ArticleJournal of oral biology and craniofacial research
Dental pulp stem cells as a novel antifibrotic therapy for oral submucous fibrosis: An in vitro study.
Article in Journal of oral biology and craniofacial research. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Role of Stem Cells and Stem Cell Markers in Oral Potentially Malignant Disorders and Malignant Transformation: A Systematic Review.Stem cells international · 2026Review
- Biomaterial-based therapeutic strategies for oral submucous fibrosis.Frontiers in cell and developmental biology · 2026Review
- Swertia purpurascens Wall: Evaluation of its antifibrotic activity in anJournal of oral and maxillofacial pathology : JOMFPArticle
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Oral submucous fibrosis (OSMF) is a chronic, potentially malignant disorder associated with areca nut consumption. It is characterized by progressive fibrosis, trismus, and a significant risk of malignancy, with limited treatment options primarily offering symptomatic relief. Dental pulp stem cells (DPSCs), a type of mesenchymal stem cells (MSCs), have shown potential for modulating fibrotic conditions through their immunomodulatory and regenerative properties. This study evaluates the antifibrotic potential of DPSCs on OSMF fibroblasts in an in vitro model. Methods: DPSCs were isolated from healthy permanent teeth and characterized using flow cytometry for MSC markers (CD73, CD90, CD44, CD105). Fibroblasts were cultured from OSMF biopsy samples and validated through magnetic sorting and morphological analysis. The antifibrotic effects of DPSCs on fibroblasts were evaluated using assays for collagen gel contraction, proliferation, TGF-β1 secretion, and morphological changes. Data were analyzed for statistical significance using appropriate tests. Results: The mean collagen gel size decreased from 3.235 mm (95 % CI: 1.65-4.82 mm) in the control group to 1.00 mm (95 % CI: -0.27 - 2.27 mm) in the DPSC-treated group. Fibroblast viability declined significantly over 72 h (p < 0.05). TGF-β1 secretion was markedly lower in DPSC-treated fibroblasts (339.38 pg/mL vs 637.61 pg/mL, p = 0.000393, Cohen's d = 19.15). Conclusion: DPSCs exhibit strong antifibrotic properties by inhibiting collagen contraction, suppressing fibroblast proliferation, and reducing TGF-β1 secretion. These findings suggest DPSCs as a promising cell-based therapy for OSMF. Further in vivo studies are warranted for clinical translation. Trial registration number: Not applicable.
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