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The aim of the study was to evaluate the effects of polymeric computer-aided design/computer-aided manufacturing CAD/CAM materials on antagonistic primary tooth wear. Five CAD/CAM polymeric materials were examined: Vipi Block Monocolor (VBM), Yamahachi polymethylmethacrylate (PMMA) (YAP), Mazic Duro (MZD), Vita Enamic (ENA), and Pekkton (PEK). All of the specimens were tested in a thermomechanical loading machine with the primary canine as the antagonist (50 N, 1.2 x 105 cycles, 1.7 Hz, 5/55 °C). The wear losses of the antagonist tooth and the restorative materials were calculated using reverse modelling software and an electronic scale. VBM and ENA showed significantly higher antagonist tooth wear than PEK (p < 0.05), but there was no significant difference observed among VBM, YAP, MZD and ENA (p > 0.05). PEK showed the largest value in both material volumetric and weight losses. In terms of material volumetric losses, there was no significant difference between all of the groups (p > 0.05). In terms of material weight losses, PEK was significantly larger than ENA (p < 0.05), but there was no significant difference between VBM, YAP, MZD and ENA (p > 0.05). Volumetric and weight losses of materials showed similar wear behaviour. However, the wear patterns of antagonists and materials were different, especially in PEK. [ABSTRACT FROM AUTHOR]

Mucin hypersecretion and overproduction are frequent manifestations of respiratory disease. Determining the physiological function of airway mucin is presently considered more important than identifying the relevant signaling pathways. The lack of a full-length human mucin 8 (MUC8) cDNA sequence has hindered the generation of a Muc8 knockout mouse line. Thus, the precise physiological functions of MUC8 are unclear. Herein, we investigated the function of MUC8 using a small-interfering RNA (siRNA)-mediated genetic silencing approach in human airway epithelial cells. Herein, intracellular IL-1α production was stimulated by an ATP/P2Y2 complex. While ATP/P2Y2 increased IL-1α secretion in a time-dependent manner, treatment with P2Y2-specific siRNA significantly decreased IL-1α secretion. Moreover, ATP increased P2Y2-mediated upregulation of MUC8 expression; however, IL-1α significantly decreased the extent to which ATP/P2Y2 upregulated MUC8 expression. Interestingly, treatment with MUC8-specific siRNA decreased the production of anti-inflammatory cyto-kines (TGF-β and IL-1 receptor antagonist) and increased the production of inflammatory cytokines (IL-1α and IL-6) in our system. In addition, siRNA-mediated knockdown of MUC8 expression dramatically increased the secretion of inflammatory chemokines and resulted in an approximately threefold decrease in cell chemotaxis. We propose that MUC8 may function as an anti-inflammatory mucin that participates in inflammatory response by attracting immune cells/cytokines to the site of inflammation. Our results provide new insight into the physiological function of MUC8 and enhance our understanding of mucin overproduction during airway inflammation. [ABSTRACT FROM AUTHOR]