Evidence map›Paper›PMID 30147688›Full record

ArticleFrontiers in immunology2018

CCR2 Contributes to F4/80+ Cells Migration Along Intramembranous Bone Healing in Maxilla, but Its Deficiency Does Not Critically Affect the Healing Outcome.

Claudia Cristina Biguetti, Andreia Espindola Vieira, Franco Cavalla, Angélica Cristina Fonseca, Priscila Maria Colavite, Renato Menezes Silva, Ana Paula Favaro Trombone, Gustavo Pompermaier Garlet

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

17 citing papers in PubMed, 31 citations in OpenAlex.

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  9. Frontiers in bioengineering and biotechnology · 2023
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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

8 authors at 3 institutions in 2 countries.

Claudia Cristina BiguettiDepartment of Biological Sciences, Bauru School of Dentistry, University of São Paulo, Bauru, Brazil.
Andreia Espindola VieiraInstitute of Biological Sciences and Health, Federal University of Alagoas, Maceió, Brazil.
Franco CavallaDepartment of Biological Sciences, Bauru School of Dentistry, University of São Paulo, Bauru, Brazil.
Angélica Cristina FonsecaDepartment of Biological Sciences, Bauru School of Dentistry, University of São Paulo, Bauru, Brazil.
Priscila Maria ColaviteDepartment of Biological Sciences, Bauru School of Dentistry, University of São Paulo, Bauru, Brazil.
Renato Menezes SilvaDepartment of Endodontics, University of Texas School of Dentistry at Houston, Houston, TX, United States.
Ana Paula Favaro TromboneDepartment of Biological and Allied Health Sciences, Universidade do Sagrado Coração, Bauru, Brazil.
Gustavo Pompermaier GarletDepartment of Biological Sciences, Bauru School of Dentistry, University of São Paulo, Bauru, Brazil.
Universidade de São Paulo · BRUniversidade Federal de Alagoas · BRUniversidade Sagrado Coração · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bone healing depends of a transient inflammatory response, involving selective migration of leukocytes under the control of chemokine system. CCR2 has been regarded as an essential receptor for macrophage recruitment to inflammation and healing sites, but its role in the intramembranous bone healing on craniofacial region remains unknown. Therefore, we investigated the role of CCR2 on F4/80+ cells migration and its consequences to the intramembranous healing outcome. C57BL/6 wild-type (WT) and CCR2KO mice were subjected to upper right incisor extraction, followed by micro-computed tomography, histological, immunological, and molecular analysis along experimental periods. CCR2 was associated with F4/80+ cells influx to the intramembranous bone healing in WT mice, and CCR2+ cells presented a kinetics similar to F4/80+ and CCR5+ cells. By contrast, F4/80+ and CCR5+ cells were significantly reduced in CCR2KO mice. The absence of CCR2 did not cause major microscopic changes in healing parameters, while molecular analysis demonstrated differential genes expression of several molecules between CCR2KO and WT mice. The mRNA expression of TGFB1, RUNX2, and mesenchymal stem cells markers (CXCL12, CD106, OCT4, NANOG, and CD146) was decreased in CCR2KO mice, while IL6, CXCR1, RANKL, and ECM markers (MMP1, 2, 9, and Col1a2) were significantly increased in different periods. Finally, immunofluorescence and FACS revealed that F4/80+ cells are positive for both CCR2 and CCR5, suggesting that CCR5 may account for the remaining migration of the F4/80+ cells in CCR2KO mice. In summary, these results indicate that CCR2+ cells play a primary role in F4/80+ cells migration along healing in intramembranous bones, but its deficiency does not critically impact healing outcome.

Indexed as

Wound HealingAnimalsBiomarkersCell MovementDisease Models, AnimalImmunohistochemistryMacrophagesMaleMaxillaMiceMice, KnockoutMonocytesReceptors, CCR2X-Ray MicrotomographyBiomarkersReceptors, CCR2bone healingbone histomorphometryintramembranous bonemacrophagesosteoimmunology

Identifiers

PMID30147688
PMCPMC6095997
OpenAlexW2885811162

What OpenQuestion holds

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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.