenesisOsteomyelitisbeta CateninGlycogen Synthase Kinase 3 betaRecombinant ProteinsWnt3A ProteinWnt3a protein, mouseBoneBone regenerationCanonical Wnt-pathwayOsteomyelitisWnt3a

Identifiers

PMID32424558
PMCPMC8526481

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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.