Evidence map›Paper›PMID 38413562›Full record

ArticleInternational journal of oral science2024

The neutrophil-osteogenic cell axis promotes bone destruction in periodontitis.

Yutaro Ando, Masayuki Tsukasaki, Nam Cong-Nhat Huynh, Shizao Zang, Minglu Yan, Ryunosuke Muro, Kazutaka Nakamura, Masatsugu Komagamine, Noriko Komatsu, Kazuo Okamoto and 5 more

Open access · goldAbstract read
In one paragraph

Article in International journal of oral science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
18.8field-weighted citation impact, top 1% 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

44 citing papers in PubMed, 47 citations in OpenAlex.

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  9. A RANKLBone research · 2026
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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

15 authors at 5 institutions in 2 countries.

Yutaro AndoDepartment of Immunology, Graduate School of Medicine and Faculty of Medicine, The University of Tokyo, 7-3-1, Hongo, Bunkyo-ku, Tokyo, Japan.
Masayuki TsukasakiDepartment of Osteoimmunology, Graduate School of Medicine and Faculty of Medicine, The University of Tokyo, 7-3-1, Hongo, Bunkyo-ku, Tokyo, Japan. tsuka-im@m.u-tokyo.ac.jp.
Nam Cong-Nhat HuynhDepartment of Immunology, Graduate School of Medicine and Faculty of Medicine, The University of Tokyo, 7-3-1, Hongo, Bunkyo-ku, Tokyo, Japan.ORCID 0000-0003-4718-7813
Shizao ZangDepartment of Immunology, Graduate School of Medicine and Faculty of Medicine, The University of Tokyo, 7-3-1, Hongo, Bunkyo-ku, Tokyo, Japan.
Minglu YanDepartment of Immunology, Graduate School of Medicine and Faculty of Medicine, The University of Tokyo, 7-3-1, Hongo, Bunkyo-ku, Tokyo, Japan.
Ryunosuke MuroDepartment of Immunology, Graduate School of Medicine and Faculty of Medicine, The University of Tokyo, 7-3-1, Hongo, Bunkyo-ku, Tokyo, Japan.
Kazutaka NakamuraDepartment of Immunology, Graduate School of Medicine and Faculty of Medicine, The University of Tokyo, 7-3-1, Hongo, Bunkyo-ku, Tokyo, Japan.
Masatsugu KomagamineDepartment of Immunology, Graduate School of Medicine and Faculty of Medicine, The University of Tokyo, 7-3-1, Hongo, Bunkyo-ku, Tokyo, Japan.
Noriko KomatsuDepartment of Immunology, Graduate School of Medicine and Faculty of Medicine, The University of Tokyo, 7-3-1, Hongo, Bunkyo-ku, Tokyo, Japan.
Kazuo OkamotoDepartment of Osteoimmunology, Graduate School of Medicine and Faculty of Medicine, The University of Tokyo, 7-3-1, Hongo, Bunkyo-ku, Tokyo, Japan.
Kenta NakanoDepartment of Laboratory Animal Medicine, Research Institute, National Center for Global Health and Medicine, Tokyo, Japan.
Tadashi OkamuraDepartment of Laboratory Animal Medicine, Research Institute, National Center for Global Health and Medicine, Tokyo, Japan.
Akira YamaguchiOral Health Science Center, Tokyo Dental College, 2-9-18, Kanda-Misaki-cho, Chiyoda-ku, Tokyo, Japan.
Kazuyuki IshiharaDepartment of Microbiology, Tokyo Dental College, 2-1-14 Kanda-Misaki-cho, Chiyoda-ku, Tokyo, Japan.ORCID 0000-0002-6567-807X
Hiroshi TakayanagiDepartment of Immunology, Graduate School of Medicine and Faculty of Medicine, The University of Tokyo, 7-3-1, Hongo, Bunkyo-ku, Tokyo, Japan. takayana@m.u-tokyo.ac.jp.ORCID 0000-0002-1462-4127
The University of Tokyo · JPTokyo Dental College · JPNational Center for Global Health and Medicine · JPKeio University · JPUniversity of Medicine and Pharmacy at Ho Chi Minh City · VN

Funding

Japan Agency for Medical Research and Development (AMED) JP20ek0410073Japan Agency for Medical Research and Development (AMED) JP22ek0410100Japan Agency for Medical Research and Development (AMED) JP23ek0410108
6 · The paper itself

Abstract

The immune-stromal cell interactions play a key role in health and diseases. In periodontitis, the most prevalent infectious disease in humans, immune cells accumulate in the oral mucosa and promote bone destruction by inducing receptor activator of nuclear factor-κB ligand (RANKL) expression in osteogenic cells such as osteoblasts and periodontal ligament cells. However, the detailed mechanism underlying immune-bone cell interactions in periodontitis is not fully understood. Here, we performed single-cell RNA-sequencing analysis on mouse periodontal lesions and showed that neutrophil-osteogenic cell crosstalk is involved in periodontitis-induced bone loss. The periodontal lesions displayed marked infiltration of neutrophils, and in silico analyses suggested that the neutrophils interacted with osteogenic cells through cytokine production. Among the cytokines expressed in the periodontal neutrophils, oncostatin M (OSM) potently induced RANKL expression in the primary osteoblasts, and deletion of the OSM receptor in osteogenic cells significantly ameliorated periodontitis-induced bone loss. Epigenomic data analyses identified the OSM-regulated RANKL enhancer region in osteogenic cells, and mice lacking this enhancer showed decreased periodontal bone loss while maintaining physiological bone metabolism. These findings shed light on the role of neutrophils in bone regulation during bacterial infection, highlighting the novel mechanism underlying osteoimmune crosstalk.

Indexed as

Alveolar Bone LossPeriodontitisAnimalsCytokinesHumansMiceNeutrophilsOsteogenesisRANK LigandCytokinesRANK Ligand

Identifiers

PMID38413562
PMCPMC10899642
OpenAlexW4392200246

What Socratic 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 Socratic graph.