Comparison of Accuracy and Reproducibility of Casts Made by Digital and Conventional Methods

Statement of problem Little peer-reviewed information is available regarding the accuracy and reproducibility of digitally fabricated casts compared to conventional nondigital methods. Purpose The purpose of this in vitro study was to compare the accuracy and reproducibility of a digital impression and cast fabrication with a conventional impression and cast fabrication. Material and methods Conventional impressions were made via a 1-step single viscosity technique with vinyl siloxanether material of a typodont master model, and conventional casts were cast from dental stone. Digital impressions were obtained with a digital scanner, and digital stereolithographic models were printed. The typodont and fabricated casts were digitized with a structured light scanner and saved in surface tessellation language (STL) format. All STL records were superimposed via a best-fit method. The digital impression and cast fabrication method was compared with the conventional impression and cast fabrication method for discrepancy, accuracy, and reproducibility. The Levene test was used to determine equality of variances, and a 1-way ANOVA was conducted to assess the overall statistical significance of differences among the groups (n=5, α=.05). Results No significant statistical difference was found between the digital cast and conventional casts in the internal area or finish line area (P\u3e.05). In addition, there was no statistically significant difference between these 2 techniques for a fixed dental prosthesis or single crown (P\u3e.05). However, statistically significant differences were observed for overall areas of the casts in terms of accuracy (PP Conclusions No statistically significant difference was found between the digital cast and conventional cast groups in the internal and finish line areas. However, in terms of the reproducibility and accuracy of the entire cast area, the conventional cast was significantly better than the digital cast

Bisphosphonate-associated osteonecrosis of the jaw is linked to suppressed TGFβ1-signaling and increased Galectin-3 expression: A histological study on biopsies

Background Bisphosphonate associated osteonecrosis of the jaw (BRONJ) implies an impairment in oral hard- and soft tissue repair. An understanding of the signal transduction alterations involved can inform therapeutic strategies. Transforming growth factor β1 (TGFβ1) is a critical regulator of tissue repair; galectin-3 mediates tissue differentiation and specifically modulates periodontopathic bacterial infection. The aim of this study was to compare the expression of TGFβ1-related signaling molecules and Galectin-3 in BRONJ-affected and healthy mucosal tissues. To discriminate between BRONJ-specific impairments in TGFβ1 signaling and secondary inflammatory changes, the results were compared to the expression of TGFβ1 and Galectin-3 in mucosal tissues with osteoradionecrosis. Methods Oral mucosal tissue samples with histologically-confirmed BRONJ (n = 20), osteoradionecrosis (n = 20), and no lesions (normal, n = 20) were processed for immunohistochemistry. Automated staining with an alkaline phosphatase-anti-alkaline phosphatase kit was used to detect TGFβ1, Smad-2/3, Smad-7, and Galectin-3. We semiquantitatively assessed the ratio of stained cells/total number of cells (labeling index, Bonferroni-adjustment). Results TGFβ1 and Smad-2/3 were significantly decreased (p < 0.032 and p(0.028, respectively) in the BRONJ samples and significantly increased (p < 0.04 and p <0.043, respectively) in the osteoradionecrosis samples compared to normal tissue. Smad-7 was significantly increased (p < 0.031) in the BRONJ group and significantly decreased (p < 0.026) in the osteoradionecrosis group. Galectin-3 staining was significantly (p < 0.025) increased in both the BRONJ and the osteoradionecrosis (p < 0.038) groups compared to the normal tissue group. However, Galectin-3 expression was significantly higher in the BRONJ samples than in the osteoradionecrosis samples (p < 0.044). Conclusion Our results showed that disrupted TGFβ1 signaling was associated with delayed periodontal repair in BRONJ samples. The findings also indicated that impairments in TGFβ1-signaling were different in BRONJ compared to osteoradionecrosis. BRONJ appeared to be associated with increased terminal osseous differentiation and decreased soft tissue proliferation. The increase in Galectin-3 reflected the increase in osseous differentiation of mucoperiosteal progenitors, and this might explain the inflammatory anergy observed in BRONJ-affected soft tissues. The results substantiated the clinical success of treating BRONJ with sequestrectomy, followed by strict mucosa closure. BRONJ can be further elucidated by investigating the specific intraoral osteoimmunologic status

PHD2 is a regulator for glycolytic reprogramming in macrophages.

