Evidence map›Paper›PMID 41786250›Full record

ArticleJournal of lipid research2026

EBV promotes alveolar trabecula resorption via extracellular vesicle remodeling by group IIA secreted phospholipase A

Akane Kanamori, Akira Hasuike, Kai Kudo, Joaquim Carreras, Takanobu Shimizu, Shunya Nakayama, Ryo Yanagiya, Ryo Koike, Yorimasa Ogata, Osamu Takeichi and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of lipid research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

16 authors.

Akane KanamoriDivision of Cellular and Molecular Biology, Department of Regulation of Infectious Cancer, Research Institute for Microbial Diseases, The University of Osaka, Suita, Osaka, Japan; Department of Molecular Life Sciences, Tokai University School of Medicine, Isehara, Kanagawa, Japan.
Akira HasuikeDepartment of Innovative Medical Science, Tokai University School of Medicine, Isehara, Kanagawa, Japan; Department of Periodontology, Nihon University School of Dentistry, Tokyo, Japan.
Kai KudoDepartment of Innovative Medical Science, Tokai University School of Medicine, Isehara, Kanagawa, Japan.
Joaquim CarrerasDepartment of Pathology, Tokai University School of Medicine, Isehara, Kanagawa, Japan.
Takanobu ShimizuDepartment of Innovative Medical Science, Tokai University School of Medicine, Isehara, Kanagawa, Japan.
Shunya NakayamaDepartment of Innovative Medical Science, Tokai University School of Medicine, Isehara, Kanagawa, Japan.
Ryo YanagiyaDivision of Cellular and Molecular Biology, Department of Regulation of Infectious Cancer, Research Institute for Microbial Diseases, The University of Osaka, Suita, Osaka, Japan.
Ryo KoikeDepartment of Microbiology and Immunology, Nihon University School of Dentistry, Tokyo, Japan.
Yorimasa OgataDepartment of Periodontology, Nihon University School of Dentistry at Matsudo, Chiba, Japan.
Osamu TakeichiDepartment of Endodontics, Nihon University School of Dentistry, Tokyo, Japan.
Shuichi SatoDepartment of Periodontology, Nihon University School of Dentistry, Tokyo, Japan.
Kiyoshi AndoDepartment of Hematology and Oncology, Tokai University School of Medicine, Isehara, Kanagawa, Japan.
Naoya NakamuraDepartment of Pathology, Tokai University School of Medicine, Isehara, Kanagawa, Japan.
Makoto MurakamiLaboratory of Microenvironmental Metabolic Health Sciences Center for Disease Biology and Integrative Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Kenichi ImaiDepartment of Microbiology and Immunology, Nihon University School of Dentistry, Tokyo, Japan. Electronic address: imai.kenichi@nihon-u.ac.jp.
Ai KotaniDivision of Cellular and Molecular Biology, Department of Regulation of Infectious Cancer, Research Institute for Microbial Diseases, The University of Osaka, Suita, Osaka, Japan; Department of Immunology, Tokai University School of Medicine, Isehara, Kanagawa, Japan. Electronic address: aikotani@k-lab.jp.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epstein-Barr virus (EBV) is an enveloped, double-stranded DNA virus that selectively infects primates. Periodontitis, a common inflammatory disease characterized by alveolar bone destruction, affects more than half of the global adult population. While EBV has been linked to periodontitis due to its pro-inflammatory effects and presence in the human periodontium, its effects on bone metabolism, particularly alveolar bone resorption, remain unclear. This study demonstrated that EBV infection in humanized mice induced osteoclast differentiation and alveolar bone resorption, resulting in sparse trabecular bone patterns and increased lacunae resorption. Extracellular vesicles (EVs) from EBV-infected cells contained M-CSF, essential for osteoclast differentiation, and increased CTSK and RANKL expression in osteoclast precursor cells after uptake. EBV infection increased the expression of group IIA-secreted phospholipase A

Indexed as

Alveolar Bone LossExtracellular VesiclesGroup II Phospholipases A2Herpesvirus 4, HumanAnimalsCell DifferentiationHumansMiceOsteoclastsGroup II Phospholipases A2bone resorptionEBVextracellular vesiclesperiodontitissPLA(2)

Identifiers

PMID41786250
PMCPMC13049295

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.