Evidence map›Paper›PMID 26069661›Full record

ArticleCartilage2013

Key Pathways to Prevent Posttraumatic Arthritis for Future Molecule-Based Therapy.

Susan Chubinskaya, Markus A Wimmer

Abstract read
In one paragraph

Article in Cartilage, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 2 pooled it
2.3field-weighted citation impact, top 12% 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

16 citing papers in PubMed, 2 syntheses or guidelines pooled it, 34 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Mitoprotective therapy preserves chondrocyte viability and prevents cartilage degeneration in an ex vivo model of posttraumatic osteoarthritis.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2018
    Article
  11. Article
  12. Mitochondrial dysfunction is an acute response of articular chondrocytes to mechanical injury.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2018
    Article
  13. Article
  14. Article
  15. Post-traumatic osteoarthritis of the ankle: A distinct clinical entity requiring new research approaches.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2017
    Review
  16. 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

2 authors at 1 institution in 1 country.

Susan ChubinskayaDepartment of Biochemistry, Internal Medicine (Section of Rheumatology), Rush University Medical Center, Chicago, IL, USA ; Department of Orthopedic Surgery, Rush University Medical Center, Chicago, IL, USA.
Markus A WimmerDepartment of Orthopedic Surgery, Rush University Medical Center, Chicago, IL, USA.
Rush University Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Joint injuries are common, especially among young adults aged 18 to 44 years. They are accompanied by a cascade of events that increase the risk of posttraumatic osteoarthritis (PTOA). Therefore, understanding of biological responses that predispose to PTOA should help in determining treatment modalities to delay and/or prevent the onset and progression of the disease. The vast majority of the literature pointed to chondrocyte death and apoptosis, inflammation and matrix damage/fragmentation being the earliest events that follow joint trauma. Together these events lead to the development of osteoarthritis-like focal cartilage lesions that if untreated have a tendency to expand and progress to fully developed disease. Currently, the only treatments available for joint trauma are surgical interventions. Experimental biologic approaches involve engineering of cartilage with the use of cells (stem cells or chondrocytes), juvenile or adult cartilage pieces, scaffolds, and various polymeric matrices. The major challenge for all of them is regeneration of normal functional mature hyaline cartilage that can sustain the load, resist compression, and most important, integrate with the host tissue. If the tissue is spontaneously repaired it fails to reproduce original structure and function and thus, may be more susceptible to re-injury. Thus, there is a critical need to develop novel molecular mechanism-based therapeutic approaches to biologic chondral and/or osteochondral repair. The focus of this review is on the earliest molecular and cellular manifestations of injury that can be grouped based on the following therapeutic options for PTOA: chondroprotection, anti-inflammatory, matrix protection, and matrix remodeling/matrix synthesis.

Indexed as

anabolic responsesanti-inflammatorychondroprotectionmatrix degradationposttraumatic osteoarthritisrepair

Identifiers

PMID26069661
PMCPMC4297064
OpenAlexW2324755165

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.