Evidence map›Paper›PMID 37425196›Full record

ArticleBone reports2023

Post-traumatic osteoarthritis: A review of pathogenic mechanisms and novel targets for mitigation.

Julian E Dilley, Margaret Anne Bello, Natoli Roman, Todd McKinley, Uma Sankar

Open access · goldAbstract read
In one paragraph

Article in Bone reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 1 pooled it
16.9field-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

66 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.

  1. Pooled it
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  14. Cross-Linked Versus Linear Hyaluronic Acid for Cartilage Repair in Rat Post-Traumatic Osteoarthritis.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2026
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6 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

5 authors at 1 institution in 1 country.

Julian E DilleyDepartment of Orthopaedic Surgery, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Margaret Anne BelloDepartment of Anatomy, Cell Biology and Physiology, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Natoli RomanDepartment of Orthopaedic Surgery, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Todd McKinleyDepartment of Orthopaedic Surgery, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Uma SankarDepartment of Anatomy, Cell Biology and Physiology, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Indiana University School of Medicine

Funding

CaMKK2 Signaling in OsteoarthritisR01AR076477 · NIAMS · INDIANA UNIVERSITY INDIANAPOLIS · PI SANKAR, UMA · 2020 to 2024
$3.0M
NIAMS NIH HHS R01 AR076477
6 · The paper itself

Abstract

Post-traumatic osteoarthritis (PTOA) develops secondary to a joint injury and accounts for 12 % of all osteoarthritis. These injuries, often of the lower extremity joints, occur due to trauma or accidents related to athletic or military activities. They primarily affect younger individuals although PTOA can occur across the spectrum of age. Pain and functional disability caused by PTOA confer a heavy economic toll on patients, in addition to detrimentally affecting their quality of life. Both high energy injuries that cause articular surface fracture with or without subchondral bone disruption and low-energy injuries involving joint dislocations or ligamentous injury cause PTOA, albeit through different mechanisms. Regardless, chondrocyte death, mitochondrial dysfunction, reactive oxygen species production, subchondral bone remodeling, inflammation and cytokine release in the cartilage and synovium play integral roles in the pathogenesis of PTOA. Evolving surgical methods are focused on stabilizing articular surface and joint structure congruity. However, to date there are no disease modifying medical therapies against PTOA. Increased recent understanding of the pathogenesis of the subchondral bone and synovial inflammation as well as that of chondrocyte mitochondrial dysfunction and apoptosis have led to the investigation of new therapeutics targeting these mechanisms to prevent or delay PTOA. This review discusses new advances in our understanding of cellular mechanisms underlying PTOA, and therapeutic approaches that are potentially effective in reducing the self-propagating cycle of subchondral bone alterations, inflammation, and cartilage degradation. Within this context, we focus therapeutic options involving anti-inflammatory and anti-apoptotic candidates that could prevent PTOA.

Indexed as

ApoptosisCartilageInflammationIntra-articular fractureMitochondriaPost-traumatic arthritisSubchondral boneSynoviumTherapeutics

Identifiers

PMID37425196
PMCPMC10323219
OpenAlexW4320341097

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.