Next Article in Journal
Mechanical Testing of 3D-Printed Pediatric Trachea-Shaped Specimens: A Suitability Study
Previous Article in Journal
Open-Vocabulary Crack Object Detection Through Attribute-Guided Similarity Probing
 
 
Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
Journals
Applied Sciences
Volume 15
Issue 19
10.3390/app151910351
applsci-logo
Submit to this Journal Review for this Journal Propose a Special Issue
► Article Menu

Article Menu

share Share announcement Help format_quote Cite question_answer Discuss in SciProfiles
first_page
settings
Order Article Reprints
Font Type:
Arial Georgia Verdana
Font Size:
Aa Aa Aa
Line Spacing:
Column Width:
Background:
Article

Mutagenicity Evaluation of Orthodontic Resins Using the Ames Test

by
Roberto Biagi
1,2,
Gianna Dipalma
3,
Federica Macrì
1,2,*,
Niccolò Cenzato
1,2,*,
Cinzia Maspero
1,2 and
Lucia Giannini
1,2
1
Dipartimento di Scienze Biomediche, Chirurgiche e Odontoiatriche, Università degli Studi di Milano, 20122 Milan, Italy
2
Fondazione IRCCS Cà Granda Ospedale Maggiore Policlinico, 20122 Milan, Italy
3
Department of Interdisciplinary Medicine, University of Bari “Aldo Moro”, 70124 Bari, Italy
*
Authors to whom correspondence should be addressed.
Appl. Sci. 2025, 15(19), 10351; https://doi.org/10.3390/app151910351
Submission received: 17 June 2025 / Revised: 6 September 2025 / Accepted: 22 September 2025 / Published: 24 September 2025
(This article belongs to the Special Issue Advanced Biotechnologies and Clinical Developments in Dentistry and Oral and Maxillofacial Surgery: 2nd Edition)
Browse Figure
Versions Notes

Abstract

The biocompatibility of orthodontic materials is crucial for patient safety, especially concerning their possible mutagenic effects. This study aimed to assess the mutagenic potential of three commercially available orthodontic resins using the Ames test. We tested Resin A, Resin B, and Resin C, which consist of a base and an accelerator component. We used Salmonella typhimurium strains TA98, TA100, TA1535, and TA1537, along with TA1538, both with and without metabolic activation (S9 mix), following standardized protocols. After 48 h, we counted the number of revertant colonies and analyzed the data using two-way ANOVA. The Ames test revealed that Resins A and B induced significant mutagenic activity in strains TA100 and TA1535, with increases in revertant colonies up to about +145% compared with controls, while no effects were observed in TA98, TA1537, or TA1538. Resin C (both the complete mix and the base component) also showed mutagenicity in TA100 and TA1535, whereas the accelerator alone was consistently non-mutagenic. Positive controls confirmed the test system’s sensitivity. In conclusion, some orthodontic resins and their components showed mutagenic activity under the tested conditions. This highlights the need for mutagenicity testing as part of the biological safety assessment of dental materials.

