Evidence map›Paper›PMID 24891761›Full record

ReviewMediators of inflammation2014

The pathology of orthopedic implant failure is mediated by innate immune system cytokines.

Stefan Landgraeber, Marcus Jäger, Joshua J Jacobs, Nadim James Hallab

Abstract readReview
In one paragraph

Review in Mediators of inflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing 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

66 citing papers in PubMed.

  1. Review
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  14. Article
  15. Biopolymeric Coatings for Local Release of Therapeutics from Biomedical Implants.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Review
  16. Article
  17. Therapeutic activity of lipoxin AFrontiers in immunology · 2023
    Article
  18. Innate Immune Response in Orthopedic Implant Failure.Journal of orthopaedics and sports medicine · 2023
    Article
  19. Metabolic Conditions and Peri-Implantitis.Antibiotics (Basel, Switzerland) · 2022
    Review
  20. Review

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

4 authors.

Stefan LandgraeberDepartment of Orthopaedics, University Hospital Essen, University of Duisburg-Essen, Hufelandstraße 55, 45122 Essen, Germany ; Department of Orthopedics, Rush University Medical Center, 1735 W Harrison MC107, Chicago, IL 60612, USA.
Marcus JägerDepartment of Orthopaedics, University Hospital Essen, University of Duisburg-Essen, Hufelandstraße 55, 45122 Essen, Germany.
Joshua J JacobsDepartment of Orthopedics, Rush University Medical Center, 1735 W Harrison MC107, Chicago, IL 60612, USA.
Nadim James HallabDepartment of Orthopedics, Rush University Medical Center, 1735 W Harrison MC107, Chicago, IL 60612, USA.

Funding

Inflammasome Danger Signaling:A Novel Target to Prevent Debris Induced OsteolysisR01AR060782 · NIAMS · RUSH UNIVERSITY MEDICAL CENTER · PI HALLAB, NADIM JAMES · 2012 to 2016
$1.5M
NIAMS NIH HHS R01 AR060782
6 · The paper itself

Abstract

All of the over 1 million total joint replacements implanted in the US each year are expected to eventually fail after 15-25 years of use, due to slow progressive subtle inflammation at the bone implant interface. This inflammatory disease state is caused by implant debris acting, primarily, on innate immune cells, that is, macrophages. This slow progressive pathological bone loss or "aseptic loosening" is a potentially life-threatening condition due to the serious complications in older people (>75 yrs) of total joint replacement revision surgery. In some people implant debris (particles and ions from metals) can influence the adaptive immune system as well, giving rise to the concept of metal sensitivity. However, a consensus of studies agrees that the dominant form of this response is due to innate reactivity by macrophages to implant debris where both danger (DAMP) and pathogen (PAMP) signalling elicit cytokine-based inflammatory responses. This paper discusses implant debris induced release of the cytokines and chemokines due to activation of the innate (and the adaptive) immune system and the subsequent formation of osteolysis. Different mechanisms of implant-debris reactivity related to the innate immune system are detailed, for example, danger signalling (e.g., IL-1β, IL-18, IL-33, etc.), toll-like receptor activation (e.g., IL-6, TNF-α, etc.), apoptosis (e.g., caspases 3-9), bone catabolism (e.g., TRAP5b), and hypoxia responses (Hif1-α). Cytokine-based clinical and basic science studies are in progress to provide diagnosis and therapeutic intervention strategies.

Indexed as

Gene Expression RegulationImmunity, InnateProsthesis FailureAdaptive ImmunityAgedBone and BonesChemokinesCytokinesHumansInflammasomesInflammationLymphocytesMacrophagesOrthopedicsOsteoblastsOsteolysisChemokinesCytokinesInflammasomes

Identifiers

PMID24891761
PMCPMC4033543

What OpenQuestion holds

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LicenceCC BY
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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.