Evidence map›Paper›PMID 28747793›Full record

ArticleScientific reports2017

Bone matrix components activate the NLRP3 inflammasome and promote osteoclast differentiation.

Yael Alippe, Chun Wang, Biancamaria Ricci, Jianqiu Xiao, Chao Qu, Wei Zou, Deborah V Novack, Yousef Abu-Amer, Roberto Civitelli, Gabriel Mbalaviele

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed, 2 pooled it
3.4field-weighted citation impact, top 7% 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

69 citing papers in PubMed, 2 syntheses or guidelines pooled it, 105 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Pyroptotic cell-derived factors promote osteoclast differentiation.bioRxiv : the preprint server for biology · 2026
    Article
  5. Article
  6. Review
  7. Article
  8. Mechanosensitive ion channels as novel targets in osteoporosis.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2026
    Review
  9. Review
  10. Review
  11. Review
  12. Review
  13. Article
  14. Pinosylvin Inhibits Inflammatory and Osteoclastogenesis via NLRP3 Inflammasome.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  15. Review
  16. Review
  17. Review
  18. NLRP3 inflammasome in health and disease (Review).International journal of molecular medicine · 2025
    Review
  19. Review
  20. Article

9 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

10 authors at 1 institution in 1 country.

Yael AlippeDivision of Bone and Mineral Diseases, Washington University School of Medicine, St. Louis, MO, 63110, United States.
Chun WangDivision of Bone and Mineral Diseases, Washington University School of Medicine, St. Louis, MO, 63110, United States.
Biancamaria RicciDepartment of Orthopedic Surgery, Washington University School of Medicine, St. Louis, MO, 63110, United States.
Jianqiu XiaoDivision of Bone and Mineral Diseases, Washington University School of Medicine, St. Louis, MO, 63110, United States.
Chao QuDivision of Bone and Mineral Diseases, Washington University School of Medicine, St. Louis, MO, 63110, United States.
Wei ZouDepartment of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO, 63110, United States.
Deborah V NovackDivision of Bone and Mineral Diseases, Washington University School of Medicine, St. Louis, MO, 63110, United States.ORCID 0000-0001-7101-5582
Yousef Abu-AmerDepartment of Orthopedic Surgery, Washington University School of Medicine, St. Louis, MO, 63110, United States.
Roberto CivitelliDivision of Bone and Mineral Diseases, Washington University School of Medicine, St. Louis, MO, 63110, United States.
Gabriel MbalavieleDivision of Bone and Mineral Diseases, Washington University School of Medicine, St. Louis, MO, 63110, United States. gmbalaviele@wustl.edu.
Washington University in St. Louis · US

Funding

WU INSTITUTE OF CLINICAL AND TRANSLATIONAL SCIENCESUL1TR002345 · NCATS · WASHINGTON UNIVERSITY · PI William G. Powderly · 2017 to 2026
$97.8M
Washington University Institute of Clinical and Translational SciencesUL1TR000448 · NCATS · WASHINGTON UNIVERSITY · PI EVANOFF, BRADLEY A · 2012 to 2016
$41.4M
The Role of the Osteoblast Secretome in Bone FormationP30AR057235 · NIAMS · WASHINGTON UNIVERSITY · PI SILVA, MATTHEW J · 2009 to 2018
$5.7M
Regulatory Mechanisms of Implant-Induced OsteolysisR01AR049192 · NIAMS · WASHINGTON UNIVERSITY · PI ABU-AMER, YOUSEF · 2004 to 2019
$4.3M
Molecular Mechanisms Underlying Tak1 Function in OsteoclastsR01AR054326 · NIAMS · WASHINGTON UNIVERSITY · PI ABU-AMER, YOUSEF · 2008 to 2017
$3.3M
NLRP3 inflammasome Regulation of Bone ResorptionR01AR064755 · NIAMS · WASHINGTON UNIVERSITY · PI MBALAVIELE, GABRIEL · 2013 to 2017
$1.6M
Role of PARP1 in the Osteoclast LineageR01AR068972 · NIAMS · WASHINGTON UNIVERSITY · PI MBALAVIELE, GABRIEL · 2016 to 2020
$1.6M
NCATS NIH HHS UL1 TR000448NCATS NIH HHS UL1 TR002345NIAMS NIH HHS P30 AR057235NIAMS NIH HHS R01 AR049192NIAMS NIH HHS R01 AR054326NIAMS NIH HHS R01 AR064755NIAMS NIH HHS R01 AR068972
6 · The paper itself

Abstract

The NLRP3 inflammasome senses a variety of signals referred to as danger associated molecular patterns (DAMPs), including those triggered by crystalline particulates or degradation products of extracellular matrix. Since some DAMPs confer tissue-specific activation of the inflammasomes, we tested the hypothesis that bone matrix components function as DAMPs for the NLRP3 inflammasome and regulate osteoclast differentiation. Indeed, bone particles cause exuberant osteoclastogenesis in the presence of RANKL, a response that correlates with NLRP3 abundance and the state of inflammasome activation. To determine the relevance of these findings to bone homeostasis, we studied the impact of Nlrp3 deficiency on bone using pre-clinical mouse models of high bone turnover, including estrogen deficiency and sustained exposure to parathyroid hormone or RANKL. Despite comparable baseline indices of bone mass, bone loss caused by hormonal or RANKL perturbations is significantly reduced in Nlrp3 deficient than in wild type mice. Consistent with the notion that osteolysis releases DAMPs from bone matrix, pharmacologic inhibition of bone resorption by zoledronate attenuates inflammasome activation in mice. Thus, signals originating from bone matrix activate the NLRP3 inflammasome in the osteoclast lineage, and may represent a bone-restricted positive feedback mechanism that amplifies bone resorption in pathologic conditions of accelerated bone turnover.

Indexed as

Cell DifferentiationAnimalsBone MatrixBone ResorptionEstrogensInflammasomesMice, Inbred C57BLMice, KnockoutModels, AnimalNLR Family, Pyrin Domain-Containing 3 ProteinOsteoclastsParathyroid HormoneRANK LigandReceptors, Cell SurfaceEstrogensInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseParathyroid HormoneRANK LigandReceptors, Cell SurfaceTnfsf11 protein, mouse

Identifiers

PMID28747793
PMCPMC5529467
OpenAlexW2736948430

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.