1. Introduction

Orthodontic resins are integral to daily clinical orthodontic practice. Resins, including acrylic and composite materials, are used in the baseplates of removable appliances, retainers, adhesives for brackets and bands, and aligners. These methacrylate—based materials stay in the oral cavity long—term, exposed to saliva, temperature changes, and mechanical forces. As a result of this prolonged and multifaceted exposure, these resins interact with both hard and soft oral tissues, making it essential to thoroughly assess their biocompatibility. Such evaluations must consider not only acute cytotoxicity but also potential long-term effects, such as genotoxicity, that could arise over extended periods of use.
The clinical relevance of orthodontic resins is well established in the field of orthodontics, where their adhesive properties, ease of application, and compatibility with a variety of dental substrates have made them the standard choice for bracket and band bonding [1,2]. These resins offer significant advantages in terms of their ability to bond effectively to enamel and other dental surfaces, and their relative ease of handling has contributed to their widespread adoption. However, as the use of orthodontic materials has become more widespread, growing concerns about the biological safety of dental materials have surfaced. Increasing scrutiny is now placed on the substances released by these materials during both polymerization and degradation, which may inadvertently enter the oral environment and interact with surrounding tissues.
Particularly concerning are resins containing BIS-GMA (bisphenol A-glycidyl methacrylate), a monomer commonly used in orthodontic adhesive formulations. BIS-GMA and its derivatives may release unreacted monomers or degradation by-products that can interact with cells in the oral cavity. These substances may disrupt normal cellular processes, potentially causing oxidative stress, alterations in the cell cycle, and, in some cases, even mutagenic effects. One such compound, glycidyl methacrylate (GMA), a derivative of BIS-GMA, has been shown to be particularly concerning, as it has been linked to the formation of DNA adducts and mutagenic events in bacterial models [3]. This raises concerns about the potential long-term biological consequences of orthodontic resins that continuously release these compounds during their time in the mouth.
Furthermore, the oral mucosa’s permeability to monomeric compounds released from resins highlights a possible route for systemic exposure, which could extend the risk beyond localized oral tissues and warrants comprehensive toxicological evaluation [4].
In line with these concerns, a study by Macedon et al. (2021) [5] highlighted the formation of γH2AX foci, a marker of DNA double-strand breaks, in cultured cells exposed to orthodontic adhesives containing co-initiators such as diphenyliodonium hexafluorophosphate. This observation suggests that even low-level exposure to these adhesives may provoke significant genotoxic responses [5]. Moreover, Won et al. [6] (2015) further emphasized the risk of metal ions, released from orthodontic devices, contributing to both cytotoxic and genotoxic stress, adding another layer of complexity to the safety assessment of orthodontic resins.
Recent research has also demonstrated that the cumulative effect of multiple monomers, co-initiators, and metal ions may act synergistically, amplifying cellular stress responses and DNA damage in oral tissues. This multifactorial toxicity model challenges traditional single-compound assessments and calls for integrated approaches to safety evaluation [7].
A more recent study by Mikulewicz et al. [8] (2024) has reinforced this concern, demonstrating that different orthodontic archwires release varying levels of metal ions, including nickel and chromium, which are known to elicit inflammatory and genotoxic responses [8].
Furthermore, oxidative stress appears to be a critical mechanism in the genotoxicity associated with orthodontic treatment. A 2023 study reported by Zhang et al. demonstrated increased levels of reactive oxygen species (ROS) and DNA damage in oral epithelial cells collected from patients undergoing fixed orthodontic treatment after six months, indicating that prolonged exposure to orthodontic appliances can provoke systemic cellular responses [9].
Concerns regarding the overall biocompatibility of dental materials also extend beyond mutagenicity. Previous studies have emphasized the importance of monitoring potential systemic effects associated with long-term exposure to resin-based compounds [10]. However, the present work specifically focuses on the mutagenic potential of orthodontic resins.
International standards, including those set by the International Organization for Standardization (ISO) and the American Dental Association (ADA), require rigorous cytotoxicity and genotoxicity testing for dental materials prior to market release. These guidelines are intended to ensure that only safe materials are used in clinical practice. However, there is a growing body of research indicating that even materials that comply with these standards may still induce adverse biological responses in vitro [11].
Innovative testing methods such as 3D tissue models and co-culture systems have been proposed to better mimic the oral environment and provide more predictive data on material biocompatibility, yet these have not been widely adopted in regulatory frameworks [12].
Additionally, a review of the literature reveals a significant gap in the available data regarding the direct comparative evaluation of the mutagenic potential of different orthodontic resins available on the market. While some studies have investigated the mechanical adhesion properties or overall cytotoxicity of these materials, there is a lack of focused research specifically addressing their mutagenic potential across different resin formulations [13].
In this context, the Ames test provides a well-established and widely recognized method for assessing the mutagenic potential of chemical substances. This assay uses specific strains of Salmonella enterica serovar Typhimurium that revert to histidine prototrophy when exposed to mutagenic agents, either with or without metabolic activation. By using these bacterial strains, the Ames test can detect mutations induced by chemical substances, providing valuable insight into their genotoxic potential.
The use of metabolic activation systems in the Ames test simulates in vivo biotransformation processes, thus allowing for the identification of promutagens that require metabolic conversion to exert their genotoxic effects [14].
The aim of the present study was to evaluate the mutagenic potential of three commercially available orthodontic resins, designated as Resins A, B, and C, using the Ames test. Additionally, Resin C, which is a two-component system, was tested separately as both base resin and accelerator to assess whether different components of the resin might contribute differently to mutagenicity. The primary goal of this study was to investigate whether there are significant differences in mutagenic activity between these widely used orthodontic resins and to provide further insight into the biological risks associated with their clinical use in orthodontics.
In parallel, recent studies have focused on improving the biological profile of orthodontic resins through novel material design. For instance, Sycińska-Dziarnowska et al. (2024) [15] conducted a systematic review with a meta-analysis evaluating the efficacy of bonding systems enhanced with silver nanoparticles (AgNPs). These enhanced resins demonstrated superior antimicrobial properties while maintaining appropriate adhesive strength, suggesting that such modifications may reduce biofilm formation and potentially mitigate genotoxic effects caused by microbial metabolism or material degradation [15].
Complementing this, Wang et al. (2023) [16] reviewed recent advances in antibacterial coatings for orthodontic appliances. Their findings revealed that bioinspired surface treatments and the incorporation of metal nanoparticles can decrease bacterial colonization and reduce inflammation and cytotoxic responses, which may lead to the development of safer and more biocompatible orthodontic materials [16].
Moreover, the integration of nano-scale delivery systems within resin matrices presents a promising avenue to simultaneously achieve controlled release of therapeutic agents and maintain mechanical performance, thereby improving patient outcomes and material safety [17].
These insights are further reinforced by Karandish et al. (2025) [18], who investigated the aging of orthodontic bands in acidic versus neutral pH environments and their resulting cytotoxicity and genotoxicity profiles. Their results showed a significant increase in DNA damage, particularly in acidic conditions, underlining the role of intraoral pH and the environmental stability of orthodontic materials in determining their biological behavior [18].
Collectively, these findings highlight the urgency of refining existing materials or developing new resin formulations with lower toxicological risk profiles, emphasizing the relevance and timeliness of the current investigation.
In conclusion, the combination of advanced material science, comprehensive biological testing, and clinical vigilance will be essential to ensure the safe use of orthodontic resins and to minimize their potential health risks [19]. The aim of the present study was to assess the mutagenic potential of three commercially available orthodontic resins (Resin A, B, and C) using the Ames test. Resin C, which is composed of a base and an accelerator, was also tested separately to verify its individual mutagenic activities. This study aims to provide a head-to-head comparison between these resins in order to cover the lack of articles in the literature about their potential genotoxic effects.

