CAD/CAM-generated all-ceramic restorations facilitate the reconstruction of deeply destroyed teeth irrespectively of the location of the cavity margins.
Objectives The aim of this study was to investigate whether file design and taper significantly influence microcrack initiation during machine preparation. Materials and methods Sixty extracted teeth with straight single canals were selected. The teeth were randomly assigned to four groups based on their root canal anatomy and the corresponding NiTi rotary file system (I, Mtwo; II, ProTaper Universal; III, F6 SkyTaper; control, no preparation and filling). The root canals of the experimental groups were filled using the single-cone technique. The tested teeth were all subjected to a mechanical chewing simulation with flat lead loading over a period of 3 years (corresponding to 150,000 cycles). The teeth were checked for dentinal defects (accumulative crack growth in length) under the digital microscope (Keyence VHX-5000) at time 0 (baseline prior to chewing simulation) and after 3, 6, 12, 24, and 36 months of loading. The cumulative crack increase was statistically analyzed using the Kruskal–Wallis test, Jonckheere–Terpstra test, and the Wilcoxon rank-sum test. The significance was set at p < 0.05. Results In contrast to preparation with greater-tapered instruments, ProTaper Universal (group II) and F6 SkyTaper (group III) instrumentation with the smaller tapered Mtwo files (group I) showed less accumulative propagation of craze lines (p < 0.05) at all time points. Conclusion Instruments with greater taper for root canal instrumentation should be used with care to avoid negative long-term effects in the form of propagation of dentinal defects over time. A positive cutting-edge angle and a smaller taper have a positive effect on a lower craze line development. Clinical relevance Instruments with a positive cutting-edge angle and a smaller taper are beneficial for the long-term preservation of dentinal tooth structure.
The nitric oxide (NO)-sensitive soluble guanylyl cyclase (sGC) is a heterodimeric enzyme with an α and β subunit. NO binds to heme of the β-subunit of sGC, activates the enzyme in the reduced heme iron state in vascular smooth muscle cells (VSMCs), and generates cGMP-inducing vasodilatation and suppression of VSMC proliferation. In the complex tumor milieu with higher levels of reactive oxygen species (ROS), sGC heme iron may become oxidized and insensitive to NO. To change sGC from an NO-insensitive to NO-sensitive state or NO-independent manner, protein expression of sGC in VSMC is required. Whether sGCαβ exists at the protein level in arterial VSMCs of oropharyngeal squamous cell carcinoma (OPSCC) is unknown. In addition, whether differences in the genetic profile between human papillomavirus (HPV)-positive and HPV-negative OPSCC contributes to the regulation of sGCαβ is unclear. Therefore, we compared the effects of HPV-positive and HPV-negative OPSCC on the expression of sGCαβ in arterial VSMCs from tumor-free and tumor-containing regions of human tissue sections using quantitative immunohistochemistry. In comparison to the tumor-free region, we found a decrease in expression of both α- and β-subunits in the arterial VSMC layer of the tumor-containing areas. The OPSCC-induced significant downregulation of the α- and β-subunits of sGC in arterial VSMC was HPV-independent. We conclude that the response of sGC to NO in tumor arterial VSMCs may be impaired by oxidation of the heme of the β-subunit, and thus, α- and β-subunits of sGC could be targeted to degradation under oxidative stress in OPSCC in an HPV-independent manner. The degradation of sGCαβ in VSMCs may result in increased proliferation of VSMCs, promoting tumor arteriogenesis in OPSCC. This can be interrupted by preserving the active heterodimer sGCαβ in arterial VSMCs.
The activity of endothelial nitric oxide synthase (eNOS) in endothelial cells increased with the phosphorylation of the enzyme at Ser1177 and decreased at Thr495. The regulation of the phosphorylation sites of eNOS at Ser1177 and Thr495 in blood vessels of the healthy and inflamed human dental pulp is unknown. To investigate this, healthy and carious human third molars were immersion-fixed and decalcified. The localization of eNOS, Ser1177, and Thr495 in healthy and inflamed blood vessels was examined in consecutive cryo-sections using quantitative immunohistochemical methods. We found that the staining intensity of Ser1177 in healthy blood vessels decreased in inflamed blood vessels, whereas the weak staining intensity of Thr495 in healthy blood vessels strongly increased in inflamed blood vessels. In blood vessels of the healthy pulp, eNOS is active with phosphorylation of the enzyme at Ser1177. The phosphorylation of eNOS at Thr495 in inflamed blood vessels leads to a decrease in eNOS activity, contributing to eNOS uncoupling and giving evidence for a decrease in NO and an increase in O2− production. Since the formation of the tertiary dentin matrix depends on intact pulp circulation, eNOS uncoupling and phosphorylation of eNOS at Thr495 in the inflamed pulp blood vessels should be considered during caries therapy.
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