Evidence map›Paper›PMID 33925019›Full record

ReviewInternational journal of molecular sciences2021

Connection between Periodontitis-Induced Low-Grade Endotoxemia and Systemic Diseases: Neutrophils as Protagonists and Targets.

Ljubomir Vitkov, Luis E Muñoz, Jasmin Knopf, Christine Schauer, Hannah Oberthaler, Bernd Minnich, Matthias Hannig, Martin Herrmann

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 2 pooled it
3.2field-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

34 citing papers in PubMed, 2 syntheses or guidelines pooled it, 54 citations in OpenAlex.

  1. Pooled it
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  4. Observational
  5. Review
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  7. Article
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  12. Exosomal miR-155-5p promote the occurrence of carotid atherosclerosis.Journal of cellular and molecular medicine · 2024
    Article
  13. Review
  14. Review
  15. Vesicular Messages from Dental Biofilms for Neutrophils.International journal of molecular sciences · 2024
    Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review
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.

Ljubomir VitkovVascular & Exercise Biology Unit, Department of Biosciences, University of Salzburg, 5020 Salzburg, Austria.ORCID 0000-0002-1249-0161
Luis E MuñozDepartment of Internal Medicine 3-Rheumatology and Immunology, Universitätsklinikum Erlangen, Friedrich-Alexander-University Erlangen-Nürnberg (FAU), 91052 Erlangen, Germany.ORCID 0000-0002-5395-804X
Jasmin KnopfDepartment of Internal Medicine 3-Rheumatology and Immunology, Universitätsklinikum Erlangen, Friedrich-Alexander-University Erlangen-Nürnberg (FAU), 91052 Erlangen, Germany.ORCID 0000-0003-2922-9370
Christine SchauerDepartment of Internal Medicine 3-Rheumatology and Immunology, Universitätsklinikum Erlangen, Friedrich-Alexander-University Erlangen-Nürnberg (FAU), 91052 Erlangen, Germany.
Hannah OberthalerVascular & Exercise Biology Unit, Department of Biosciences, University of Salzburg, 5020 Salzburg, Austria.
Bernd MinnichVascular & Exercise Biology Unit, Department of Biosciences, University of Salzburg, 5020 Salzburg, Austria.ORCID 0000-0003-1218-1913
Matthias HannigClinic of Operative Dentistry, Periodontology and Preventive Dentistry, Saarland University, 66424 Homburg, Germany.
Martin HerrmannDepartment of Internal Medicine 3-Rheumatology and Immunology, Universitätsklinikum Erlangen, Friedrich-Alexander-University Erlangen-Nürnberg (FAU), 91052 Erlangen, Germany.ORCID 0000-0002-0258-2484
Friedrich-Alexander-Universität Erlangen-Nürnberg · DEUniversity of Salzburg · ATSaarland University · DE

Funding

German Research Foundation SCHA 2040/1-1
6 · The paper itself

Abstract

Periodontitis is considered a promoter of many systemic diseases, but the signaling pathways of this interconnection remain elusive. Recently, it became evident that certain microbial challenges promote a heightened response of myeloid cell populations to subsequent infections either with the same or other pathogens. This phenomenon involves changes in the cell epigenetic and transcription, and is referred to as ''trained immunity''. It acts via modulation of hematopoietic stem and progenitor cells (HSPCs). A main modulation driver is the sustained, persistent low-level transmission of lipopolysaccharide from the periodontal pocket into the peripheral blood. Subsequently, the neutrophil phenotype changes and neutrophils become hyper-responsive and prone to boosted formation of neutrophil extracellular traps (NET). Cytotoxic neutrophil proteases and histones are responsible for ulcer formations on the pocket epithelium, which foster bacteremia and endoxemia. The latter promote systemic low-grade inflammation (SLGI), a precondition for many systemic diseases and some of them, e.g., atherosclerosis, diabetes etc., can be triggered by SLGI alone. Either reverting the polarized neutrophils back to the homeostatic state or attenuation of neutrophil hyper-responsiveness in periodontitis might be an approach to diminish or even to prevent systemic diseases.

Indexed as

AnimalsDiseaseEndotoxemiaHumansLipopolysaccharidesNeutrophilsPeriodontitisLipopolysaccharidesblood transmission of PAMPsloss of toleranceneutrophil-driven damagesneutrophil hyper-responsivenesstrained immunity

Identifiers

PMID33925019
PMCPMC8125370
OpenAlexW3159316998

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.