Evidence map›Paper›PMID 24090989›Full record

ReviewActa biomaterialia2014

Chronic inflammation in biomaterial-induced periprosthetic osteolysis: NF-κB as a therapeutic target.

Tzu-hua Lin, Yasunobu Tamaki, Jukka Pajarinen, Heather A Waters, Deanna K Woo, Zhenyu Yao, Stuart B Goodman

Abstract readReview
In one paragraph

Review in Acta biomaterialia, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed
12.5field-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

89 citing papers in PubMed, 206 citations in OpenAlex.

  1. Article
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  3. Nrf2 signaling pathway: focus on oxidative stress in osteoporosis.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2025
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  19. MAVRIC based T2 mapping assessment of infrapatellar fat pad scarring in patients with total knee arthroplasty.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2023
    Article
  20. Article

29 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

7 authors at 1 institution in 1 country.

Tzu-hua LinDepartment of Orthopaedic Surgery, Stanford University, Stanford, CA, USA.
Yasunobu Tamaki
Jukka Pajarinen
Heather A Waters
Deanna K Woo
Zhenyu Yao
Stuart B Goodman
Stanford University · US

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

Biomaterial-induced tissue responses in patients with total joint replacement are associated with the generation of wear particles, which may lead to chronic inflammation and local bone destruction (periprosthetic osteolysis). Inflammatory reactions associated with wear particles are mediated by several important signaling pathways, the most important of which involves the transcription factor NF-κB. NF-κB activation is essential for macrophage recruitment and maturation, as well as the production of pro-inflammatory cytokines and chemokines such as TNF-α, IL-1β, IL-6 and MCP1. In addition, NF-κB activation contributes to osteoclast differentiation and maturation via RANK/RANKL signaling, which increases bone destruction and reduces bone formation. Targeting individual downstream cytokines directly (such as TNF-α or IL-1β) may not effectively prevent wear particle induced osteolysis. A more logical upstream therapeutic approach may be provided by direct modulation of the core IκB/IKKα/β/NF-κB signaling pathway in the local environment. However, the timing, dose and strategy for administration should be considered. Suppression of chronic inflammation via inhibition of NF-κB activity in patients with malfunctioning joint replacements may be an effective strategy to mitigate wear particle induced periprosthetic osteolysis.

Indexed as

AnimalsBiocompatible MaterialsChronic DiseaseHumansInflammationJoint ProsthesisNF-kappa BOsteolysisSignal TransductionBiocompatible MaterialsNF-kappa BBiomaterialsChronic inflammationNF-κBPeriprosthetic osteolysis

Identifiers

PMID24090989
PMCPMC3849197
OpenAlexW2027496373

What OpenQuestion holds

Textmetadata
LicenceTDM
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.