Evidence map›Paper›PMID 39709535›Full record

ArticleMicrobiology and immunology2025

Experimental Murine Periodontitis Increases Salivary Gland IgA-Producing B Cells Following Oral Dysbiosis.

Mai Nara, Mie Kurosawa, Momoe Itsumi, Hirobumi Morisaki, Haruka Fukamachi, Nobuo Okahashi, Noriyuki Suzuki, Hirotaka Kuwata

Abstract read
In one paragraph

Article in Microbiology and immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

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

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Pathogenic effects ofCurrent research in microbial sciences · 2025
    Article
  6. 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.

Mai NaraDepartment of Conservative Dentistry, Division of Endodontology, Showa University Graduate School of Dentistry, Ota-ku, Tokyo, Japan.ORCID http://orcid.org/0009-0004-1376-2618
Mie KurosawaDepartment of Oral Microbiology and Immunology, Showa University Graduate School of Dentistry, Shinagawa-ku, Tokyo, Japan.ORCID http://orcid.org/0000-0002-8348-6311
Momoe ItsumiDepartment of Oral Microbiology and Immunology, Showa University Graduate School of Dentistry, Shinagawa-ku, Tokyo, Japan.ORCID http://orcid.org/0000-0003-2292-8523
Hirobumi MorisakiDepartment of Oral Microbiology and Immunology, Showa University Graduate School of Dentistry, Shinagawa-ku, Tokyo, Japan.
Haruka FukamachiDepartment of Oral Microbiology and Immunology, Showa University Graduate School of Dentistry, Shinagawa-ku, Tokyo, Japan.
Nobuo OkahashiDepartment of Oral Microbiology and Immunology, Showa University Graduate School of Dentistry, Shinagawa-ku, Tokyo, Japan.
Noriyuki SuzukiDepartment of Conservative Dentistry, Division of Endodontology, Showa University Graduate School of Dentistry, Ota-ku, Tokyo, Japan.
Hirotaka KuwataDepartment of Oral Microbiology and Immunology, Showa University Graduate School of Dentistry, Shinagawa-ku, Tokyo, Japan.ORCID http://orcid.org/0000-0002-5023-1777

Funding

This work was supported by the Japan Society for the Promotion of Science (JSPS) (KAKENHI Grant Numbers JP24K12900, JP24K12889, and JP23K09144).
6 · The paper itself

Abstract

The oral microbiome is closely involved in the maintenance of host health and the development of systemic diseases. The salivary glands play an essential role in homeostasis in the oral cavity. Here, we investigated the effects of periodontal inflammation on salivary gland function and the oral microbiome. In experimental periodontitis model mice, an increase in IgA⁺ cells in the salivary glands were observed 1 week after treatment. Alteration of the oral microbiome was also induced in this model. Gene expression analysis of the salivary glands showed changes in the expression of genes related to B-cell maturation and plasma cell differentiation and an increase in the expression of genes related to macrophage activation upon experimental periodontitis induction. Furthermore, the relationship between disruption of oral microflora and salivary gland function was examined using a cohousing model in which experimental periodontitis model mice and untreated mice were reared in the same cage. We found that cohoused normal mice underwent alteration of the oral microbiome, with increases in IgA⁺ cells and macrophages in the salivary glands. In summary, our results suggest that, in the oral cavity, there is a close link between oral bacterial flora and immune cells in the salivary glands. Our results also show that localized inflammation disrupts the homeostasis in the oral cavity, inducing pathological conditions such as dysbiosis. Our study suggests the importance of the interaction among local oral inflammation, salivary gland function, and oral microflora, and provides new insights into the mechanisms by which oral health is maintained.

Indexed as

B-LymphocytesDysbiosisImmunoglobulin AMouthPeriodontitisSalivary GlandsAnimalsDisease Models, AnimalMacrophagesMaleMiceMice, Inbred C57BLMicrobiotaImmunoglobulin AdysbiosisIgAmucosal immunologyoral microbiomeperiodontal inflammationsalivary gland

Identifiers

PMID39709535
PMCPMC11789210

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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.