Journal of oral biology and craniofacial research · 2025
Dental pulp stem cells as a novel antifibrotic therapy for oral submucous fibrosis: An in vitro study.
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Narvekar Snehalata, Baliga Shridhar D, Angadi Punnya V
Аннотация
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.
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.