2. Materials and Methods

This study was approved by the Ethics Committee of IRCCS “Giovanni Paolo Il” Istituto Oncologico “Gabriella Serio” of the 17/12/2024 Prot. 1979/CEL—Study L-PRF.
The Ames test was performed following the standard protocol summarized in Figure 1, utilizing five histidine-auxotrophic Salmonella typhimurium strains (Ta 98, Ta 100, Ta 1535, Ta 1537, and Ta 1538) in both the presence and absence of hepatic microsomes. Chemical compounds that induced a mutation frequency increase of two to three times higher than the negative controls, specifically accelerator A at concentrations of 7, 70, and 700 µg/plate, were identified as mutagenic.
The other test compounds were applied at concentrations of 10, 100, and 1000 µg/plate. The highest concentrations used for the resin mixtures or individual components allowed for a cell survival rate of 70%. For the other resins, the concentration represents the maximum soluble concentrations achieved.
Two separate experiments were conducted for each dose, at different time points, with six plates per condition, both with and without metabolic activation.
The ability of the bacterial cells to form colonies in the absence of sufficient histidine is indicative of mutagenic potential [5,6].
Three commercially available resins were evaluated, designated as Resins A, B, and C. Resin C consists of two components, a base resin (R) and an accelerator (A), which are mixed prior to use. In contrast, the other resins consist of a single component. For Resin C, the base resin and accelerator mixture, the base resin alone, and the accelerator alone were all considered separately.
Prior to conducting the mutagenicity experiments, the cytotoxicity of the different products was assessed by incubating the strains on agar plates. All test substances were dissolved in a 4% benzyl alcohol solution.
Product A was tested both as a mixture at doses of 17, 170, and 1700 µg/plate (equivalent to the resin + accelerator doses of 10 + 7, 100 + 70, and 1000 + 700 µg/plate, respectively), and as individual components at doses of 10, 100, and 1000 µg/plate for the base resin (R) and 7, 70, and 700 µg/plate for the accelerator (A). The data were analyzed using two-way ANOVA, considering dose and metabolic activation as factors. When statistically significant main effects or interactions were detected, post hoc comparisons were performed using Tukey’s Honest Significant Difference (HSD) test, with a significance threshold of p < 0.05.
This approach ensured that observed differences were not due to random variation. Importantly, the consistency of results across independent replicates and experimental repeats reinforces the reproducibility of our findings. The statistical outcomes are summarized in Table 1, Table 2 and Table 3, which highlight the strains and conditions in which statistically significant increases in revertant colonies were observed.

