AIM: To determine the incremental and total enamel loss when enamel surfaces are exposed to multiple etching cycles and to assess the relative attenuation coefficient after multiple etching cycles and resin infiltration treatment.
METHODS: Ninety extracted sound human premolars teeth were divided into 9 groups (n = 10); with each consecutive group having one additional etching cycle up to 9 cycles. The teeth were scanned with optical coherence tomography and enamel loss and attenuation coefficient were measured with MATLAB software. Enamel loss (one-way ANOVA, p ≤ 0.05) and attenuation coefficient (two-way ANOVA, p ≤ 0.05) were statistically analyzed.
RESULTS: There was a significant total enamel loss of more than 33% found at the 7th etching cycle and more. There was no statistically significant difference in the incremental mean depth of penetration of resin between various etching cycles (F(8, 134) = [2.016], one-way ANOVA, p = 0.185).
CONCLUSION: This study recommends that etching should not be repeated more than seven cycles to prevent excessive enamel loss. Following eight etching cycles, resin infiltration penetration appears approximately equal to that of healthy enamel.
AIM OF THE STUDY: The molecular mechanisms of the anti-inflammatory properties of M. accedens are not yet understood. Therefore, we examined those mechanisms using a methanol extract of M. accedens (Ma-ME) and determined the target molecule in macrophages.
MATERIALS AND METHODS: We evaluated the anti-inflammatory effects of Ma-ME in lipopolysaccharide (LPS)-stimulated RAW264.7 cells and in an HCl/EtOH-triggered gastritis model in mice. To investigate the anti-inflammatory activity, we performed a nitric oxide (NO) production assay and ELISA assay for prostaglandin E2 (PGE2). RT-PCR, luciferase gene reporter assays, western blotting analyses, and a cellular thermal shift assay (CETSA) were conducted to identify the mechanism and target molecule of Ma-ME. The phytochemical composition of Ma-ME was analyzed by HPLC and LC-MS/MS.
RESULTS: Ma-ME suppressed the production of NO and PGE2 and the mRNA expression of proinflammatory genes (iNOS, IL-1β, and COX-2) in LPS-stimulated RAW264.7 cells without cytotoxicity. Ma-ME inhibited NF-κB activation by suppressing signaling molecules such as IκBα, Akt, Src, and Syk. Moreover, the CETSA assay revealed that Ma-ME binds to Syk, the most upstream molecule in the NF-κB signal pathway. Oral administration of Ma-ME not only alleviated inflammatory lesions, but also reduced the gene expression of IL-1β and p-Syk in mice with HCl/EtOH-induced gastritis. HPLC and LC-MS/MS analyses confirmed that Ma-ME contains various anti-inflammatory flavonoids, including quercetin, daidzein, and nevadensin.
CONCLUSIONS: Ma-ME exhibited anti-inflammatory activities in vitro and in vivo by targeting Syk in the NF-κB signaling pathway. Therefore, we propose that Ma-ME could be used to treat inflammatory diseases such as gastritis.