Evidence map›Paper›PMID 22480275›Full record

Trial reportBMC musculoskeletal disorders2012

Local biochemical and morphological differences in human Achilles tendinopathy: a case control study.

Pingel J, Fredberg U, Qvortrup K, Larsen J O, Schjerling P, Heinemeier K, Kjaer M, Langberg H

Open access · goldAbstract readRandomized Controlled Trial
In one paragraph

Trial report in BMC musculoskeletal disorders, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 3 pooled it
6.3field-weighted citation impact, top 3% 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

20 citing papers in PubMed, 3 syntheses or guidelines pooled it, 64 citations in OpenAlex.

  1. Pooled it
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  6. Article
  7. Transcriptional Adaptations to Muscle Loading in a Murine Model of Achilles Tendinopathy.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2026
    Article
  8. Article
  9. Tendinopathy: The Interplay between Mechanical Stress, Inflammation, and Vascularity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
  10. Characterization of anMatrix biology plus · 2024
    Article
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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

8 authors at 3 institutions in 1 country.

Pingel JInstitute of Sports Medicine, Department of Orthopedic Surgery M, Bispebjerg Hospital and Center for Healthy Aging, Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark. jessica.pingel@gmx.de
Fredberg U
Qvortrup K
Larsen J O
Schjerling P
Heinemeier K
Kjaer M
Langberg H
Bispebjerg Hospital · DKUniversity of Copenhagen · DKRegionshospitalet Silkeborg · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe incidence of Achilles tendinopathy is high and underlying etiology as well as biochemical and morphological pathology associated with the disease is largely unknown. The aim of the present study was to describe biochemical and morphological differences in chronic Achilles tendinopathy. The expressions of growth factors, inflammatory mediators and tendon morphology were determined in both chronically diseased and healthy tendon parts.

methodsThirty Achilles tendinopathy patients were randomized to an expression-study (n = 16) or a structural-study (n = 14). Biopsies from two areas in the Achilles tendon were taken and structural parameters: fibril density, fibril size, volume fraction of cells and the nucleus/cytoplasm ratio of cells were determined. Further gene expressions of various genes were analyzed.

resultsSignificantly smaller collagen fibrils and a higher volume fraction of cells were observed in the tendinopathic region of the tendon. Markers for collagen and its synthesis collagen 1, collagen 3, fibronectin, tenascin-c, transforming growth factor-β fibromodulin, and markers of collagen breakdown matrix metalloproteinase-2, matrix metalloproteinase-9 and metallopeptidase inhibitor-2 were significantly increased in the tendinopathic region. No altered expressions of markers for fibrillogenesis, inflammation or wound healing were observed.

conclusionThe present study indicates that an increased expression of factors stimulating the turnover of connective tissue is present in the diseased part of tendinopathic tendons, associated with an increased number of cells in the injured area as well as an increased number of smaller and thinner fibrils in the diseased tendon region. As no fibrillogenesis, inflammation or wound healing could be detected, the present data supports the notion that tendinopathy is an ongoing degenerative process.

trial registrationCurrent Controlled Trials ISRCTN20896880.

Indexed as

Achilles TendonBiopsyCase-Control StudiesChi-Square DistributionChronic DiseaseCollagenasesDenmarkFibrillar CollagensGene Expression RegulationGenetic MarkersHumansInflammation MediatorsIntercellular Signaling Peptides and ProteinsMicroscopy, Electron, TransmissionPolymerase Chain ReactionRNA, MessengerCollagenasesFibrillar CollagensGenetic MarkersInflammation MediatorsIntercellular Signaling Peptides and ProteinsRNA, MessengerTissue Inhibitor of Metalloproteinases

Identifiers

PMID22480275
PMCPMC3341204
OpenAlexW1976543803

What OpenQuestion holds

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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.