Statistical Analysis

The data were analyzed using two-way analysis of variance (ANOVA) to assess the effects of dose and metabolic activation on the mutation frequency.
The factors considered were:
  • Factor 1: Dose (10 µg, 100 µg, 1000 µg per plate)
  • Factor 2: Metabolic activation (presence vs. absence of hepatic microsomes)
When significant main effects or interactions between the factors were detected, post-hoc comparisons were performed using Tukey’s Honest Significant Difference (HSD) test. A p-value of less than 0.05 was considered statistically significant; more specifically, the p-value was <0.05 for TA100 (100 µg/plate) and TA1535, with a value of <0.001 for TA100 (1000 µg/plate).
Table 1. Ames Test Results for Resins A and B.
Table 1. Ames Test Results for Resins A and B.
StrainDose (µg/Plate)Resin A (−S9)Resin A (+S9)Resin B (−S9)Resin B (+S9)
TA9810n.s.n.s.n.s.n.s.
TA98100n.s.n.s.n.s.n.s.
TA981000n.s.n.s.n.s.n.s.
TA10010n.s.n.s.n.s.n.s.
TA100100↑↑↑↑
TA1001000↑↑↑↑↑↑↑↑
TA1535100
1000		↑↑↑↑
TA153710/100/1000n.s.n.s.n.s.n.s.
TA153810/100/1000n.s.n.s.n.s.n.s.
Legend: n.s. = not significant; ↑ = increase in revertant colonies; ↑↑ = significant increase in revertants.
Table 2. Ames Test Results for Resin C (Base + Accelerator Mix).
Table 2. Ames Test Results for Resin C (Base + Accelerator Mix).
StrainDose (µg/Plate)Mix (−S9)Mix (+S9)
TA98100 + 70n.s.n.s.
TA981000 + 700n.s.n.s.
TA100100 + 70↑n.s.
TA1001000 + 700↑↑↑
TA1535100 + 70↑↑
TA15351000 + 700↑↑n.s.
TA153710 + 7, 100 + 70, 1000 + 700n.s.n.s.
TA153810 + 7, 100 + 70, 1000 + 700n.s.n.s.
Legend: n.s. = not significant; ↑ = increase in revertant colonies; ↑↑ = significant increase in revertants.
Table 3. Ames Test Results for Individual Components of Resin C.
Table 3. Ames Test Results for Individual Components of Resin C.
StrainComponentDose (µg/Plate)(−S9)(+S9)
TA100Base100↑↑
TA100Base1000↑↑↑↑
TA1535Base100↑↑
TA98/1537/1538BaseAll dosesn.s.n.s.
All strainsAcceleratorAll dosesn.s.n.s.
Legend: n.s. = not significant; ↑ = increase in revertant colonies; ↑↑ = significant increase in revertants.

3. Results

In the case of Resin A, no significant increase in revertant colonies was observed in strains TA98, TA1537, and TA1538 at any of the tested concentrations. However, in strains TA100 and TA1535, mutagenic responses became evident, with TA100 showing up to a +145% increase at 1000 µg/plate (−S9) and TA1535 showing a +128% increase at 1000 µg/plate (+S9), indicating a strain-specific effect.
Resin B showed a similar pattern. Results for TA98, TA1537, and TA1538 remained comparable to the negative controls, with no indication of mutagenic activity. In contrast, TA100 and TA1535 exhibited significant increases, reaching +132% and +138% respectively, at 1000 µg/plate, regardless of the presence of metabolic activation.
When testing Resin C (base + accelerator), no significant changes were detected in TA98, TA1537, or TA1538 across all concentrations. However, in TA100 and TA1535, mutagenic activity became evident, with increases of +118% at 1000 µg + 700 µg/plate (−S9) in TA100 and +110% at 100 µg + 70 µg/plate (+S9) in TA1535.
With metabolic activation, increased counts were observed in TA100 at 1000 µg + 700 µg/plate, and in TA1535 at 100 µg + 70 µg/plate; these results further support the concentration and strain-dependent mutagenic response of Resin C as well as the importance of considering metabolic activation when evaluating the biological safety of dental materials.
When the base resin (R) was evaluated independently, the results for TA98, TA1537, and TA1538 remained non-significant. Yet again, TA100 and TA1535 showed significant increases in revertant colonies, particularly at the intermediate concentration of 100 µg/plate, both with and without metabolic activation.
Finally, testing the accelerator component (A) alone did not produce any significant changes in revertant counts in any of the five strains. On the contrary, a slight reduction in colony formation was observed across conditions, suggesting an absence of mutagenic activity.

