Evidence map›Paper›PMID 27126447›Full record

ArticleJournal of dental research2016

SOCS-3 Regulates Alveolar Bone Loss in Experimental Periodontitis.

E Papathanasiou, A Kantarci, A Konstantinidis, H Gao, T E Van Dyke

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of dental research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

25 citing papers in PubMed, 41 citations in OpenAlex.

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  7. JAK/STAT as a Potential Therapeutic Target for Osteolytic Diseases.International journal of molecular sciences · 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

5 authors at 3 institutions in 2 countries.

E PapathanasiouDepartment of Applied Oral Sciences, Center for Periodontology, Forsyth Institute, Cambridge, MA, USA Department of Periodontology, Tufts University School of Dental Medicine, Boston, MA, USA Department of Preventive Dentistry, Periodontology and Implant Biology, Dental School, Aristotle University of Thessaloniki, Thessaloniki, Greece.
A KantarciDepartment of Applied Oral Sciences, Center for Periodontology, Forsyth Institute, Cambridge, MA, USA.
A KonstantinidisDepartment of Preventive Dentistry, Periodontology and Implant Biology, Dental School, Aristotle University of Thessaloniki, Thessaloniki, Greece.
H GaoCenter for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
T E Van DykeDepartment of Applied Oral Sciences, Center for Periodontology, Forsyth Institute, Cambridge, MA, USA tvandyke@forsyth.org.
Aristotle University of Thessaloniki · GRBrigham and Women's Hospital · USTufts University · US

Funding

Mechanisms of Resolvin E1 in Periodontal RegenerationR01DE025020 · NIDCR · ADA FORSYTH INSTITUTE, INC. · PI GUASTALDI, FERNANDO, VAN DYKE, THOMAS ELLIOTT · 2015 to 2023
$4.9M
Hypoxia and PMN Function in PeriodontitisR21DE020906 · NIDCR · ADA FORSYTH INSTITUTE, INC. · PI KANTARCI, IBRAHIM ALPDOGAN · 2011 to 2012
$478k
NIDCR NIH HHS R01 DE025020NIDCR NIH HHS R21 DE020906
6 · The paper itself

Abstract

The host immune response plays a key role in bacteria-induced alveolar bone resorption. Endogenous control of the magnitude and duration of inflammatory signaling is considered an important determinant of the extent of periodontal pathology. Suppressor of cytokine signaling (SOCS) proteins are inhibitors of cytokine signaling pathways and may play a role in restraining periodontal inflammation. We hypothesized that SOCS-3 regulates alveolar bone loss in experimental periodontitis. Periodontal bone loss was induced in 16-wk-old myeloid-specific SOCS-3-knockout and wild-type (WT) C57Bl6-B.129 mice by oral inoculation 9 times with 10(9) colony-forming units of Porphyromonas gingivalis A7436 through an oral gavage model for periodontitis. Sham controls for both types of mice received vehicle without bacteria. The mice were euthanized 6 wk after the last oral inoculation. Increased bone loss was demonstrated in P. gingivalis-infected SOCS-3-knockout mice as compared with P. gingivalis-infected WT mice by direct morphologic measurements, micro-computed tomography analyses, and quantitative histology. Loss of SOCS-3 function resulted in an increased number of alveolar bone osteoclasts and increased RANKL expression after P. gingivalis infection. SOCS-3 deficiency in myeloid cells also promotes a higher P. gingivalis lipopolysaccharide-induced inflammatory response with higher secretion of IL-1β, IL-6, and KC (IL-8) by peritoneal macrophages as compared with WT controls. Our data implicate SOCS-3 as a critical negative regulator of alveolar bone loss in periodontitis.

Indexed as

Alveolar Bone LossAnimalsDisease Models, AnimalMaleMiceMice, Inbred C57BLMice, KnockoutOsteoclastsPeriodontitisPorphyromonas gingivalisSuppressor of Cytokine Signaling 3 ProteinSuppressor of Cytokine Signaling ProteinsX-Ray MicrotomographySocs3 protein, mouseSuppressor of Cytokine Signaling 3 ProteinSuppressor of Cytokine Signaling Proteinsanimal modelcytokinesinflammationmacrophagesosteoclastsPorphyromonas gingivalis

Identifiers

PMID27126447
PMCPMC4959623
OpenAlexW2343782389

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.