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Objectives: To investigate the clinical performance of chairside fabricated tooth-supported posterior single crowns from lithium disilicate ceramic. Materials and methods: Thirty-four crowns (IPS e.max CAD, Ivoclar Vivadent, Schaan, Liechtenstein) were inserted between 2006 and 2007 and again evaluated after 15 years. Survival and success rates were calculated according to Kaplan–Meier, and the quality of the crowns was evaluated by using modified United States Public Health (USPHS) criteria. Results: Twenty-two crowns were available for recall; six patients were defined as dropouts. The mean observation period was 15.2 years (± 0.2). Six failures occurred (1 technical/5 biological) resulting in a survival rate of 80.1%. The success rate was 64.2%. The roughness of the crowns increased (p = 0.021) and the majority of adhesive gaps were discolored (p = 0.001) in comparison to baseline. The color, tooth, and crown integrity remained stable over the follow-up period (p ≥ 0.317). Conclusion: The fabrication of tooth-supported lithium disilicate crowns using a chairside approach yielded acceptable long-term survival and success rates. Due to discoloration, the long-term use of dual-cure self-adhesive resin cements might result in unpleasing esthetic results. Clinical relevance: The performance of posterior lithium disilicate single crowns revealed excellent to good clinical quality and an acceptable number of events after 15 years of clinical service. [ABSTRACT FROM AUTHOR]

Desialylation of cell surface glycoproteins carried out by sialidases affects various immunological processes. However, the role of neuraminidase 1 (NEU1), one of the four mammalian sialidases, in inflammation and autoimmune disease is not completely unraveled to date. In this study, we analyzed the retinal expression of NEU1 in equine recurrent uveitis (ERU), a spontaneous animal model for autoimmune uveitis. Mass spectrometry revealed significantly higher abundance of NEU1 in retinal Müller glial cells (RMG) of ERU-diseased horses compared to healthy controls. Immunohistochemistry uncovered NEU1 expression along the whole Müller cell body in healthy and uveitic states and confirmed higher abundance in inflamed retina. Müller glial cells are the principal macroglial cells of the retina and play a crucial role in uveitis pathogenesis. To determine whether higher expression levels of NEU1 in uveitic RMG correlate with the desialylation of retinal cells, we performed lectin-binding assays with sialic acid-specific lectins. Through these experiments, we could demonstrate a profound loss of both α2-3- and α2-6-linked terminal sialic acids in uveitis. Hence, we hypothesize that the higher abundance of NEU1 in uveitic RMG plays an important role in the pathogenesis of uveitis by desialylation of retinal cells. As RMG become activated in the course of uveitis and actively promote inflammation, we propose that NEU1 might represent a novel activation marker for inflammatory RMG. Our data provide novel insights in the expression and implication of NEU1 in inflammation and autoimmune disease. [ABSTRACT FROM AUTHOR]

Retinal Müller glial cells (RMG) are involved in virtually every retinal disease; however, the role of these glial cells in neuroinflammation is still poorly understood. Since cell surface proteins play a decisive role in immune system signaling pathways, this study aimed at characterizing the changes of the cell surface proteome of RMG after incubation with prototype immune system stimulant lipopolysaccharide (LPS). While mass spectrometric analysis of the human Müller glia cell line MIO-M1 revealed 507 cell surface proteins in total, with 18 proteins significantly more abundant after stimulation (ratio ≥ 2), the surfaceome of primary RMG comprised 1425 proteins, among them 79 proteins with significantly higher abundance in the stimulated state. Pathway analysis revealed notable association with immune system pathways such as "antigen presentation", "immunoregulatory interactions between a lymphoid and a non-lymphoid cell" and "cell migration". We could demonstrate a higher abundance of proteins that are usually ascribed to antigen-presenting cells (APCs) and function to interact with T-cells, suggesting that activated RMG might act as atypical APCs in the course of ocular neuroinflammation. Our data provide a detailed description of the unstimulated and stimulated RMG surfaceome and offer fundamental insights regarding the capacity of RMG to actively participate in neuroinflammation in the retina. [ABSTRACT FROM AUTHOR]