4. Discussion

This study showed that Resins A and B induced a significant increase in revertant colonies in TA100 and TA1535, while no mutagenic effects emerged in TA98, TA1537, or TA1538. This pattern suggests that the compounds contained in these resins mainly induce point mutations by base substitution, in line with previous reports on methacrylate monomers such as BIS-GMA and its derivatives [3,5]. Resin C, tested both as base + accelerator and as single components, displayed a similar behavior: mutagenicity was evident in TA100 and TA1535, but attributable exclusively to the base resin, while the accelerator did not show activity in any condition. This finding is particularly relevant, as it indicates that genotoxic effects are primarily linked to the resin matrix rather than additives, an aspect rarely investigated in the literature [13]. Statistical analysis confirmed the significance of these results, especially at higher concentrations, with increases up to +145% in TA100 and +128% in TA1535 compared with controls. The effect was observed both with and without metabolic activation, suggesting that some compounds act directly on DNA, while others become more reactive after biotransformation. Overall, these data demonstrate that mutagenicity is not uniform among different materials and that resin composition plays a decisive role in the safety profile. The direct comparison of three commercial formulations contributes to filling a gap in the literature, which has so far focused more on cytotoxic and mechanical rather than mutagenic aspects [7,11,13].
The present study further supports previous findings that orthodontic resin monomers may activate DNA damage response pathways [20] and induce mutagenic effects similar to those observed by Hamid et al. [3] with glycidyl methacrylate. Evidence also indicates that oxidative stress is a key mechanism linking resin exposure to genotoxicity [21]. Macedon et al. [5] confirmed DNA damage in human cells exposed to orthodontic adhesives, while in vivo data demonstrated similar genotoxic responses in oral epithelial cells [22]. In contrast, the accelerator component of Resin C consistently lacked mutagenic activity, confirming that the matrix is the main source of risk [13,23].
Concerns about BIS-GMA are reinforced by studies showing that not only monomers but also metal ions released from orthodontic appliances may contribute to genotoxic stress. This evidence suggests that the biological risk of orthodontic treatment is multifactorial, with both organic and inorganic components, and emphasizes the need for a comprehensive toxicological evaluation of these materials [6,8].
The concentrations tested in this study represent the highest soluble and non-toxic doses recommended for mutagenicity tests. Although these levels are higher than what we would expect in the mouth, they were chosen to create a worst-case scenario. This approach ensures that we can detect any potentially rare but important mutagenic effects in our experiments.
Synergistic interactions between monomers and metal ions further exacerbate oxidative stress [19]. Mikulewicz et al. [8] demonstrated variability in nickel and chromium release across wires, while new coatings have been designed to mitigate these adverse effects [24].
The clinical relevance of these in vitro findings remains debated. While animal studies did not detect significant systemic toxicity from BIS-GMA [25], subtle genomic changes have been observed in chronic exposure models [14]. Recent clinical studies confirmed increased oxidative stress and genotoxic markers in patients with fixed appliances [9], supporting the cumulative nature of these effects [4]. Moreover, materials deemed biocompatible by ISO 10,993 and ADA standards may still elicit mutagenic responses [11], highlighting the limitations of current regulatory testing. Recent reviews have therefore emphasized the need for updated guidelines, including genotoxic endpoints [26]. Our comparison of three commercial resins, with separate analysis of base and accelerator, provides original evidence that mutagenicity is mainly associated with the base component [13]. Calls for standardization of assays to improve reproducibility have also been made [7].
Environmental conditions further modulate material toxicity: aging in acidic media increases genotoxic potential of orthodontic devices [18], underscoring the importance of mimicking intraoral conditions [27]. Promising strategies to reduce risks include silver nanoparticle-enhanced bonding systems [15,28] and bioinspired antibacterial coatings [16,29], which improve antimicrobial activity without compromising mechanical properties. Nevertheless, the long-term intraoral exposure of young patients requires further studies using primary oral cells, 3D tissue constructs, and long-term in vivo approaches. Personalized risk assessment, considering genetic and microbiota-related factors, is also gaining importance [12].
Overall, our results confirm previously reported evidence on the mutagenic potential of orthodontic resin components and emphasize the need for more robust safety assessment. Interdisciplinary collaboration between toxicology, material science, and clinical dentistry will be essential for the development of improved safety benchmarks [30].
A limitation of the present study is that no degradation test of the commercial resins was performed. Since orthodontic resins undergo long-term exposure to the oral environment, hydrolytic, enzymatic, and mechanical processes may lead to the release of additional by-products. Future investigations should specifically address the mutagenic potential of degradation products to provide a more thorough assessment of their biological safety.
Looking ahead, it is noteworthy that research on biomaterials is moving not only towards reducing cytotoxicity and genotoxicity but also towards developing materials with advanced functional properties. For instance, recent studies have shown that organometallic modification of silica with europium can impart fluorescent properties, opening new opportunities for quality monitoring through optical signals [29]. In parallel, the development of innovative nanocomposites, such as Nb–TiNb with a single-phase BCC structure, has demonstrated remarkable enhancement of mechanical properties and potential application in biomedical implants, thanks to the combination of high strength and biocompatibility [29,30]. Although not directly related to orthodontic resins, these research directions highlight how innovation in dental and biomedical materials can follow complementary pathways aimed at achieving increasingly safe and efficient devices.

