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Fluoride can harm various tissues depending on its concentration and exposure duration. While its effects on mineralized tissues like bones and teeth are known, few studies have explored its impact on preosteoblastic cells. This study examined the effects of fluoride on differentiating osteoblastic cells. M3CT3-E1 preosteoblastic cells were cultured for 24 h or 3, 5, or 7 days with fluoride concentrations of 1, 10, or 100 μg/mL. Cell viability, oxidative stress biomarkers, mitochondrial membrane potential, cell cycle distribution, apoptosis, and morphology were assessed. After statistical analysis, At 100 μg/mL, fluoride modulated cell viability in a dose- and time-dependent manner, increasing reactive oxygen species levels and lipid peroxidation (1.382 ± 0.163 vs. 0.826 ± 0.081; p = 0.0125). Oxidative stress markers such as superoxide dismutase (SOD) (4.008 ± 0.425 vs. 0.724 ± 0.474; p = 0.0025) and glutathione (GSH) (78.38 ± 4.506 vs. 45.65 ± 2.900; p = 0.0003) were also elevated. High fluoride concentrations impaired mitochondrial activity and disrupted the cell cycle, affecting the G0/G1, S, and G2/M phases. These changes caused irreversible damage, including apoptosis and alterations in cell morphology. High fluoride concentrations can significantly damage preosteoblastic cells, reducing viability, altering redox status, impairing mitochondrial function, and disrupting the cell cycle, leading to cell death. These findings underscore that fluoride toxicity is concentration-dependent and reinforce the safety of exposure to doses of fluoride such as those found in the optimally fluoridated water.
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http://dx.doi.org/10.1016/j.tice.2025.103000 | DOI Listing |
FASEB Bioadv
August 2025
Laboratory of Molecular Signaling and Stem Cells Therapy, Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction Beijing Stomatological Hospital, School of Stomatology, Capital Medical University Beijing China.
Previous studies reported the pro-osteogenic ability of L-Tryptophan (L-Trp) and Calcium-Sensing RCeceptor (CaSR) respectively. Recent researchers found L-Trp could activate CaSR. Therefore, this study investigated the osteogenic mechanisms of L-Trp through CaSR activation.
View Article and Find Full Text PDFTissue Cell
August 2025
State Key Laboratory of Oral Diseases & National Center for Stomatology & National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China; Department of Oral Implantology, West China Hospital of Stomatology, Sichuan University, Chengdu, Chi
Lysophosphatidic acid (LPA) is a small bioactive lysophospholipid that elicits diverse biological activities in bone homeostasis and diseases. However, the specific functions of LPA and intrinsic mechanism underlying these processes is not well understood. In this study, we identified that LPA regulated cell proliferation, migration, and osteogenic differentiation primarily via LPA in MC3T3-E1 pre-osteoblastic cells.
View Article and Find Full Text PDFInt Dent J
September 2025
Discipline of Endodontology, Division of Restorative Dental Sciences, Faculty of Dentistry, The University of Hong Kong, Hong Kong SAR, China. Electronic address:
Objectives: This study aimed to evaluate the cytotoxicity and osteogenic potential of three sealers, including a strontium silicate-based sealer, C-Root SP (C-R), and two calcium silicate-based sealers, iRoot SP (i-R) and AH Plus Bioceramic Sealer (AHPbcs), compared with AH Plus (AHP) on MC3T3-E1 pre-osteoblasts.
Materials And Methods: Standardized sealer discs were eluted in a culture medium to assess cytotoxicity using the CCK-8 assay at various dilutions (1:1, 1:2, 1:5, and 1:10). Osteogenic differentiation was evaluated by culturing cells in osteogenic medium supplemented with 1:5 diluted sealer extract.
Adv Healthc Mater
September 2025
Department of Chemical and Biochemical Engineering, School of Biomedical Engineering, Department of Chemistry, The Centre for Advanced Materials and Biomaterials Research, The University of Western Ontario, London, ON, N6A 5B9, Canada.
Severe bone defects resulting from traumatic injuries or infections are severe skeletal deficiencies that are unable to regenerate on their own. Despite their effectiveness, current treatments including allografts and artificial bone substitutes, have several drawbacks. This includes poor osseointegration, low biocompatibility and biodegradability, limited cell infiltration, and adverse side effects arising from drug-loaded substitutes.
View Article and Find Full Text PDFCells
August 2025
School of Stomatology, Xuzhou Medical University, Xuzhou 221004, China.
Healing large bone defects remains challenging. Gelatin scaffolds are biocompatible and biodegradable, but lack osteoinductive activity. Plant-derived exosomes carry miRNAs, growth factors, and proteins that modulate osteogenesis, but free exosomes suffer from poor stability, limited targeting, and low bioavailability in vivo.
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