Evidence map›Paper›PMID 25747032›Full record

ArticleJournal of long-term effects of medical implants2014

Innate immunity sensors participating in pathophysiology of joint diseases: a brief overview.

Jiri Gallo, Milan Raska, Yrjo T Konttinen, Christophe Nich, Stuart B Goodman

Abstract read
In one paragraph

Article in Journal of long-term effects of medical implants, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

5 citing papers in PubMed.

  1. The Metabolic Syndrome, a Human Disease.International journal of molecular sciences · 2024
    Review
  2. Review
  3. Review
  4. Identification ofAging and disease · 2018
    Article
  5. 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

5 authors.

Jiri GalloDepartment of Orthopedics, University Hospital and Faculty of Medicine and Dentistry, Palacky University, Olomouc 775 20, Czech Republic.
Milan RaskaDepartment of Immunology, Faculty of Medicine & Dentistry, Palacky University, Hnevotinska 3, 775 15 Olomouc, Czech Republic.
Yrjo T KonttinenDepartment of Clinical Medicine, University of Helsinki and ORTON Orthopaedic Hospital of the Invalid Foundation, Helsinki, Finland.
Christophe NichLaboratoire de Biomecanique et Biomateriaux Osteo-Articulaires - UMR CNRS 7052, Faculte de Medecine - Universite Paris 7, Paris, France; Department of Orthopaedic Surgery, European Teaching Hospital, Assistance Publique - Hopitaux de Paris.
Stuart B GoodmanDepartment of Orthopaedic Surgery Stanford University Medical Center Redwood City, CA.

Funding

Wear Particle Disease and NF-kappa B SignalingR01AR063717 · NIAMS · STANFORD UNIVERSITY · PI GOODMAN, STUART B · 2012 to 2021
$3.5M
Chemokine Directed Cell Trafficking during Continuous Infusion of Wear ParticlesR01AR055650 · NIAMS · STANFORD UNIVERSITY · PI GOODMAN, STUART B · 2007 to 2016
$3.3M
NIAMS NIH HHS R01 AR055650NIAMS NIH HHS R01 AR063717
6 · The paper itself

Abstract

The innate immune system consists of functionally specialized "modules" that are activated in response to a particular set of stimuli via sensors located on the surface or inside the tissue cells. These cells screen tissues for a wide range of exogenous and endogenous danger/damage-induced signals with the aim to reject or tolerate them and maintain tissue integrity. In this line of thinking, inflammation evolved as an adaptive tool for restoring tissue homeostasis. A number of diseases are mediated by a maladaptation of the innate immune response, perpetuating chronic inflammation and tissue damage. Here, we review recent evidence on the cross talk between innate immune sensors and development of rheumatoid arthritis, osteoarthritis, and aseptic loosening of total joint replacements. In relation to the latter topic, there is a growing body of evidence that aseptic loosening and periprosthetic osteolysis results from long-term maladaptation of periprosthetic tissues to the presence of by-products continuously released from an artificial joint.

Indexed as

Arthritis, RheumatoidHumansImmunity, InnateJoint ProsthesisLectins, C-TypeNod Signaling Adaptor ProteinsOsteoarthritisOsteolysisReceptor for Advanced Glycation End ProductsReceptors, Cytoplasmic and NuclearReceptors, ImmunologicToll-Like ReceptorsLectins, C-TypeNod Signaling Adaptor ProteinsReceptor for Advanced Glycation End ProductsReceptors, Cytoplasmic and NuclearReceptors, ImmunologicToll-Like Receptors

Identifiers

PMID25747032
PMCPMC4369672

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Registered trials

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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.