The prolyl-4-hydroxylase domain (PHD) enzymes are regarded as the molecular oxygen sensors. There is an interplay between oxygen availability and cellular metabolism, which in turn has significant effects on the functionality of innate immune cells, such as macrophages. However, if and how PHD enzymes affect macrophage metabolism are enigmatic. We hypothesized that macrophage metabolism and function can be controlled via manipulation of PHD2. We characterized the metabolic phenotypes of PHD2-deficient RAW cells and primary PHD2 knockout bone marrow-derived macrophages (BMDM). Both showed typical features of anaerobic glycolysis, which were paralleled by increased pyruvate dehydrogenase kinase 1 (PDK1) protein levels and a decreased pyruvate dehydrogenase enzyme activity. Metabolic alterations were associated with an impaired cellular functionality. Inhibition of PDK1 or knockout of hypoxia-inducible factor 1 alpha (HIF-1 alpha) reversed the metabolic phenotype and impaired the functionality of the PHD2-deficient RAW cells and BMDM. Taking these results together, we identified a critical role of PHD2 for a reversible glycolytic reprogramming in macrophages with a direct impact on their function. We suggest that PHD2 serves as an adjustable switch to control macropha(g)e behavior

Wearing complete dental prostheses - Effects on perioral morphology

Background: To adequately perform rehabilitation of edentulous patients by a complete removable dental prosthesis (CRDP) is from basic interest to dentists to understand the morphologic changes caused by re-establishment of a physiologic jaw relationship. Anthropometric analyses of standardized frontal view and profile photographs may help elucidate such changes. Material and Methods: Photographs of 31 edentulous patients were compared in relaxed lip closure and after insertion of a CRDP in stable occlusion. 2232 anthropometric distances were raised. Eighteen anthropometric indices reflecting the perioral morphology and its integration in the vertical facial harmony were investigated. Results: The intercanthal – mouth width index ( p <.001), medial – lateral cutaneous upper lip height index ( p= .007), lower vermilion contour index ( p= .022), vermilion – total upper lip height index ( p= .018), cutaneous – total up - per lip height index ( p= .023), upper lip – nose height index ( p= .001), nose – upper face height index ( p= .002), chin – mandible height index ( p= .013), upper lip – mandible height index ( p= .045), nose – lower face height index ( p= .018), and nose - face height index ( p= .029) showed significant pre- to post-treatment changes. Conclusions: The investigated anthropometric indices presented reproducible results related to an increase in occlusal vertical dimension. Their application may be helpful in assessment, planning, and explanation of morphologic effects of CRDPs on the perioral and overall facial morphology, which may helps to improve the aesthetic outcome

EMD in periodontal regenerative surgery modulates cytokine profiles: A randomised controlled clinical trial

The enamel matrix derivative (EMD) contains hundreds of peptides in different levels of proteolytic processing that may provide a range of biological effects of importance in wound healing. The aim of the present study was to compare the effect of EMD and its fractions on the cytokine profiles from human gingival fibroblasts in vitro and in gingival crevicular fluid (GCF) in a randomized controlled split-mouth clinical study (n = 12). Levels of cytokines in cell culture medium and in GCF were measured by Luminex over a 2-week period. In the clinical study, levels of pro-inflammatory cytokines and chemokines were increased, whereas the levels of transforming growth factor-α (TGF-α) and platelet-derived growth factor-BB (PDGF-BB) were reduced. The in vitro study showed that EMD and its high and low molecular weight fractions reduced the secretion of pro-inflammatory cytokines and chemokines compared to untreated cells. EMD had an effect on levels of cytokines related to fibroplasia, angiogenesis, inflammation and chemotaxis both in vitro and in vivo, however, the anti-inflammatory effect induced by EMD observed in the in vitro study could not be confirmed clinically

Prolyl hydroxylase 2 inactivation enhances glycogen storage and promotes excessive neutrophilic responses.

Fully activated innate immune cells are required for effective responses to infection, but their prompt deactivation and removal are essential for limiting tissue damage. Here, we have identified a critical role for the prolyl hydroxylase enzyme Phd2 in maintaining the balance between appropriate, predominantly neutrophil-mediated pathogen clearance and resolution of the innate immune response. We demonstrate that myeloid-specific loss of Phd2 resulted in an exaggerated inflammatory response to Streptococcus pneumonia, with increases in neutrophil motility, functional capacity, and survival. These enhanced neutrophil responses were dependent upon increases in glycolytic flux and glycogen stores. Systemic administration of a HIF-prolyl hydroxylase inhibitor replicated the Phd2-deficient phenotype of delayed inflammation resolution. Together, these data identify Phd2 as the dominant HIF-hydroxylase in neutrophils under normoxic conditions and link intrinsic regulation of glycolysis and glycogen stores to the resolution of neutrophil-mediated inflammatory responses. These results demonstrate the therapeutic potential of targeting metabolic pathways in the treatment of inflammatory disease.This work was principally supported by a Wellcome Trust Senior Clinical Fellowship award (098516 to SRW), Medical Research Council (MRC) Clinical Training Fellowship awards (G0802255 to AART; MR/K023845/1 to RSD), an Academy of Medical Sciences (AMS) starter grant (to AART), a Wellcome Trust Senior Clinical Fellowship award (076945 to DHD), British Lung Foundation Fellowship (F05/7 to HMM), and a Engineering and Physical Sciences Research Council and Medical Research Council grant (EP/L016559/1, JAW). The MRC /University of Edinburgh Centre for Inflammation Research is supported by an MRC Centre Grant. The work of PC is supported by long-term structural funding-Methusalem funding from the Flemish Government. CJS thanks the Wellcome Trust and Cancer Research UK for support