Evidence map›Paper›PMID 29415458›Full record

ArticleInternational journal of molecular sciences2018

Alterations of Subchondral Bone Progenitor Cells in Human Knee and Hip Osteoarthritis Lead to a Bone Sclerosis Phenotype.

Daniel Bianco, Atanas Todorov, Tomislav Čengić, Geert Pagenstert, Stefan Schären, Cordula Netzer, Thomas Hügle, Jeroen Geurts

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

17 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Innate Immunity and Synovitis: Key Players in Osteoarthritis Progression.International journal of molecular sciences · 2024
    Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. From Pathogenesis to Therapy in Knee Osteoarthritis: Bench-to-Bedside.International journal of molecular sciences · 2021
    Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Subchondral Bone Remodeling: A Therapeutic Target for Osteoarthritis.Frontiers in cell and developmental biology · 2020
    Review
  16. Article
  17. 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

8 authors at 2 institutions in 1 country.

Daniel BiancoOrthopaedic Department, University Hospital of Basel, 4031 Basel, Switzerland. danbiancocot@gmail.com.
Atanas TodorovTissue Engineering, Department of Biomedicine, University Hospital of Basel, 4031 Basel, Switzerland. atanastodo@gmail.com.
Tomislav ČengićOrthopaedic Department, University Hospital of Basel, 4031 Basel, Switzerland. cengict@me.com.ORCID 0000-0002-3211-9925
Geert PagenstertOrthopaedic Department, University Hospital of Basel, 4031 Basel, Switzerland. pagenstert@praxisclarahof.ch.
Stefan SchärenDepartment of Spine Surgery, University Hospital of Basel, 4031 Basel, Switzerland. Stefan.Schaeren@usb.ch.
Cordula NetzerDepartment of Spine Surgery, University Hospital of Basel, 4031 Basel, Switzerland. Cordula.Netzer@usb.ch.
Thomas HügleDepartment of Rheumatology, University Hospital Lausanne (CHUV), 1005 Lausanne, Switzerland. Thomas.Hugle@chuv.ch.
Jeroen GeurtsOrthopaedic Department, University Hospital of Basel, 4031 Basel, Switzerland. Jeroen.Geurts@usb.ch.ORCID 0000-0002-4367-4641
University Hospital of Basel · CHUniversity Hospital of Lausanne · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Subchondral bone tissue plays a key role in the initiation and progression of human and experimental osteoarthritis and has received considerable interest as a treatment target. Elevated bone turnover and remodeling leads to subchondral bone sclerosis that is characterized by an increase in bone material that is less mineralized. The aim of this study was to investigate whether perturbations in subchondral bone-resident progenitor cells might play a role in aberrant bone formation in osteoarthritis. Colony formation assays indicated similar clonogenicity of progenitor cells from non-sclerotic and sclerotic subchondral trabecular bone tissues of osteoarthritic knee and hip joints compared with controls from iliac crest bone. However, the osteogenic potential at the clonal level was approximately two-fold higher in osteoarthritis than controls. An osteogenic differentiation assay indicated an efficient induction of alkaline phosphatase activity but blunted in vitro matrix mineralization irrespective of the presence of sclerosis. Micro-computed tomography and histology demonstrated the formation of de novo calcified tissues by osteoblast-like cells in an ectopic implantation model. The expression of bone sialoprotein, a marker for osteoblast maturation and mineralization, was significantly less in sclerotic progenitor cells. Perturbation of resident progenitor cell function is associated with subchondral bone sclerosis and may be a treatment target for osteoarthritis.

Indexed as

PhenotypeAgedAged, 80 and overBone and BonesCell DifferentiationCells, CulturedFemaleHumansMaleMiddle AgedOsteoarthritis, HipOsteoarthritis, KneeOsteoblastsOsteogenesisSclerosisStem Cellsclonogenicitycomputed tomographyectopic bone formationosteoarthritisosteogenic differentiationosteoprogenitorssubchondral bone

Identifiers

PMID29415458
PMCPMC5855697
OpenAlexW2792541430

What OpenQuestion holds

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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.