Evidence map›Paper›PMID 40382634›Full record

ArticleJournal of nanobiotechnology2025

Outer membrane vesicles of Porphyromonas gingivalis impede bone regeneration by inducing ferroptosis via the Hippo-YAP signaling pathway.

Xinghong Luo, Yanzhen Wang, Tingting Ning, Qian Lei, Hao Cui, Xianghui Zou, Yan Chen, Shuoling Chen, Xinyao Zhang, Shenglong Tan and 1 more

Abstract read
In one paragraph

Article in Journal of nanobiotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

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

  1. Pooled it
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  9. Clinical features ofFrontiers in cellular and infection microbiology · 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

11 authors.

Xinghong Luo *Department of Endodontics, Stomatological Hospital, School of Stomatology, Southern Medical University, No. 366 Jiangnan Avenue South, Guangzhou, 510280, Guangdong, China.
Yanzhen Wang *Stomatological Hospital, School of Stomatology, Southern Medical University, No. 366 Jiangnan Avenue South, Guangzhou, 510280, Guangdong, China.
Tingting Ning *Department of Endodontics, Stomatological Hospital, School of Stomatology, Southern Medical University, No. 366 Jiangnan Avenue South, Guangzhou, 510280, Guangdong, China.
Qian LeiDepartment of Endodontics, Stomatological Hospital, School of Stomatology, Southern Medical University, No. 366 Jiangnan Avenue South, Guangzhou, 510280, Guangdong, China.
Hao CuiStomatological Hospital, School of Stomatology, Southern Medical University, No. 366 Jiangnan Avenue South, Guangzhou, 510280, Guangdong, China.
Xianghui ZouStomatological Hospital, School of Stomatology, Southern Medical University, No. 366 Jiangnan Avenue South, Guangzhou, 510280, Guangdong, China.
Yan ChenDepartment of Pediatric Dentistry, Stomatological Hospital, School of Stomatology, Southern Medical University, No 366 Jiangnan Avenue South, Guangzhou, 510280, Guangdong, China.
Shuoling ChenStomatological Hospital, School of Stomatology, Southern Medical University, No. 366 Jiangnan Avenue South, Guangzhou, 510280, Guangdong, China.
Xinyao ZhangStomatological Hospital, School of Stomatology, Southern Medical University, No. 366 Jiangnan Avenue South, Guangzhou, 510280, Guangdong, China.
Shenglong TanDepartment of Endodontics, Stomatological Hospital, School of Stomatology, Southern Medical University, No. 366 Jiangnan Avenue South, Guangzhou, 510280, Guangdong, China.
Dandan MaDepartment of Endodontics, Stomatological Hospital, School of Stomatology, Southern Medical University, No. 366 Jiangnan Avenue South, Guangzhou, 510280, Guangdong, China. mdd@smu.edu.cn.

Funding

Guangzhou Municipal Basic and Applied Basic Research Project Funding by Science and Technology Projects in Guangzhou 2024A04J6614National Natural Science Foundation of China 82470963Scientific research. Science research cultivation program of stomatological hospital, Southern medical university PY2023027
6 · The paper itself

Abstract

backgroundAlthough increasing evidence confirms that oral microbiota imbalance is a critical factor inhibiting bone regeneration, the specific mechanisms have remained unexplored. This study aims to use periodontitis as a model of oral microbiota imbalance to investigate the specific mechanisms that inhibit bone regeneration in extraction sockets.

methodsCone Beam Computed Tomography (CBCT) data of extraction sockets were collected from patients with and without periodontitis to confirm the influence of the periodontitis microenvironment on bone regeneration in extraction sockets. Furthermore, GW4869-pretreated Porphyromonas gingivalis (Pg) and normal Pg were used to build a periodontitis model, and then the bone regeneration in extraction sockets under these conditions was detected by H&E staining, Masson's staining and micro-CT analysis. In vitro, the effect of Pg-derived OMVs on osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) was examined. RNA sequencing, FerroOrange, malondialdehyde assay, transmission electron microscopy, qRT‒PCR, and western blotting analysis were performed.

resultsCBCT analysis showed that periodontitis significantly inhibited new bone formation in the extraction sockets in patients. Micro-CT and Histological analysis revealed that inhibiting OMVs released from Pg alleviated the inhibition of bone regeneration in extraction sockets under Pg imbalance. Moreover, Pg-derived OMVs treatment deteriorated bone regeneration in extraction sockets. In vitro, results showed that Pg-derived OMVs inhibited osteogenic differentiation of BMSCs. Furthermore, the results indicated a significant upregulation of ferroptosis in OMVs-treated BMSCs. Notably, targeting ferroptosis promoted osteogenic differentiation of BMSCs and bone regeneration in extraction sockets, as compared with the OMVs-treated group. Mechanistic studies have shown that Pg-derived OMVs promoted BMSCs ferroptosis via the Hippo- Yes-associated protein (YAP) pathway.

conclusionThis study shows that a Pg microbiota imbalance inhibits bone regeneration by secreting OMVs from Pg to induce ferroptosis in BMSCs. Mechanically, we illustrated that OMVs induce ferroptosis through the Hippo-YAP pathway. These findings might provide a new insight and potential therapeutic target to promote bone regeneration under oral microbiota imbalance.

Indexed as

Bone RegenerationFerroptosisPorphyromonas gingivalisAnimalsCell DifferentiationFemaleHippo Signaling PathwayHumansMaleMesenchymal Stem CellsMiddle AgedOsteogenesisPeriodontitisSignal TransductionYAP-Signaling ProteinsYAP-Signaling ProteinsBMSCsBone regenerationFerroptosisOMVsOral microbiota imbalance

Identifiers

PMID40382634
PMCPMC12084903

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.