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Introduction. The aim of this study was to evaluate the fracture resistance of endodontically treated mandibular molars using traditional and conservative access cavity preparation. Materials and Methods. In this in vitro study, 100 extracted healthy human mandibular molars were selected and divided into 10 groups ( n = 10 ). Healthy teeth in one group were considered the control group. In three groups, traditional access cavity preparation was done (groups A) without two marginal ridges (A1), with one marginal ridge (A2), and with two marginal ridges (A3). In three groups (group B), two separate access cavities with a dentinoenamel roof without two marginal ridges (B1), with one marginal ridge (B2), and with two marginal ridges (B3) were prepared. In three other groups (groups C), two separate access cavities were prepared only with a dentinal roof without two marginal ridges (C1), with one marginal ridge (C2), and with two marginal ridges (C3), on which root canal treatment was performed afterward. Then, these teeth were subjected to force until fracture. The fracture force and fracture mode of each tooth were recorded and compared between groups by ANOVA, Tukey’s post hoc, and chi-square tests using SPSS ver. 23 (IBM, Somers, NJ, USA). Results. The control teeth had the highest mean fracture force ( 2804.5 ± 338.5  N), followed by a conservative access cavity with a dentinoenamel roof and two marginal ridges ( 2360.4 ± 181.72  N) and a conservative access cavity with a dentinoenamel roof and one marginal ridge ( 1812.8 ± 263.9  N), respectively. The lowest mean fracture force was found for the conventional access cavity group without two marginal ridges ( 399.4 ± 95.2  N). Conclusion. In the condition of this study, with two separate access cavities in mandibular molars and maintenance of the marginal ridges, it is possible to provide teeth with higher fracture resistance against occlusal forces.

Background Systemic lupus erythematosus (SLE) is an autoimmune disease resulting from impaired inflammatory responses. Given the role of air pollution on increasing inflammatory mediators, thus, we aimed to systematically review and meta-analyze evidence regarding an association between short-term exposure to air pollution and SLE onset, activity, and hospitalization. Methods Electronic databases including Web of Science, PubMed, Scopus, and Embase were searched for all published articles until July 5, 2021. Newcastle Ottawa Scale (NOS) checklist was used to assess the quality of individual studies. Relevant demographic data and the intended results of the selected studies were extracted, and their adjusted risk ratios (RRs) were pooled using random and fixed effect analysis based on the heterogeneity index. Findings Twelve studies were entered in our systematic review, and finally, six publications were enrolled in meta-analysis. Overall, Meta-analysis showed no significant association between an increase of PM2.5 on the third day and SLEDAI score with pooled adjusted RR of 1.212 (95% CI, 0,853–1.721), p-value = 0.284. However, there was a positive relationship between 6 days increase of Particulate matter (PM) 2.5 and the systemic lupus erythematosus disease activity Index (SLEDAI) score (pooled adjusted RR 1.112; 95% CI, 1.005–1.231), p-value = 0.040. There was no significant association between carbon monoxide (CO), nitrogen dioxide (NO2), PM2.5, and PM10 increase in the air and hospitalization of SLE patients with pooled RR of 1.021 (95% CI, 0,986–1.1.057), p-value = 0.249, 1.034 (95% CI, 0.996–1.068); p-value = 0.079, 1.042 (95% CI, 0.994–1.092); p-value = 0.084 and 1.004 (95% CI, 0.996–1.013); p-value = 0.323, respectively. Also, analysis showed a significant relation between ozone (O3) increase and hospitalization with a pooled RR of 1.076 (95% CI, 1.009–1.147); p-value = 0.025. Finally, analysis of SO2 increase and risk of hospitalization demonstrated no significant relationship with the pooled RR of 1.011; (95% CI, 0.962–1.062), p-value = 0.0.671. Conclusion Our findings prove that PM2.5 was associated with increased SLE risk. We also showed that only O3 was associated with increased hospital admissions of SLE patients.

Background Air pollution exposure can trigger a wide range of thyroid dysfunction in different population groups. This systematic review and meta-analysis aimed to find the association between air pollution and thyroid dysfunction in the general population and neonate, pregnant and cancerous people. Methods Electronic databases, including Web of Science, PubMed, Scopus, and Embase, were searched for all published articles from 27 October 2021. The Newcastle Ottawa Scale checklist was used to assess the quality of individual studies. Relevant demographic data and the intended results of the selected studies were extracted, and their adjusted odds ratios were pooled using random and fixed effect analysis based on the heterogenicity index. Results After applying the search strategies, twenty-six articles were included in our study. Overall, the association between air pollution and thyroid cancer, neonatal hypothyroidism, maternal thyroid function, and thyroid function in the general population was discussed in four, eight, ten, and four studies, respectively. There was a significant association between PM2.5 exposure and maternal hypothyroxinemia with pooled OR of 1.241 (95%CI, 1.089–1.415), p-value < 0.001. No positive relationship existed between NO2 exposure and maternal hypothyroxinemia with pooled OR of 1.007 (95%CI, 0.840–1.207), p-value = 0.941. The investigation of the relationship between PM2.5 exposure and congenital hypothyroxinemia showed a significant association between them, with pooled OR of 1.017 (95%CI, 1.002–1.032), p-value = 0.024. Conclusions Air pollution could influence thyroid function, especially in pregnant women and newborn infants. This study and similar investigations provide evidence of air pollution toxicity for healthcare systems.