Evidence map›Paper›PMID 29616218›Full record

ReviewFrontiers in bioengineering and biotechnology2018

Recent Insights into the Contribution of the Changing Hypertrophic Chondrocyte Phenotype in the Development and Progression of Osteoarthritis.

Ellen G J Ripmeester, Ufuk Tan Timur, Marjolein M J Caron, Tim J M Welting

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in bioengineering and biotechnology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 1 pooled it
10.1field-weighted citation impact, top 1% 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

52 citing papers in PubMed, 1 synthesis or guideline pooled it, 98 citations in OpenAlex.

  1. Pooled it
  2. Programmed cell death in osteoarthritis.Apoptosis : an international journal on programmed cell death · 2026
    Review
  3. Pararamosis, a Neglected Tropical Disease Induced byInternational journal of molecular sciences · 2024
    Article
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  20. Autophagic LC3Science advances · 2022
    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

4 authors at 1 institution in 1 country.

Ellen G J RipmeesterLaboratory for Experimental Orthopedics, Department of Orthopedic Surgery, Maastricht University Medical Center, Maastricht, Netherlands.
Ufuk Tan TimurLaboratory for Experimental Orthopedics, Department of Orthopedic Surgery, Maastricht University Medical Center, Maastricht, Netherlands.
Marjolein M J CaronLaboratory for Experimental Orthopedics, Department of Orthopedic Surgery, Maastricht University Medical Center, Maastricht, Netherlands.
Tim J M WeltingLaboratory for Experimental Orthopedics, Department of Orthopedic Surgery, Maastricht University Medical Center, Maastricht, Netherlands.
Maastricht University · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteoarthritis (OA) is an extremely prevalent age-related condition. The economic and societal burden due to the cost of symptomatic treatment, inability to work, joint replacement, and rehabilitation is huge and increasing. Currently, there are no effective medical therapies that delay or reverse the pathological manifestations of OA. Current treatment options are, without exception, focused on slowing down progression of the disease to postpone total joint replacement surgery for as long as possible and keeping the associated pain and joint immobility manageable. Alterations in the articular cartilage chondrocyte phenotype might be fundamental in the pathological mechanisms of OA development. In many ways, the changing chondrocyte phenotype in osteoarthritic cartilage resembles the process of endochondral ossification as seen, for instance, in developing growth plates. However, the relative contribution of endochondral ossification to the changing chondrocyte phenotype in the development and progression of OA remains poorly described. In this review, we will discuss the current knowledge regarding the cartilage endochondral phenotypic changes occurring during OA development and progression, as well as the molecular and environmental effectors driving these changes. Understanding how these molecular mechanisms determine the chondrocyte cell fate in OA will be essential in enabling cartilage regenerative approaches in future treatments of OA.

Indexed as

cartilagechondrocytesendochondral ossificationhypertrophyosteoarthritisphenotype

Identifiers

PMID29616218
PMCPMC5867295
OpenAlexW2789533472

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.