Evidence map›Paper›PMID 28569732›Full record

ReviewThe Journal of clinical investigation2017

Inflammatory osteolysis: a conspiracy against bone.

Gabriel Mbalaviele, Deborah V Novack, Georg Schett, Steven L Teitelbaum

Open access · bronzeAbstract readReview
In one paragraph

Review in The Journal of clinical investigation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 151 papers.

0numbers the graph read from it
0cells of the map it votes in
151citing papers in PubMed
10.0field-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

151 citing papers in PubMed, 249 citations in OpenAlex.

  1. S100A9 Induces RANKL Expression in Osteocytes Utilizing IL-6/sIL-6R Combination and gp130 Signaling Pathways.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  2. Article
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  4. Activation of the noncanonical inflammasome-GSDMD pathway triggers pyroptosis in bone marrow and promotes periosteal bone formation.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2026
    Article
  5. Osteomyelitis.Nature reviews. Disease primers · 2026
    Review
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91 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 at 2 institutions in 2 countries.

Gabriel MbalavieleDepartment of Medicine, Division of Bone and Mineral Diseases, and.
Deborah V NovackDepartment of Medicine, Division of Bone and Mineral Diseases, and.
Georg SchettDepartment of Internal Medicine 3, Rheumatology and Immunology, University of Erlangen-Nuremberg, Erlangen, Germany.
Steven L TeitelbaumDepartment of Medicine, Division of Bone and Mineral Diseases, and.
Washington University in St. Louis · USFriedrich-Alexander-Universität Erlangen-Nürnberg · DE

Funding

The Role of the Osteoblast Secretome in Bone FormationP30AR057235 · NIAMS · WASHINGTON UNIVERSITY · PI SILVA, MATTHEW J · 2009 to 2018
$5.7M
MECHANISMS OF AVB3 INTEGRIN MEDIATED BONE RESORPTIONR01AR046523 · NIAMS · WASHINGTON UNIVERSITY · PI TEITELBAUM, STEVEN L · 2000 to 2009
$4.0M
Mechanisms of AVB3 Integrin Mediated Bone ResorptionR37AR046523 · NIAMS · WASHINGTON UNIVERSITY · PI TEITELBAUM, STEVEN L · 2010 to 2019
$3.3M
NF-kB SUBUNITS p65 AND RelB IN OSTEOCLASTSR01AR052705 · NIAMS · WASHINGTON UNIVERSITY · PI VEIS, DEBORAH J · 2006 to 2015
$3.0M
Role of Mitochondrial Dynamics In Bone HomeostasisR01AR070030 · NIAMS · WASHINGTON UNIVERSITY · PI VEIS, DEBORAH J · 2016 to 2020
$1.8M
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
NIAMS NIH HHS P30 AR057235NIAMS NIH HHS R01 AR046523NIAMS NIH HHS R01 AR052705NIAMS NIH HHS R01 AR064755NIAMS NIH HHS R01 AR068972NIAMS NIH HHS R01 AR070030NIAMS NIH HHS R37 AR046523
6 · The paper itself

Abstract

There are many causes of inflammatory osteolysis, but regardless of etiology and cellular contexts, the osteoclast is the bone-degrading cell. Thus, the impact of inflammatory cytokines on osteoclast formation and function was among the most important discoveries advancing the treatment of focal osteolysis, leading to development of therapeutic agents that either directly block the bone-resorptive cell or do so indirectly via cytokine arrest. Despite these advances, a substantial number of patients with inflammatory arthritis remain resistant to current therapies, and even effective anti-inflammatory drugs frequently do not repair damaged bone. Thus, insights into events such as those impacted by inflammasomes, which signal through cytokine-dependent and -independent mechanisms, are needed to optimize treatment of inflammatory osteolysis.

Indexed as

AnimalsBone and BonesCytokinesHumansInflammasomesOsteoclastsOsteocytesOsteolysisCytokinesInflammasomes

Identifiers

PMID28569732
PMCPMC5451216
OpenAlexW2619932350

What OpenQuestion holds

Textmetadata
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.