Evidence map›Paper›PMID 29993312›Full record

ArticleJournal of dental research2018

Resolving Macrophages Counter Osteolysis by Anabolic Actions on Bone Cells.

A Viniegra, H Goldberg, Ç Çil, N Fine, Z Sheikh, M Galli, M Freire, Y Wang, T E Van Dyke, M Glogauer and 1 more

Open access · greenAbstract read
In one paragraph

Article in Journal of dental research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
3.3field-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

52 citing papers in PubMed, 92 citations in OpenAlex.

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  17. Therapeutic delivery of CCL2 modulates immune response and restores host-microbe homeostasis.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  18. Article
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  20. Tim4 deficiency reduces CD301bInternational journal of oral science · 2024
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 4 institutions in 2 countries.

A Viniegra1 Matrix Dynamics Group, Faculty of Dentistry, University of Toronto, Toronto, ON, Canada.
H Goldberg1 Matrix Dynamics Group, Faculty of Dentistry, University of Toronto, Toronto, ON, Canada.
Ç Çil1 Matrix Dynamics Group, Faculty of Dentistry, University of Toronto, Toronto, ON, Canada.
N Fine1 Matrix Dynamics Group, Faculty of Dentistry, University of Toronto, Toronto, ON, Canada.
Z Sheikh1 Matrix Dynamics Group, Faculty of Dentistry, University of Toronto, Toronto, ON, Canada.
M Galli1 Matrix Dynamics Group, Faculty of Dentistry, University of Toronto, Toronto, ON, Canada.
M Freire3 Department of Genomic Medicine and Infectious Diseases, J. Craig Venter Institute, La Jolla, CA, USA.ORCID 0000-0003-4906-7698
Y Wang1 Matrix Dynamics Group, Faculty of Dentistry, University of Toronto, Toronto, ON, Canada.
T E Van Dyke4 Center for Clinical and Translational Research, The Forsyth Institute, Cambridge, MA, USA.ORCID 0000-0003-0856-3396
M Glogauer1 Matrix Dynamics Group, Faculty of Dentistry, University of Toronto, Toronto, ON, Canada.
C Sima4 Center for Clinical and Translational Research, The Forsyth Institute, Cambridge, MA, USA.ORCID 0000-0003-3526-4850
University of Toronto · CAHarvard University · USJ. Craig Venter Institute · USMount Sinai Hospital · CA

Funding

M1/M2 Regulation of Inflammation in T2D-Associated PeriodontitisK99DE024575 · NIDCR · ADA FORSYTH INSTITUTE, INC. · PI SIMA, CORNELIU · 2015 to 2016
$244k
CIHR TBO-122068NIDCR NIH HHS K99 DE024575
6 · The paper itself

Abstract

Progression of inflammatory osteolytic diseases, including rheumatoid arthritis and periodontitis, is characterized by increased production of proinflammatory mediators and matrix-degrading enzymes by macrophages and increased osteoclastic activity. Phenotypic changes in macrophages are central to the healing process in virtually all tissues. Using a murine model of periodontitis, we assessed the timing of macrophage phenotypic changes and the impact of proresolving activation during inflammatory osteolysis and healing. Proinflammatory macrophage activation and TNF-α overproduction within 3 wk after induction of periodontitis was associated with progressing bone loss. Proresolving activation within 1 wk of stimulus removal and markers of resolving macrophages (IL-10, TGF-β, and CD206) correlated strongly with bone levels. In vivo macrophage depletion with clodronate liposomes prevented bone resorption but impaired regeneration. Induction of resolving macrophages with rosiglitazone, a PPAR-γ agonist, led to reduced bone resorption during inflammatory stimulation and increased bone formation during healing. In vitro assessment of primary bone marrow-derived macrophages activated with either IFN-γ and LPS (proinflammatory activation) or IL-4 (proresolving activation) showed that IL-4-activated cells have enhanced resolving functions (production of anti-inflammatory cytokines; migration and phagocytosis of aged neutrophils) and exert direct anabolic actions on bone cells. Cystatin C secreted by resolving but not inflammatory macrophages explained, in part, the macrophage actions on osteoblasts and osteoclasts. This study supports the concept that therapeutic induction of proresolving functions in macrophages can recouple bone resorption and formation in inflammatory osteolytic diseases.

Indexed as

OsteogenesisAnimalsDisease Models, AnimalInterferon-gammaInterleukin-4LipopolysaccharidesMacrophagesMaleMetabolismMiceMice, Inbred C57BLOsteolysisPeriodontitisReverse Transcriptase Polymerase Chain ReactionX-Ray MicrotomographyInterferon-gammaInterleukin-4Lipopolysaccharidesbone regenerationinflammation resolutioninnate immunityosteoblastosteoclastsperiodontitis

Identifiers

PMID29993312
PMCPMC6169030
OpenAlexW2838594489

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.