Evidence map›Paper›PMID 22140600›Full record

ArticleInternational journal of clinical and experimental medicine2011

Pathogenetic mechanisms of posttraumatic osteoarthritis: opportunities for early intervention.

William C Kramer, Kelly J Hendricks, Jinxi Wang

Abstract read
In one paragraph

Article in International journal of clinical and experimental medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed, 1 pooled it
3.2field-weighted citation impact, top 9% 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

62 citing papers in PubMed, 1 synthesis or guideline pooled it, 99 citations in OpenAlex.

  1. Guideline
  2. Trial
  3. Review
  4. Article
  5. 2050: An Arthroplasty Odyssey.Healthcare (Basel, Switzerland) · 2025
    Article
  6. TJournal of magnetic resonance imaging : JMRI · 2025
    Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Characteristics of distal femoral articular cartilage in 6 weeks posttraumatic osteoarthritis by a subcritical impact.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2024
    Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. [Short- and mid-term effectiveness of unicompartmental knee arthroplasty for post-traumatic arthritis of knee].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2023
    Article
  19. Article
  20. Article

2 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

William C KramerDepartment of Orthopedic Surgery, University of Kansas Medical Center 3901 Rainbow Boulevard, Kansas City, Kansas 66160, USA.
Kelly J Hendricks
Jinxi Wang
University of Kansas Medical Center · US

Funding

Transcription Factor NFAT1 Deficiency and OsteoarthritisR01AR059088 · NIAMS · UNIVERSITY OF KANSAS MEDICAL CENTER · PI WANG, JINXI · 2011 to 2015
$1.7M
NIAMS NIH HHS R01 AR059088
6 · The paper itself

Abstract

Osteoarthritis (OA) is characterized by joint pain and stiffness with radiographic evidence of joint space narrowing, osteophytes, and subchondral bone sclerosis. Posttraumatic OA (PTOA) arises from joint trauma, which accounts for a fraction of all patients with OA. Articular cartilage breakdown can occur soon or for years after a joint injury. Even with the current care of joint injuries, such as anatomic reduction and rigid fixation of intra-articular fractures and reconstruction of ruptured ligaments with successful restoration of joint biomechanics, the risk of PTOA after joint injuries ranges from 20% to more than 50%. The time course for the progression of PTOA is highly variable and risk of PTOA increases with patient age at the time of joint injury, suggesting that biologic factors may be involved in the progression of PTOA. Therapeutic options are limited due largely to the lack of information on the mechanisms underlying the progression of PTOA. This review summarizes the current studies on the pathogenetic mechanisms of PTOA, with a main focus on the metabolic changes in articular cartilage in the acute posttraumatic phase and the early chronic phase, a clinically asymptomatic period. Recent studies have revealed that mechanical damage to the articular tissues may lead to changes in gene expression and cartilage metabolism, which could trigger a cascade of events leading to degradation of articular cartilage and pathologic changes in other joint tissues. Understanding the mechanobiologic, molecular and cellular changes that lead to continued cartilage degradation in the relatively early phases after joint injury may open up new opportunities for early clinical intervention.

Indexed as

articular cartilagejoint injuryligamentmeniscusOsteoarthritisposttraumatic osteoarthritis

Identifiers

PMID22140600
PMCPMC3228584
OpenAlexW35361850

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.