Evidence map›Paper›PMID 39233381›Full record

ReviewPeriodontology 20002024

Microbiota-immune-brain interactions: A new vision in the understanding of periodontal health and disease.

Torbjørn Jarle Breivik, Per Gjermo, Yngvar Gundersen, Per Kristian Opstad, Robert Murison, Anders Hugoson, Stephan von Hörsten, Inge Fristad

Abstract readReview
In one paragraph

Review in Periodontology 2000, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

8 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. 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.

Torbjørn Jarle BreivikDepartment of Periodontology, Faculty of Dentistry, Institute of Clinical Odontology, University of Oslo, Oslo, Norway.
Per GjermoDepartment of Periodontology, Faculty of Dentistry, Institute of Clinical Odontology, University of Oslo, Oslo, Norway.
Yngvar GundersenDivision for Protection, Norwegian Defence Research Establishment, Kjeller, Norway.
Per Kristian OpstadDivision for Protection, Norwegian Defence Research Establishment, Kjeller, Norway.
Robert MurisonDepartment of Biological and Medical Psychology, Faculty of Psychology, University of Bergen, Bergen, Norway.
Anders HugosonDepartment of Periodontology, Institute of Odontology, The Sahlgrenska Academy at University of Gothenburg and School of Health and Welfare, Gothenburg, Sweden.
Stephan von HörstenDepartment for Experimental Therapy, University Hospital Erlangen, Preclinical Experimental Center, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), Erlangen, Germany.
Inge FristadDepartment of Clinical Dentistry, Faculty of Medicine, University of Bergen, Bergen, Norway.ORCID 0000-0002-3054-6501

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This review highlights the significance of interactions between the microbiota, immune system, nervous and hormonal systems, and the brain on periodontal health and disease. Microorganisms in the microbiota, immune cells, and neurons communicate via homeostatic nervous and hormonal systems, regulating vital body functions. By modulating pro-inflammatory and anti-inflammatory adaptive immune responses, these systems control the composition and number of microorganisms in the microbiota. The strength of these brain-controlled responses is genetically determined but is sensitive to early childhood stressors, which can permanently alter their responsiveness via epigenetic mechanisms, and to adult stressors, causing temporary changes. Clinical evidence and research with humans and animal models indicate that factors linked to severe periodontitis enhance the responsiveness of these homeostatic systems, leading to persistent hyperactivation. This weakens the immune defense against invasive symbiotic microorganisms (pathobionts) while strengthening the defense against non-invasive symbionts at the gingival margin. The result is an increased gingival tissue load of pathobionts, including Gram-negative bacteria, followed by an excessive innate immune response, which prevents infection but simultaneously destroys gingival and periodontal tissues. Thus, the balance between pro-inflammatory and anti-inflammatory adaptive immunity is crucial in controlling the microbiota, and the responsiveness of brain-controlled homeostatic systems determines periodontal health.

Indexed as

BrainMicrobiotaAdaptive ImmunityAnimalsHomeostasisHumansImmune SystemImmunity, InnatePeriodontal DiseasesPeriodontitisenvironmentepigeneticsgeneticsgingivitismicrobiota‐immune‐brain‐communicationperiodontitis

Identifiers

PMID39233381
PMCPMC11579829

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.