Evidence map›Paper›PMID 28672826›Full record

ReviewJournal of clinical medicine2017

Pathophysiology of Hemophilic Arthropathy.

Daniela Melchiorre, Mirko Manetti, Marco Matucci-Cerinic

Open access · goldAbstract readReview
In one paragraph

Review in Journal of clinical medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed, 2 pooled it
9.5field-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

73 citing papers in PubMed, 2 syntheses or guidelines pooled it, 169 citations in OpenAlex.

  1. Pooled it
  2. Surgery for chronic arthropathy in people with haemophilia.The Cochrane database of systematic reviews · 2022
    Pooled it
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Magnetic resonance imaging of knee arthropathies: A pictorial review.Journal of clinical orthopaedics and trauma · 2025
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Biomarkers Involved in the Pathogenesis of Hemophilic Arthropathy.International journal of molecular sciences · 2024
    Review
  18. Article
  19. Article
  20. Article

13 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 2 institutions in 1 country.

Daniela MelchiorreSection of Internal Medicine, Department of Experimental and Clinical Medicine, University of Florence, 50134 Florence, Italy. daniela.melchiorre@unifi.it.
Mirko ManettiSection of Anatomy and Histology, Department of Experimental and Clinical Medicine, University of Florence, 50134 Florence, Italy. mirko.manetti@unifi.it.
Marco Matucci-CerinicSection of Internal Medicine, Department of Experimental and Clinical Medicine, University of Florence, 50134 Florence, Italy. marco.matuccicerinic@unifi.it.
Azienda Ospedaliero-Universitaria Careggi · ITUniversity of Florence · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Spontaneous joint bleeding and repeated hemarthroses lead to hemophilic arthropathy-a debilitating disease with a significant negative impact on mobility and quality of life. Iron, cytokines, and angiogenic growth factors play a pivotal role in the onset of the inflammatory process that involves the synovial tissue, articular cartilage, and subchondral bone, with early damages and molecular changes determining the perpetuation of a chronic inflammatory condition. Synovitis is one of the earliest complications of hemarthrosis, and is characterized by synovial hypertrophy, migration of inflammatory cells, and a high degree of neo-angiogenesis with subsequent bleeding. The pathogenic mechanisms and molecular pathways by which blood in the joint cavity causes articular cartilage and subchondral bone destruction have yet to be fully elucidated. Both cytokines and matrix metalloproteinases and hydroxyl radicals may induce chondrocyte apoptosis. Members of the tumor necrosis factor receptor superfamily (such as the molecular triad: osteoprotegerin-OPG; receptor activator of nuclear factor κB-RANK; RANK ligand-RANKL) seem instead to play a major role in the inflammatory process. These pathogenic processes interact with each other and ultimately lead to a fibrotic joint and the disabling condition characteristic of hemophilic arthropathy.

Indexed as

hemarthrosishemophiliahemophilic arthropathysynovitis

Identifiers

PMID28672826
PMCPMC5532571
OpenAlexW2702036786

What OpenQuestion holds

Textmetadata
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.