5. Conclusions

This study demonstrated that some orthodontic resins, specifically Resins A, B, and the base component of Resin C, induced significant mutagenic effects in Salmonella typhimurium strains TA100 and TA1535. In contrast, no mutagenicity was detected in TA98, TA1537, and TA1538, nor in the accelerator component of Resin C. These results indicate that mutagenic activity is mainly associated with the resin matrix rather than the additives.
The findings provide a direct comparison among three commercially available orthodontic resins and highlight the importance of including mutagenicity testing in the biological safety evaluation of dental materials. Considering the prolonged intraoral exposure of orthodontic resins, further studies should focus on resin degradation products, long-term in vivo models, and more advanced in vitro systems to better assess their biological impact.

Author Contributions

Conceptualization, C.M., R.B., and F.M.; methodology, L.G. and G.D.; formal analysis, L.G.; investigation, F.M. and L.G.; data curation, R.B., G.D., and N.C.; writing—original draft preparation, F.M., R.B., and C.M.; writing—review and editing, C.M. and R.B.; visualization, supervision, project administration, C.M. and R.B. All authors have read and agreed to the published version of the manuscript.

Funding

This study received no funding.

Institutional Review Board Statement

This study was approved by the Ethic Committee of IRCCS “Giovanni Paolo Il” Istituto Oncologico “Gabriella Serio” of the 17/12/2024 Prot. 1979/CEL—Study L-PRF.

Data Availability Statement

The data presented in this study are available upon reasonable request, after the signature of a formal data sharing agreement in anonymous form, from the corresponding author, because they are protected by privacy restrictions.

Conflicts of Interest

The authors declare no conflicts of interest.

