RESUMO
Background/purpose: Recent advancements in dental technology has led clinicians to convert from traditional methods to digital workflows. The purpose of this study was to analyze the effect of various finish line designs and occlusal morphologies on the accuracy of digital impressions. Materials and methods: Six maxillary molar crown preparations were designed by using a digital sculpting software program. The samples differed in finish line design and occlusal surface morphology. Three different finish line designs (shoulder, chamfer, and shoulder with internal round angle) and two different occlusal morphologies (sharp and rounded) were used, giving six groups. Using three different intraoral scanners, each group was scanned and compared with a reference scan obtained from an industrial scanner. The accuracy of each scan was studied, and the data were statistically analyzed. Results: A total of 180 scans were acquired by utilizing three different intraoral scanners. The reference scan was compared with the scans from each group and overall differences (marginal, axial, and occlusal) were assessed. A crown preparation with a chamfer finish line showed the lowest marginal discrepancy of 13.2 ± 4.18 µm while preparation with a shoulder finish line reported the highest discrepancy of 34.8 ± 7.9 µm (P < 0.05). Also, the occlusal discrepancies of the samples with rounded and sharp occlusal morphologies were 12.55 ± 3.09 µm and 19.13 ± 2.3 µm, respectively (P < 0.05). Conclusion: It has been suggested that chamfer finish line design and rounded occlusal anatomy may produce more accurate digital impression for single crown restorations.
RESUMO
Bacterial lipopolysaccharide (LPS) association with their connate receptor TLR4 triggers Type I interferon signaling cascade through its MyD88 independent downstream. Compared to plethora of reported empirical data on both TLR4 and Type I interferon pathways, there is no known model to decipher crosstalk mechanisms between these two crucial innate immune pathogen activated pathways regulating vital transcriptional factors such as nuclear factor-κB (NFκB), IFNß, the interferon-stimulated gene factor-3 (ISGF3) and an important cancer drug target protein kinase-R (PKR). Innate immune system is based on a sensitive balance of intricate interactions. In elucidating these interactions, in silico integration of pathways has great potential. Attempts confined to single pathway may not be effective in truly addressing source of real systems behavior. This is the first report combining toll-like receptor-4 (TLR4) and interferon beta (IFNß) pathways in a single in silico model, analyzing their interactions, pinpointing the source of delay in PKR late phase activity and limiting the transcription of IFN and PKR by using a method including an statistical physics technique in reaction equations. The model quite successfully recapitulates published interferon regulatory factor-3 (IRF3) and IFNß data from mouse macrophages and PKR data from mouse embryonic fibroblast cell lines. The simulations end up with an estimate of IRF3, IFNß, ISGF3 dose dependent profiles mimicking nonlinear dose response characteristic of the system. Involvement of concomitant PKR downstream can unravel elusive mechanisms in specific profiles like NFκB regulation.
