Genotoxicity induced by endodontic sealers: A systematic review.

Introduction: This systematic review aimed to help further elucidate the following question: are endodontics sealers able to induce DNA damage in vitro or in vivo? Methods: This study was conducted following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement 2020 criteria. A total of 23 studies were carefully selected by the authors. Results: Regarding the general characteristics, most studies evaluated, on average, 3-5 types of sealers (resin epoxy, salicylate, salicylate + MTA, zinc oxide-eugenol, bioceramic products, calcium hydroxide), performing comparisons between them. Our results demonstrate that endodontic sealers may be a genotoxic agent since most studies demonstrated positive findings, with the resin-based ones being the most potentially genotoxic. Conclusion: The type of genotoxicity assay, material evaluated, and dilution concentration levels influenced the outcome. This study clarifies whether and to what extent endodontic sealers are capable of inducing DNA injury in oral tissues.

Is micronucleus assay in oral cells suitable biomarker for evaluating the risk of carcinogenesis in gas station attendants? A systematic review.

This study aimed to evaluate all studies which used the micronucleus assay using oral cells in the attempt to understand whether such technique is efficient in evaluating genotoxicity in gas station attendants. Full manuscripts from 16 studies were carefully selected by the authors. Our results demonstrate that continuous exposure to derivatives of petroleum may lead to genotoxic effects since all studies demonstrated positive findings (16 out of 16) and 11 of them had a strong or moderate final rating. In summary, our results reveal that gas station attendants are occupationally exposed to genotoxic agents and that the micronucleus assay in oral mucosa is indeed an effective method to evaluate genotoxicity in this specific case. Such findings are very important for protecting these professionals who are continuously exposed to chemicals for long periods.

CXCR3 chemokine receptor contributes to specific CD8+ T cell activation by pDC during infection with intracellular pathogens.

Chemokine receptor type 3 (CXCR3) plays an important role in CD8+ T cells migration during intracellular infections, such as Trypanosoma cruzi. In addition to chemotaxis, CXCR3 receptor has been described as important to the interaction between antigen-presenting cells and effector cells. We hypothesized that CXCR3 is fundamental to T. cruzi-specific CD8+ T cell activation, migration and effector function. Anti-CXCR3 neutralizing antibody administration to acutely T. cruzi-infected mice decreased the number of specific CD8+ T cells in the spleen, and those cells had impaired in activation and cytokine production but unaltered proliferative response. In addition, anti-CXCR3-treated mice showed decreased frequency of CD8+ T cells in the heart and numbers of plasmacytoid dendritic cells in spleen and lymph node. As CD8+ T cells interacted with plasmacytoid dendritic cells during infection by T. cruzi, we suggest that anti-CXCR3 treatment lowers the quantity of plasmacytoid dendritic cells, which may contribute to impair the prime of CD8+ T cells. Understanding which molecules and mechanisms guide CD8+ T cell activation and migration might be a key to vaccine development against Chagas disease as those cells play an important role in T. cruzi infection control.

CXCR3 chemokine receptor guides Trypanosoma cruzi-specific T-cells triggered by DNA/adenovirus ASP2 vaccine to heart tissue after challenge.

CD8+ T lymphocytes play an important role in controlling infections by intracellular pathogens. Chemokines and their receptors are crucial for the migration of CD8+ T-lymphocytes, which are the main IFNγ producers and cytotoxic effectors cells. Although the participation of chemokine ligands and receptors has been largely explored in viral infection, much less is known in infection by Trypanosoma cruzi, the causative agent of Chagas disease. After T. cruzi infection, CXCR3 chemokine receptor is highly expressed on the surface of CD8+ T-lymphocytes. Here, we hypothesized that CXCR3 is a key molecule for migration of parasite-specific CD8+ T-cells towards infected tissues, where they may play their effector activities. Using a model of induction of resistance to highly susceptible A/Sn mice using an ASP2-carrying DNA/adenovirus prime-boost strategy, we showed that CXCR3 expression was upregulated on CD8+ T-cells, which selectively migrated towards its ligands CXCL9 and CXCL10. Anti-CXCR3 administration reversed the vaccine-induced resistance to T. cruzi infection in a way associated with hampered cytotoxic activity and increased proapoptotic markers on the H2KK-restricted TEWETGQI-specific CD8+ T-cells. Furthermore, CXCR3 receptor critically guided TEWETGQI-specific effector CD8+ T-cells to the infected heart tissue that express CXCL9 and CXCL10. Overall, our study pointed CXCR3 and its ligands as key molecules to drive T. cruzi-specific effector CD8+ T-cells into the infected heart tissue. The unveiling of the process driving cell migration and colonization of infected tissues by pathogen-specific effector T-cells is a crucial requirement to the development of vaccine strategies.

Cytogenetic biomonitoring of peripheral blood and oral mucosa cells from car painters.

The aim of the present study was to comparatively evaluate genomic damage and cellular death in exfoliated oral mucosa cells and peripheral blood from car painters. A total of 24 car painters and 19 healthy controls (non-exposed individuals) were included in this setting. Individuals had epithelial cells from cheek mucosa (left and right side) mechanically exfoliated, placed in fixative and dropped in clean slides which were checked for the specific nuclear phenotypes. A total of 5 µL from peripheral blood was collected for the single cell gel (comet) assay. The results pointed out statistically significant differences (p < 0.05) of micronucleated oral mucosa cells from car painters. In addition, DNA damage was detected in peripheral blood cells by single cell gel (comet) assay. Nevertheless, exposure to car paints did not cause increases other nuclear alterations closely related to cytotoxicity such as karrhyorexis, pyknosis and karyolysis in buccal mucosa cells. In summary, the results of the present study suggest that car painters comprise a high risk group since paints can induce genotoxic and mutagenic effects in peripheral blood and oral mucosa cells, respectively.

Cytogenetic biomonitoring in children submitting to a complete set of radiographs for orthodontic planning.

OBJECTIVES: To evaluate the DNA damage (micronucleus) and cellular death (pyknosis, karyolysis, and karyorrhexis) in exfoliated buccal mucosa cells from children undergoing orthodontic radiographs. MATERIALS AND METHODS: A total of 25 healthy children undergoing orthodontic therapy partook in a complete set of orthodontic radiographs (lateral cephalographic, posteroanterior cephalographic, panoramic, full periapical exam, and bitewing). The micronucleus test in the buccal exfoliated cells was applied. The paired-samples t-test and the Wilcoxon test were used to compare the frequencies of alterations before and after X-ray exposure. RESULTS: We found no statistically significant differences (P > .05) between micronucleated buccal mucosa cells before and after exposure to radiation. However, radiation did cause other nuclear alterations closely related to cytotoxicity (P  =  .007). CONCLUSION: According to the micronucleus test, the complete set of radiographs requested in the orthodontic planning may not be a factor that induces chromosomal damage, but it is able to promote cytotoxicity.