A comparative evaluation of the sealing ability of two calcium silicate based sealers and a resin epoxy-based sealer through scanning electron microscopy and bond strength: an in vitro study

Aim: this study aimed to compare the sealing ability of two types of commercially available calcium silicate bioceramic based root canal sealers and a resin based root canal sealer. Methods: Twenty one single-rooted teeth were used, samples (n= 21) were randomly divided into three groups according to the sealer used (group A; ADSEAL, group B; Wellroot, group C; Ceraseal). Roots were then cleaved longitudinally in the labiolingual direction; all samples were then sectioned at three, six, and nine mm from the root tip. The penetration of sealers into the dentinal tubules was examined at 1000x with a scanning electron microscope. Data were tested for normality using Shapiro Wilk test. ANOVA test was used for analyzing normally distributed data followed by Bonferroni post hoc test for pair-wise comparison. Significance level p≤0.001. Results: groups B and C showed better sealing ability than group A in all the three sections. The coronal section showed higher sealing ability than the middle section followed by the apical section in the three tested groups. Conclusion: it can be concluded that both calcium silicate-based sealers had better sealing ability and higher bond strength than the resin epoxy- based sealer

Thromboembolic injury and systemic toxicity induced by nicotine in mice.

Nicotine is involved in the pathogenesis of hematological and cardiopulmonary diseases. The understanding of the pathophysiological mechanisms underlying these undesirable effects is however unclear. Cigarette smoking, nicotine gums and patches are common sources for nicotine ingestion. We have investigated the nicotine's effect on cerebral microvessel thrombosis and systemic toxicity. Mice received either nicotine (1 mg/kg, i.p.) or saline (control), once a day for 21 days. Briefly, after bolus intravenous fluorescein injection, a photo insult of cerebral microvessel was done. The platelet aggregation in microvessels was video recorded and analyzed. In conjunction, the plasma levels of superoxide dismutase (SOD), lactate dehydrogenase (LDH), liver enzymes, creatinine and blood urea nitrogen (BUN); and histopathological studies were carried out. Our results revealed a significant prothrombotic effect following nicotine exposure. Significant decrease in SOD indicates the occurrence of oxidative stress involved in the tissue damages and increase in the LDH emphasize the systemic toxicity. Substantial rise in the liver aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels were observed. Lungs histology showed intra-vascular hemorrhagic infarction with necrosis, macrophage and neutrophils infiltration. Liver histology showed intravascular thrombosis and portal inflammation. We conclude that the sub-acute nicotine exposure causes an increase in thrombosis in cerebral microvessels and systemic, hepatic and pulmonary toxicity.