Evidence map›Paper›PMID 27994716›Full record

ReviewCartilage2017

Peculiarities in Ankle Cartilage.

Matthew J Kraeutler, Tanyaporn Kaenkumchorn, Cecilia Pascual-Garrido, Markus A Wimmer, Susanna Chubinskaya

Open access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cartilage, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 3 pooled it
2.1field-weighted citation impact, top 14% 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

19 citing papers in PubMed, 3 syntheses or guidelines pooled it, 41 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Article
  5. Article
  6. Synovial Dysregulation in Ankle Osteoarthritis: Molecular Insights and Pathogenetic Pathways.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2025
    Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Ankle Osteoarthritis Aetiology.Journal of clinical medicine · 2021
    Review
  16. Article
  17. Article
  18. Article
  19. 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

5 authors at 2 institutions in 1 country.

Matthew J KraeutlerDepartment of Orthopedics, University of Colorado School of Medicine, Aurora, CO, USA.
Tanyaporn KaenkumchornDepartment of Pediatrics, Rush University Medical Center, Chicago, IL, USA.
Cecilia Pascual-GarridoDepartment of Orthopedics, University of Colorado School of Medicine, Aurora, CO, USA.
Markus A WimmerDepartment of Orthopedic Surgery, Rush University Medical Center, Chicago, IL, USA.
Susanna ChubinskayaDepartments of Pediatrics, Orthopedics, Biochemistry, and Internal Medicine, Rush University Medical Center, Chicago, IL, USA.
Rush University Medical Center · USUniversity of Colorado Denver · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Posttraumatic osteoarthritis (PTOA) is the most common form of osteoarthritis (OA) of the ankle joint. PTOA occurs as a result of several factors, including the poor regenerative capacity of hyaline articular cartilage as well as increased contact stresses following trauma. The purpose of this article is to review the epidemiology, pathogenesis, and potential targets for treatment of PTOA in the ankle joint. Previous reviews primarily addressed clinical approaches to ankle PTOA, while the focus of the current article will be specifically on the newly acquired knowledge of the cellular mechanisms that drive PTOA in the ankle joint and means for potential targeted therapeutics that might halt the progression of cartilage degeneration and/or improve the outcome of surgical interventions. Three experimental treatment strategies are discussed in this review: (1) increasing the anabolic potential of chondrocytes through treatment with growth factors such as bone morphogenetic protein-7; (2) limiting chondrocyte cell death either through the protection of cell membrane with poloxamer 188 or inhibiting activity of intracellular proteases, caspases, which are responsible for cell death by apoptosis; and (3) inhibiting catabolic/inflammatory responses of chondrocytes by treating them with anti-inflammatory agents such as tumor necrosis factor-α antagonists. Future studies should focus on identifying the appropriate timing for treatment and an appropriate combination of anti-inflammatory, chondro- and matrix-protective biologics to limit the progression of trauma-induced cartilage degeneration and prevent the development of PTOA in the ankle joint.

Indexed as

ankleanti-inflammatorycartilagechondroprotectionposttraumatic osteoarthritis

Identifiers

PMID27994716
PMCPMC5154419
OpenAlexW2326901501

What OpenQuestion holds

Textmetadata
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.