The purpose of this study was to compare the bond strengths and debonded interfaces achieved with light-cured resin-modified glass ionomer cement (RMGIC) and conventional light-cured composite resin. In addition, the effects of acid etching and water contamination were examined. One hundred human premolars were randomly divided into five equal groups. The mini Dyna-lock upper premolar bracket was selected for testing. The first four groups were treated with light-cured RMGIC with or without 15 per cent phosphoric acid-etching treatment and with or without water contamination preceding bracket bonding. The control samples were treated with the conventional light-cured Transbond composite resin under acid etching and without water contamination. Subsequently, the brackets were debonded by tensile force using an Instron machine. The modified adhesive remnant index (ARI) scores were assigned to the bracket base of the debonded interfaces using a scanning electron microscope. The bond strength and modified ARI scores were determined and analysed statistically by one-way analysis of variance and chi-square test. Under all four conditions, the bond strength of the light-cure RMGIC was equal to or higher than that of the conventional composite resin. The highest bond strength was achieved when using RMGIC with acid etching but without water contamination. The modified ARI scores were 2 for Fuji Ortho LC and 3 for Transbond. No enamel detachment was found in any group. Fifteen per cent phosphoric acid etching without moistening the enamel of Fuji Ortho LC provided the more favourable bond strength. Enamel surfaces, with or without water contamination and with or without acid etching, had the same or a greater bond strength than Transbond.
Hypertension is a complex disorder with high prevalence rates worldwide. Many patients take dihydropyridines, such as nifedipine, amlodipine, nicardipine, and felodipine, to control their blood pressure. Patients with dihydropyridine-induced gingival overgrowth (DIGO) are frequently found in periodontal clinic (Figure 1).Several proinflammatory cytokines secreted into the gingival crevicular fluid (GCF), including interleukin (IL)-1β, tumor necrosis factor-α, IL-6, and IL-8, can induce periodontal tissue destruction (Ruhl et al., 2004). IL-1 and IL-6 are the most active proinflammatory cytokines involved in inflammatory diseases such as periodontitis (Cardoso et al., 2018). As a principal mediator of inflammatory responses, IL-1β can be monitored as a standard biomarker to predict the prognosis when treating chronic periodontitis (Lu & Chei, 2005). IL-6 is a multifunctional cytokine mainly produced by lymphocytes, monocytes, and fibroblasts. Elevated IL-6 levels in the blood or biological fluids were reported to be associated with immunopathologies such as tissue injury, allergies, and some inflammatory diseases (Hirano et al., 1990;Young et al., 2014).Moreover, IL-6 was demonstrated to play a major role in collagen
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