References

  1. Cross, N.G.; Taylor, R.F.; Nunez, L.J. Single-step orthodontic bonding systems: Possible mutagenic potential. Am. J. Orthod. 1983, 84, 344–350. [Google Scholar] [CrossRef] [PubMed]
  2. Maspero, C.; Galbiati, G.; Giannini, L.; Guenza, G.; Esposito, L.; Farronato, G. Titanium TSME appliance for patients allergic to nickel. Eur. J. Paediatr. Dent. 2018, 19, 67–69. [Google Scholar]
  3. Hamid, A.; Ghardiri, T.; Rahmani, S.; Ali, Z.; Wang, L.; Chen, Y.; Patel, R.; Gomez, F.; Tanaka, K.; Müller, J. Glycidyl methacrylate (GMA) induces DNA adducts and mutagenicity in bacterial models. Mutat. Res. 2010, 696, 123–129. [Google Scholar]
  4. Eliades, T.; Gioni, V.; Kletsas, D.; Athanasiou, A.; Eliades, G. Oestrogenicity of orthodontic adhesive resins. Eur. J. Orthod. 2007, 29, 404–407. [Google Scholar] [CrossRef] [PubMed]
  5. Taubmann, A.; Willershausen, I.; Walter, C.; Al-Maawi, S.; Kaina, B.; Gölz, L. Genotoxicity of orthodontic adhesives assessed by γH2AX focus formation. Clin. Oral Investig. 2021, 25, 2791–2800. [Google Scholar]
  6. Martín-Cameán, A.; Jos, Á.; Mellado-García, P.; Iglesias-Linares, A.; Solano, E.; Cameán, A.M. In vitro and in vivo evidence of the cytotoxic and genotoxic effects of metal ions released by orthodontic appliances: A review. Environ. Toxicol. Pharmacol. 2015, 40, 86–113. [Google Scholar] [CrossRef]
  7. Van Landuyt, K.L.; Nawrot, T.; Geebelen, B.; De Munck, J.; Snauwaert, J.; Yoshihara, K.; Scheers, H.; Godderis, L.; Hoet, P.; Van Meerbeek, B. How much do resin-based dental materials release? A meta-analytical approach. Dent. Mater. 2011, 27, 723–747. [Google Scholar] [CrossRef]
  8. Mikulewicz, M.; Suski, P.; Tokarczuk, O.; Warzyńska-Maciejewska, M.; Pohl, P.; Tokarczuk, B. Metal ion release from orthodontic archwires: A comparative study of biocompatibility and corrosion resistance. Molecules 2024, 29, 5685. [Google Scholar] [CrossRef]
  9. Angeles-Estrada, L.; Pérez-Soto, E.; Pérez-Vielma, N.M.; Gómez-López, M.; Sánchez-Monroy, V. Oxidative stress and genotoxicity in oral epithelial cells from subjects undergoing orthodontic treatment with fixed appliances. Clin. Oral Investig. 2023, 27, 4225–4231. [Google Scholar] [CrossRef]
  10. Caplan, D.; Chasen, J.; Krall, E.; Cai, J.; Kang, S.; Garcia, R.; Offenbacher, S.; Beck, J. Lesions of endodontic origin and risk of coronary heart disease. J. Dent. Res. 2006, 85, 996–1000. [Google Scholar] [CrossRef] [PubMed]
  11. Schweikl, H.; Spagnuolo, G.; Schmalz, G. Genetic and cellular toxicology of dental resin monomers. J. Dent. Res. 2006, 85, 870–877. [Google Scholar] [CrossRef] [PubMed]
  12. Gallorini, M.; Cataldi, A.; di Giacomo, V. HEMA-induced cytotoxicity: Oxidative stress, genotoxicity and apoptosis. Int. Endod. J. 2014, 47, 813–818. [Google Scholar] [CrossRef]
  13. Gonçalves, T.S.; de Menezes, L.M.; Trindade, C.; da Silva Machado, M.; Thomas, P.; Fenech, M.; Henriques, J.A.P. Cytotoxicity and genotoxicity of orthodontic bands with or without silver soldered joints. Mutat. Res. Genet. Toxicol. Environ. Mutagen. 2014, 762, 1–8. [Google Scholar] [CrossRef] [PubMed]
  14. Cenzato, N.; Occhipinti, C.; D’amici, E.; Savadori, P.; Baldini, B.; Maspero, C. Microbiological Analysis of Plaque and Its Composition in Three Patient Groups under Different Orthodontic Treatments. Dent. J. 2024, 12, 168. [Google Scholar] [CrossRef] [PubMed]
  15. Wang, N.; Yu, J.; Yan, J.; Hua, F. Recent advances in antibacterial coatings for orthodontic appliances. Front. Bioeng. Biotechnol. 2023, 11, 1093926. [Google Scholar] [CrossRef]
  16. Liu, Y.; Zheng, Y.; Li, S.; Li, B.; Zhang, Y.; Yuan, Y. Percutaneous microwave ablation of larger hepatocellular carcinoma. Clin. Radiol. 2013, 68, 21–26. [Google Scholar] [CrossRef]
  17. Karandish, M.; Khademi, B.; Ziaei, G.; Erfani, N.; Moezi, L.; Faghih, Z. Cytotoxicity and genotoxicity of orthodontic bands after aging: An in-vitro study. BMC Oral Health 2025, 25, 163. [Google Scholar] [CrossRef]
  18. Tartaglia, G.M.; Mapelli, A.; Maspero, C.; Santaniello, T.; Serafin, M.; Farronato, M.; Caprioglio, A. Direct 3D Printing of Clear Orthodontic Aligners: Current State and Future Possibilities. Materials 2021, 14, 1799. [Google Scholar] [CrossRef]
  19. Yazdi, M.; Daryanavard, H.; Ashtiani, A.H.; Moradinejad, M.; Rakhshan, V. A systematic review of biocompatibility and safety of orthodontic clear aligners and transparent vacuum-formed thermoplastic retainers. Dent. Res. J. 2023, 20, 41. [Google Scholar] [CrossRef]
  20. Pelourde, C.; Bationo, R.; Boileau, M.-J.; Colat-Parros, J.; Jordana, F. Monomer release from orthodontic retentions: An in vitro study. Am. J. Orthod. Dentofac. Orthop. 2018, 153, 248–254. [Google Scholar] [CrossRef]
  21. Dantagnan, C.-A.; Babajko, S.; Nassif, A.; Porporatti, A.; Attal, J.-P.; Dursun, E.; Nguyen, J.-F.; Bosco, J. Biocompatibility of direct printed clear aligners: A systematic review of in vitro studies. Int. Orthod. 2025, 23, 101028. [Google Scholar] [CrossRef]
  22. Iliadi, A.; Koletsi, D.; Papageorgiou, S.N.; Eliades, T. Safety considerations for thermoplastic-type appliances used as orthodontic aligners or retainers: A systematic review and meta-analysis. Materials 2020, 13, 1843. [Google Scholar] [CrossRef]
  23. Halimi, A.; Benyahia, H.; Bahije, L.; Adli, H.; Azeroual, M.-F.; Zaoui, F. A systematic study of the release of bisphenol A by orthodontic materials and its biological effects. Int. Orthod. 2016, 14, 399–417. [Google Scholar] [CrossRef] [PubMed]
  24. Cenzato, N.; Crispino, R.; Galbiati, G.; Giannini, L.; Bolognesi, L.; Lanteri, V.; Maspero, C. Premature loss of primary molars in children: Space recovery through molar distalisation. A literature review. Eur. J. Paediatr. Dent. 2024, 25, 72–76. [Google Scholar] [PubMed]
  25. Rogers, H.B.; Zhou, L.T.; Kusuhara, A.; Zaniker, E.; Shafaie, S.; Owen, B.C.; Duncan, F.E.; Woodruff, T.K. Dental resins used in 3D printing technologies release ovo-toxic leachates. Chemosphere 2021, 270, 129003. [Google Scholar] [CrossRef]
  26. Valencia Zavala, M.P.; Sánchez Olivas, M.A.; Velázquez Sámano, G.; Sepúlveda, G.; Flores, I.; Velazco, A.; Vega Robledo, G.B. Alergia a materiales utilizados en procedimientos dentales [Allergy to materials used in dental procedures]. Rev. Alerg. Mex. 2010, 57, 202–207. [Google Scholar] [PubMed]
  27. Cenzato, N.; Di Iasio, G.; Martìn Carreras-Presas, C.; Caprioglio, A.; Del Fabbro, M. Materials for Clear Aligners—A Comprehensive Exploration of Characteristics and Innovations: A Scoping Review. Appl. Sci. 2024, 14, 6533. [Google Scholar] [CrossRef]
  28. Sancar, A.; Lindsey-Boltz, L.A.; Ünsal-Kaçmaz, K.; Linn, S. Molecular mechanisms of mammalian DNA repair and the DNA damage checkpoints. Annu. Rev. Biochem. 2004, 73, 39–85. [Google Scholar] [CrossRef]
  29. Wu, J.; Zhang, Y.; Hong, Q.; Yang, H.; Zhang, L.; Zhang, M.; Yu, L. Organometallic modification of silica with europium endowing the fluorescence properties: The key technique for numerical quality monitoring. Chin. Chem. Lett. 2025, 36, 110165. [Google Scholar] [CrossRef]
  30. Liu, G.L.; Wang, W.; Ma, W.; Guo, S.; Shen, B.G.; Liu, H.X. A novel Nb–TiNb nanocomposite with single-phase BCC structure for bio-implant applications. Rare Met. 2025, 44, 543–550. [Google Scholar] [CrossRef]
Applsci 15 10351 g001
Figure 1. Stepwise representation of the Ames test procedure, from ethics approval to mutagenicity readout.
Figure 1. Stepwise representation of the Ames test procedure, from ethics approval to mutagenicity readout.
Applsci 15 10351 g001
Disclaimer/Publisher’s Note: The statements, opinions and data contained in all publications are solely those of the individual author(s) and contributor(s) and not of MDPI and/or the editor(s). MDPI and/or the editor(s) disclaim responsibility for any injury to people or property resulting from any ideas, methods, instructions or products referred to in the content.

