MTA does not induce oxidative stress and apoptotic response, or calcium-related cellular stress and preserves
Okan Sancer1, Deniz Yanık Nalbantoğlu2, Ahmet Mert Nalbantoğlu3
1Genetic Research Unit, Innovative Technologies Application and Research Center, Süleyman Demirel University, Isparta, Turkey.
Background:
This study aimed to investigate the time-dependent biological effects of mineral trioxide aggregate (MTA) on cellular viability and the gene expressions associated with oxidative stress response (Nrf2), apoptosis-related signaling (p53), calcium homeostasis (CALB1), and extracellular matrix regulation (FN) in L-929 fibroblasts.
Methods And Results:
MTA specimens were allowed to set for 4, 6, 8, and 24 h. Eluates were obtained according to ISO-10993-12 guidelines and applied to cells. Cell viability was assessed by MTT assay. Relative mRNA expressions of Nrf2, p53, CALB1, and FN were analyzed by real-time PCR. One-way ANOVA and post-hoc Tukey's were used. Higher cell viability than the positive control was obtained. Viability remained above the 70% biocompatibility threshold in all time periods. A time-dependent fluctuation in viability was observed, with differences between 4 h and 6 h and between 4 h and 8 h (p < 0.05). No significant differences were detected in Nrf2, p53, CALB1, or FN expression levels between the negative control and MTA-treated groups at any time point (p > 0.05).
Conclusion:
MTA preserved cellular viability and molecular homeostasis without inducing oxidative, apoptotic, or calcium-related imbalance. The inclusion of Nrf2 and CALB1 as previously unexplored parameters provides additional mechanistic insight into the biocompatibility profile of MTA. MTA maintained cellular homeostasis throughout its critical setting phase without activating oxidative stress, apoptosis-related signaling, or calcium imbalance pathways. The stable expression of Nrf2, p53, and CALB1 suggests that the favorable clinical performance may depend not only on biocompatibility but also on its ability to preserve intracellular equilibrium during early tissue contact.
Insights
Mineral Trioxide Aggregate (MTA) maintained cell viability and molecular balance in fibroblasts over time. MTA did not trigger oxidative stress, apoptosis, or calcium imbalance, indicating good biocompatibility.
Area of Science:
- Biomaterials Science
- Cell Biology
- Molecular Biology
Background:
- Mineral Trioxide Aggregate (MTA) is widely used in dentistry.
- Understanding its early biological effects is crucial for clinical application.
- Investigating time-dependent cellular responses to MTA is essential.
Purpose of the Study:
- To evaluate the time-dependent biological effects of MTA on L-929 fibroblasts.
- To assess MTA's impact on cellular viability and gene expression.
- To analyze gene expression related to oxidative stress, apoptosis, calcium homeostasis, and extracellular matrix.
Main Methods:
- L-929 fibroblasts were exposed to MTA eluates at different time points (4, 6, 8, 24 hours).
- Cell viability was measured using the MTT assay.
- Gene expression levels of Nrf2, p53, CALB1, and FN were analyzed via real-time PCR.
Main Results:
- Cell viability remained above the 70% biocompatibility threshold across all tested time points.
- A statistically significant fluctuation in cell viability was observed between 4h and 6h, and 4h and 8h.
- No significant differences in Nrf2, p53, CALB1, or FN gene expression were found between MTA-treated and control groups.
Conclusions:
- MTA demonstrates biocompatibility by preserving cellular viability and molecular homeostasis.
- MTA does not induce oxidative stress, apoptosis, or calcium imbalance during its setting phase.
- Stable gene expression suggests MTA's ability to maintain intracellular equilibrium contributes to its favorable clinical performance.
Related Concept Videos
Cellular Injury V: Apoptosis and Autophagy
Cellular Injury I: Introduction
Regulation of the Unfolded Protein Response
Cellular Injury IV: Necrosis
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
The Intrinsic Apoptotic Pathway
