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Background <p>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.</p> Methods and results <p>MTA specimens were allowed to set for 4, 6, 8, and 24&#xa0;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&#xa0;h and 6&#xa0;h and between 4&#xa0;h and 8&#xa0;h (<i>p</i> &lt; 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 (<i>p</i> &gt; 0.05).</p> Conclusion <p>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.</p>

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MTA does not induce oxidative stress and apoptotic response, or calcium-related cellular stress and preserves extracellular matrix homeostasis

  • 期刊论文

  • 发表日期：

    2026年7月24日

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  • Okan Sancer,
  • Deniz Yanık Nalbantoğlu,
  • Ahmet Mert Nalbantoğlu

摘要

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.