Evidence map›Paper›PMID 38517621›Full record

ArticleAnnals of biomedical engineering2024

Wnt16 Increases Bone-to-Implant Contact in an Osteopenic Rat Model by Increasing Proliferation and Regulating the Differentiation of Bone Marrow Stromal Cells.

Michael B Berger, Kyla Bosh, Jingyao Deng, Thomas W Jacobs, D Joshua Cohen, Barbara D Boyan, Zvi Schwartz

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Annals of biomedical engineering, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. Article
  2. Article
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

7 authors at 3 institutions in 1 country.

Michael B BergerDepartment of Biomedical Engineering, College of Engineering, Virginia Commonwealth University, 601 West Main Street, Richmond, VA, 23284, USA.
Kyla BoshDepartment of Biomedical Engineering, College of Engineering, Virginia Commonwealth University, 601 West Main Street, Richmond, VA, 23284, USA.
Jingyao DengDepartment of Biomedical Engineering, College of Engineering, Virginia Commonwealth University, 601 West Main Street, Richmond, VA, 23284, USA.
Thomas W JacobsDepartment of Biomedical Engineering, College of Engineering, Virginia Commonwealth University, 601 West Main Street, Richmond, VA, 23284, USA.
D Joshua CohenDepartment of Biomedical Engineering, College of Engineering, Virginia Commonwealth University, 601 West Main Street, Richmond, VA, 23284, USA.
Barbara D BoyanDepartment of Biomedical Engineering, College of Engineering, Virginia Commonwealth University, 601 West Main Street, Richmond, VA, 23284, USA. bboyan@vcu.edu.ORCID http://orcid.org/0000-0002-9642-0311
Zvi SchwartzDepartment of Biomedical Engineering, College of Engineering, Virginia Commonwealth University, 601 West Main Street, Richmond, VA, 23284, USA.
Virginia Commonwealth University · USGeorgia Institute of Technology · USThe University of Texas Health Science Center at San Antonio · US

Funding

Mechanisms Mediating Osseointegration of 3D Printed Titanium ConstructsR01AR072500 · NIAMS · VIRGINIA COMMONWEALTH UNIVERSITY · PI BOYAN, BARBARA D. · 2019 to 2023
$2.9M
NIAMS NIH HHS R01 AR072500NIAMS NIH HHS R01AR072500
6 · The paper itself

Abstract

Osseointegration is a complex biological cascade that regulates bone regeneration after implant placement. Implants possessing complex multiscale surface topographies augment this regenerative process through the regulation of bone marrow stromal cells (MSCs) that are in contact with the implant surface. One pathway regulating osteoblastic differentiation is Wnt signaling, and upregulation of non-canonical Wnts increases differentiation of MSCs on these titanium substrates. Wnt16 is a non-canonical Wnt shown to regulate bone morphology in mouse models. This study evaluated the role of Wnt16 during surface-mediated osteoblastic differentiation of MSCs in vitro and osseointegration in vivo. MSCs were cultured on Ti substrates with different surface properties and non-canonical Wnt expression was determined. Subsequently, MSCs were cultured on Ti substrates +/-Wnt16 (100 ng/mL) and anti-Wnt16 antibodies (2 μg/mL). Wnt16 expression was increased in cells grown on microrough surfaces that were processed to be hydrophilic and have nanoscale roughness. However, treatment MSCs on these surfaces with exogenous rhWnt16b increased total DNA content and osteoprotegerin production, but reduced osteoblastic differentiation and production of local factors necessary for osteogenesis. Addition of anti-Wnt16 antibodies blocked the inhibitor effects of Wnt16. The response to Wnt16 was likely independent of other osteogenic pathways like Wnt11-Wnt5a signaling and semaphorin 3a signaling. We used an established rat model of cortical and trabecular femoral bone impairment following botox injections (2 injections of 8 units/leg each, starting and maintenance doses) to assess Wnt16 effects on whole bone morphology and implant osseointegration. Wnt16 injections did not alter whole bone morphology significantly (BV/TV, cortical thickness, restoration of trabecular bone) but were effective at increasing cortical bone-to-implant contact during impaired osseointegration in the botox model. The mechanical quality of the increased bone was not sufficient to rescue the deleterious effects of botox. Clinically, these results are important to understand the interaction of cortical and trabecular bone during implant integration. They suggest a role for Wnt16 in modulating bone remodeling by reducing osteoclastic activity. Targeted strategies to temporally regulate Wnt16 after implant placement could be used to improve osseointegration by increasing the net pool of osteoprogenitor cells.

Indexed as

Cell DifferentiationCell ProliferationMesenchymal Stem CellsOsseointegrationRats, Sprague-DawleyWnt ProteinsAnimalsBone Diseases, MetabolicCells, CulturedDisease Models, AnimalMaleRatsTitaniumTitaniumWnt ProteinsBone marrow stromal cellsBotoxCortical boneMSCsSurface propertiesTitanium

Identifiers

PMID38517621
PMCPMC11082046
OpenAlexW4393094410

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.