ArticleBMC oral health2018
Oral lichen-planus-associated fibroblasts acquire myofibroblast characteristics and secrete pro-inflammatory cytokines in response to Porphyromonas gingivalis lipopolysaccharide stimulation.
Article in BMC oral health, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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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.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- DnaK of Parvimonas micra extracellular vesicles interacts with the host fibroblasts BAG3-IKK-γ axis to accelerate TNF-α secretion in oral lichen planus.Microbiome · 2025Article
- Complexities ofDentistry journal · 2025Review
- Exploring the oral bacteria-oral lichen planus connection: mechanisms, clinical implications and future directions.Archives of microbiology · 2025Review
- Roles of intralesional bacteria in the initiation and progression of oral squamous cell carcinoma.Cancer medicine · 2024Review
- Probiotics as Potential Biological Immunomodulators in the Management of Oral Lichen Planus: What's New?International journal of molecular sciences · 2022Review
- Microbiome landscape of lesions and adjacent normal mucosal areas in oral lichen planus patient.Frontiers in microbiology · 2022Article
- Oral lichen planus: a microbiologist point of view.International microbiology : the official journal of the Spanish Society for Microbiology · 2021Review
- Pathological and Therapeutic Approach to Endotoxin-Secreting Bacteria Involved in Periodontal Disease.Toxins · 2021Review
- Interleukin-6 released by oral lichen planus myofibroblasts promotes angiogenesis.Experimental and therapeutic medicine · 2021Article
- N‑acetyl cysteine inhibits the lipopolysaccharide‑induced inflammatory response in bone marrow mesenchymal stem cells by suppressing the TXNIP/NLRP3/IL‑1β signaling pathway.Molecular medicine reports · 2020Article
- Study on the Role of Salivary Flora and NF-κB Inflammatory Signal Pathway in Oral Lichen Planus.Inflammation · 2020Article
- Pain-Related PANoptosis Gene Signature Predicts Prognosis and Guides Therapy in Oral Squamous Cell Carcinoma.Technology in cancer research & treatmentArticle
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundOral lichen planus (OLP) is a chronic inflammatory oral mucosal disease in which comprehensive inflammation-related cytokines are involved. These cytokines are commonly produced by immune cells and specific nonimmune cells including keratinocytes, endothelial cells and fibroblasts. This raises the question of whether fibroblasts in OLP lesions contribute to the inflammatory process upon inflammatory simulation.
methodsPrimary cultured Oral lichen-planus-associated fibroblasts (OLP AFs, n = 5) and normal buccal mucosal fibroblasts (NFs, n = 5) were examined by immunohistochemistry, Western blotting and reverse transcription-polymerase chain reactions (RT-PCR). Various inflammatory mediators were evaluated with a multiplex assay. Differences among groups were assessed using a Student's test or repeated measures one-way ANOVA, as appropriate.
resultsOLP AFs express significantly higher levels of α-smooth muscle actin (α-SMA) than NFs, indicating the presence of myofibroblasts. Myofibroblasts secrete Interleukin (IL)-6, IL-8, and tumor necrosis factor-α (TNF-α) in response to Porphyromonas gingivalis lipopolysaccharide (pg. LPS).
conclusionOLP AFs demonstrated α-SMA expression and secreted pro-inflammatory cytokines in response to pg. LPS stimulation.
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Registered trials
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