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Purpose: To evaluate the effectiveness of Vanish XT in preventing white spot lesions (WSLs) when placed around orthodontic brackets. The efficacy of Vanish XT was compared with that of Pro Seal, a commercially available product already proven in preventing demineralization., Materials and Methods: Sixty extracted human canine teeth were divided into three groups (n = 20). The two experimental groups were treated with either Vanish XT or Pro Seal. A third group received no treatment (control). Ethidium bromide with DNA was added to and mixed with the products to produce fluorescence to verify retention of the experimental products. The teeth were submersed in a lactic acid solution for 32 days to create WSLs. All sample teeth were brushed twice daily with a non-fluoride toothpaste to evaluate retention of the experimental products. Photos were taken under fluorescence microscopy and white light at three time intervals. Demineralization was quantified utilizing computer software, and photos were analyzed to obtain values for percent surface area of demineralization and surface color change., Results: Percent surface area of WSL data, both under white light conditions and fluorometric analysis, revealed a significant difference between Pro Seal and Vanish XT when compared with the control group. No significant differences were found between Pro Seal and Vanish XT treated teeth. Fluorescence evaluation revealed that both experimental products were largely removed by 32 days of brushing and acid exposure., Conclusion: Vanish XT is effective in preventing demineralization around orthodontic brackets. Its preventive efficacy is equivalent to that of Pro Seal.

The aim of our study was to evaluate the immunohistochemical expression of SOX11, PAX5, TTF-1 and ISL-1 in medulloblastoma (MB) to investigate their diagnostic usefulness., Methods: Immunohistochemical expression of PAX5 (two antibodies: Dako, DAK-Pax5; and BD, clone 24), TTF-1 (Dako, 8G7G3/1), SOX11 (CL0142; Abcam) and ISL-1 (1 H9, Abcam) was analyzed using the h-score and Remmele score in 25 cases of MB., Results: There were 18 MBs of classic and 7 of desmoplastic type. SOX11 was strongly expressed in all tumors. The expression of PAX5 was higher and more frequent in a case of DAK-Pax5 clone (25/25) than clone 24 (6/25). ISL-1 was positive in 11 (44%) and TTF-1 in 3 (12%) cases. ISL-1 expression correlated positively (p<0.001), while TTF-1 correlated negatively with the age of patients (p=0.039). PAX5 expression correlated with ISL-1 (p=0.039) and showed a trend toward higher expression in the desmoplastic subtype (p=0.069)., Conclusions: SOX11 is strongly and robustly expressed in MBs. PAX5 expression pattern differs substantially among two antibody clones. TTF-1 and ISL-1 is associated with the age of patients., (Copyright © 2016 Elsevier GmbH. All rights reserved.)

CD99 is a protein initially described in the Ewing sarcoma family of tumors, but growing evidence has shown its expression in other tumors of mesenchymal, hematopoietic and even epithelial origin. Some articles report CD99 in metaplastic carcinoma of the breast, a subtype of breast carcinoma (BC) with pronounced epithelial to mesenchymal (EMT) phenotype. Our aim was to analyse the potential relationship between CD99 and selected EMT (vimentin, E-cadherin, Twist) and proliferation markers (Ki-67, c-myc, cyclin D1, topoisomerase 2), molecular subtypes of BC, as well as overall survival (OS) and progression-free survival (PFS). In a group of 122 cases CD99 membrane expression was seen in 14 (11.5%) cases: strong in 11 (9%) and moderate in 3 (2.5%). Expression of CD99 correlated with low cyclin D1 index, high level of topoisomerase 2 expression and lack of progesterone receptor (PR) but not with EMT characteristics. Additionally, strong expression of CD99 correlated with triple negative molecular BC phenotype. CD99 was prognostically irrelevant for OS and PFS. CD99 correlates with selected proliferative markers and low ER/PR receptor status but not with patients' outcome in BC. Further studies are required to explain precisely its role in molecular pathogenesis of BC.