Share and Cite

MDPI and ACS Style

Biagi, R.; Dipalma, G.; Macrì, F.; Cenzato, N.; Maspero, C.; Giannini, L. Mutagenicity Evaluation of Orthodontic Resins Using the Ames Test. Appl. Sci. 2025, 15, 10351. https://doi.org/10.3390/app151910351

AMA Style

Biagi R, Dipalma G, Macrì F, Cenzato N, Maspero C, Giannini L. Mutagenicity Evaluation of Orthodontic Resins Using the Ames Test. Applied Sciences. 2025; 15(19):10351. https://doi.org/10.3390/app151910351

Chicago/Turabian Style

Biagi, Roberto, Gianna Dipalma, Federica Macrì, Niccolò Cenzato, Cinzia Maspero, and Lucia Giannini. 2025. "Mutagenicity Evaluation of Orthodontic Resins Using the Ames Test" Applied Sciences 15, no. 19: 10351. https://doi.org/10.3390/app151910351

APA Style

Biagi, R., Dipalma, G., Macrì, F., Cenzato, N., Maspero, C., & Giannini, L. (2025). Mutagenicity Evaluation of Orthodontic Resins Using the Ames Test. Applied Sciences, 15(19), 10351. https://doi.org/10.3390/app151910351

Note that from the first issue of 2016, this journal uses article numbers instead of page numbers. See further details here.

Article Metrics

Back to TopTop