Evidence map›Paper›PMID 40874052›Full record

ArticleFrontiers in cellular and infection microbiology2025

Gingipains disrupt bone homeostasis via dual regulation of osteogenesis and osteoclastogenesis through exosomal miR-146a-5p/TRAF6 signaling.

Jiachen Dong, Yue Liao, Mengjun Sun, Huiwen Chen, Kecong Zhou, Huanyu Zhang, Wei Zhou, Zhongchen Song

Abstract read
In one paragraph

Article in Frontiers in cellular and infection microbiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
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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

8 authors.

Jiachen Dong *Department of Periodontology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yue Liao *Department of Periodontology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Mengjun SunDepartment of Periodontology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Huiwen ChenDepartment of Periodontology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Kecong ZhouDepartment of Periodontology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Huanyu ZhangDepartment of Periodontology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Wei ZhouDepartment of Periodontology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Zhongchen SongDepartment of Periodontology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Gingipains are virulence factors released by Methods: Clinical samples of gingival crevicular fluid, subgingival plaque, and gingival tissues were collected from 15 patients with stage III-IV periodontitis and 15 healthy controls. The effects of gingipains on bone marrow mesenchymal stem cells (BMSCs) and RAW264.7 macrophages were assessed using cell proliferation assays, qPCR, western blot, microarray analysis, and dual-luciferase reporter assays. A rat periodontitis model was used to validate the findings Results: Periodontitis patients exhibited elevated levels of lysine- and arginine-specific gingipains, C5a, and RANKL (p < 0.05). Gingipains inhibited BMSCs proliferation and osteogenic differentiation in a dose-dependent manner while promoting osteoclastogenesis in RAW264.7 macrophages through BMSCs-derived exosomes. Gingipains reduced the levels of miR-146a-5p in exosomes, which enhanced osteoclast differentiation through the miR-146a-5p/TRAF6 signaling pathway. Animal models confirmed that gingipains aggravated alveolar bone loss, which was mitigated by miR-146a-5p overexpression. Conclusion: Gingipains disrupt bone metabolism by inhibiting BMSCs osteogenesis and promoting osteoclastogenesis through communication via exosomes. Targeting miR-146a-5p offers a potential therapeutic approach to counter gingipain-induced periodontal destruction.

Indexed as

Bone and BonesExosomesGingipain Cysteine EndopeptidasesMicroRNAsOsteogenesisTNF Receptor-Associated Factor 6AnimalsCell DifferentiationCell ProliferationDisease Models, AnimalFemaleHomeostasisHumansIntracellular Signaling Peptides and ProteinsMacrophagesMaleGingipain Cysteine EndopeptidasesIntracellular Signaling Peptides and ProteinsMicroRNAsMIRN146 microRNA, humanRANK LigandTifab protein, humanTNF Receptor-Associated Factor 6gingipainsKgpMiR-146a-5posteoclastic differentiationRGPTRAF6

Identifiers

PMID40874052
PMCPMC12378552

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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.