ArticleInflammation2025
Bacterial Extracellular Vesicles as Potential Promoting Factors for Oral Lichen Planus Pathogenesis.
Article in Inflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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.
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.
Who cites it
4 citing papers in PubMed.
- Biological properties and potential pathogenic mechanisms of oral bacterial-derived extracellular vesicles in oral and systemic diseases.Extracellular vesicles and circulating nucleic acids · 2026Review
- Heterogeneous mechanisms, risk stratification, and translational advances in the malignant transformation of oral potentially malignant disorders to oral squamous cell carcinoma.Frontiers in molecular biosciences · 2026Review
- Characteristics of salivary IgA responses to oral microbiota in patients with oral lichen planus.Scientific reports · 2025Article
- Epinephrine as a potential driver of oral lichen planus pathogenesis.Animal cells and systems · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
Abstract
Oral lichen planus (OLP) is a chronic inflammatory disease characterized by an intensive infiltration of cytotoxic T cells, which causes keratinocyte death. Abnormal changes within keratinocytes might be critical for OLP onset and progression, but the pathogenic mechanism of OLP is still uncertain. The human oral microbiota, consisting of approximately 50-100 billion bacterial entities, encompasses around 200 dominant bacterial species. These bacteria continuously produce and release extracellular vesicles (EVs), which play a significant role in host-microbe interactions. However, the impact of these bacterial EVs on the progression of OLP has not been fully elucidated. In this study, through comprehensive database analysis and experimental validation, we observed that OLP lesions exhibit elevated inflammatory signatures and significantly increased phosphorylation of STAT3 compared to non-OLP tissues. Notably, EVs derived from key periodontal pathogens, Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans, were shown to induce an inflammatory response and activate STAT3 signaling pathways, closely mirroring the pathophysiological features observed in OLP. These results underscore the potential role of bacterial EVs in the pathogenesis of OLP and highlight STAT3 as a critical mediator in this process.
Indexed as
Identifiers
39305391What OpenQuestion holds
Registered trials
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.