Formulation and characterization of antibacterial orthodontic adhesive

ABSTRACT Objective: The objective of this study was to formulate experimental orthodontic bracket adhesives and test their mechanical properties, fluoride release and antibacterial activity. Methods: Four experimental antibacterial orthodontic bracket adhesives were prepared with different compositions of synthesized antibacterial monomers replacing total 5% of dental monomers in the control Transbond XT (3M): 5%C11, 3.5%C11+1.5%C2, 5%C16, and 3.5%C16+1.5%C2. Transbond XT alone was used as control. These groups were used to bond premolar brackets to extracted premolars. Shear bond strength (SBS) was tested using an Instron machine. For antibacterial test, disk specimens (10mm diameter, 1mm thick, n=4) were fabricated and incubated with cultures of cariogenic Streptococcus mutans for 48h, and following gentle sonication, S. mutans biofilms in colony-forming-units (CFU) on the disks were enumerated by plating on agar medium. The data were analyzed using ANOVA and Tukey test (α=0.05). Results: All experimental groups had similar shear bond strength (no significant difference) to the control. All experimental groups showed significant inhibitory effect against S. mutans biofilm formation, when compared to the control, but there was no significant difference between experimental groups. Conclusion: Antibacterial orthodontic adhesive can be fabricated to have similar mechanical properties but better caries-inhibitory effect than current adhesive.

RESUMO Objetivo: o objetivo do presente estudo foi formular, experimentalmente, adesivos para colagem de braquetes ortodônticos e testar as suas propriedades mecânicas, sua liberação de flúor e sua atividade antibacteriana. Métodos: quatro adesivos ortodônticos antibacterianos foram preparados experimentalmente usando monômeros sintéticos antibacterianos com diferentes composições, substituindo-se 5% do monômero do grupo controle (Transbond XT, 3M) por: 5%C11; 3,5%C11 + 1,5%C2; 5%C16; ou 3,5%C16 + 1,5%C2. O Transbond XT original foi utilizado como controle. Esses diferentes adesivos foram usados para colar braquetes de pré-molares em pré-molares extraídos. A resistência da colagem ao cisalhamento (RCC) foi testada utilizando-se uma máquina Instron. Para os testes antibacterianos, amostras em formato de disco (10 mm de diâmetro, 1 mm de espessura, n = 4) foram fabricadas e incubadas por 48 horas com culturas cariogênicas de Streptococcus mutans. Após leve sonicação, os discos contendo os biofilmes de S. mutans em unidades formadoras de colônia (UFC) foram colocados em placas com meio de cultura ágar e numerados. Os dados foram analisados utilizando-se ANOVA e teste de Tukey (α?#8197;= 0,05). Resultados: todos os grupos experimentais apresentaram RCC semelhante (sem diferença significativa) ao grupo controle. Todos os grupos experimentais apresentaram significativo efeito inibitório contra a formação do biofilme de S. mutans, em comparação ao grupo controle, porém sem diferença significativa entre os grupos experimentais. Conclusão: adesivos ortodônticos antibacterianos podem ser produzidos para alcançar propriedades mecânicas semelhantes às dos adesivos atuais, porém com melhores efeitos inibitórios de cáries.

Role of Estrogen Receptor-alpha in the Regulation of Claudin-6 Expression in Breast Cancer Cells / 한국유방암학회지

PURPOSE: In our previous studies we showed that upregulating claudin-6 (CLDN6) expression may contribute to preventing breast cancer, and that 17beta-estradiol induces a concentration- and time-related effect on CLDN6 mRNA and protein expression in MCF-7 cells. However, the mechanisms of 17beta-estradiol regulation of CLDN6 are still unclear. We determined the role of estrogen receptors in the regulation of CLDN6 expression in human breast cancer tissues and a cell line. METHODS: CLDN6, estrogen receptor alpha (ERalpha) and estrogen receptor beta (ERbeta) expression in breast cancer tissues were examined using immunohistochemistry. The human breast cancer cell line, MCF-7, which expresses ERalpha but not ERbeta was used. CLDN6 and ERalpha expression were measured by reverse transcriptase-PCR, Western blotting and immunofluorescent staining. Treatments with propyl pyrazole triol (PPT) and ICI 182, 780 (ICI) were performed. RESULTS: The results revealed that CLDN6 expression was related to ERalpha in breast cancer tissues (p=0.033). PPT, an ERalpha-selective ligand, upregulated CLDN6 expression at 10-5 mol/L after 24 hours. The effect of PPT on regulating CLDN6 expression in MCF-7 cells was blocked by ICI. CONCLUSION: These findings suggest that Eralpha reulates CLDN6 expression in breast cancer tissues and that 17beta-estradiol induces CLDN6 expression through an ERalpha pathway in MCF-7 cells.