Quercetin reduces erosive dentin wear: Evidence from laboratory and clinical studies

Objective. The aim of the present study was to evaluate the effect of quercetin on the acid resistance of human dentin through both laboratory and clinical studies. Methods. Two hundred and twelve dentin blocks (2 mm x 2 mm x 2 mm) were prepared and used. For the laboratory study, dentin specimens were randomly divided into 8 groups (n = 12): deionized water, ethanol, 1.23 x 10(4) mu g/ml sodium fluoride (NaF), 120 mu g/ml chlorhexidine, 183.2 mu g/ml epigallocatechin gallate (EGCG), and 75 mu g/ml, 150 g/ml, and 300 mu g/ml quercetin (Q75, Q150, and Q300). The specimens were treated with the respective solutions for 2 min and then subjected to in vitro erosion (4 cycles/d for 7 d). The surface microhardness loss (%SMH1), erosive dentin wear, and surface morphology were evaluated and compared. For the impact on MMP inhibition, the release of crosslinked carboxyterminal telopeptide of type I collagen (ICTP) and the thickness of the demineralized organic matrix (DOM) were measured using additional dentin specimens. For the clinical study, the specimens were treated with NaF or Q300 for 2 min and then subjected to in vivo erosion (4 cycles/d for 7 d). The %SMH1 and erosive dentin wear of the specimens were measured to determine whether quercetin similarly inhibits erosion in situ. Results. The quercetin-treated group had a significantly lower SMH1 and erosive dentin wear than any other group, and the effect was concentration-dependent in vitro (P < 0.05). Dentin treated with quercetin produced significantly less ICTP and had a thicker DOM than the control dentin (P < 0.05). After in vivo erosion, the %SMH1 and erosive dentin wear of the Q300 group were significantly lower than those of the control group (P < 0.05). Significance. The application of quercetin was shown, for the first time, to increase the acid resistance of human dentin, possibly through MMP inhibition and DOM preservation. (C) 2020 The Academy of Dental Materials. Published by Elsevier Inc. All rights reserved.