RESUMO
From the point of view of oral rehabilitation, the treatment of extensive tooth wear requires a prosthetic approach. Physiological tooth wear is considered as a normal processand generally does not require treatment, but excessive tooth wear causes problems like inadequate occlusion and esthetics. Changes of occlusal vertical dimension should bemade through accurate diagnosis and analysis. Also, the patient’s adaptation to the changed occlusal vertical dimension should be assessed over time. This case was a60-year-old male patient who complained of a decrease in chewing function and esthetics due to severe tooth wear. Full-mouth rehabilitation was performed with a tooth supportedfixed prosthesis. An occlusal stabilization splint and provisional restoration were used to evaluate the adaptation to increased occlusal vertical dimension and induce astable centric relation position. After that, monolithic zirconia prosthesis was delivered. We report this as a satisfactory functional recovery and esthetics. (J Korean AcadProsthodont 2020;58:121-9)
RESUMO
Flavonoids have been shown to affect calcium signaling in neurons. However, there are no reports on the effect of apigenin on glutamate-induced calcium signaling in neurons. We investigated whether apigenin affects glutamate-induced increase of free intracellular Ca2+concentration ([Ca2+]i) in cultured rat hippocampal neurons, using fura-2-based digital calcium imaging and microfluorimetry. The hippocampal neurons were used between 10 and 13 days in culture from embryonic day 18 rats. Pretreatment of the cells with apigenin (1micrometerto 100micrometer for 5 min inhibited glutamate (100 micrometer 1 min) induced [Ca2+]i increase, concentration-dependently. Pretreatment with apigenin (30micrometer for 5 min significantly decreased the [Ca2+]i responses induced by two ionotropic glutamate receptor agonists, alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic (AMPA, 10 micrometer 1 min) and N-methyl-D-aspartate (NMDA, 100 micrometer 1 min), and significantly inhibited the AMPA-induced peak currents. Treatment with apigenin also significantly inhibited the [Ca2+]i response induced by 50 mM KCl solution, decreased the [Ca2+]i responses induced by the metabotropic glutamate receptor agonist, (S)-3,5-dihydroxyphenylglycine (DHPG, 100micrometer 90 s), and inhibited the caffeine (10 mM, 2 min)-induced [Ca2+]i responses. Furthermore, treatment with apigenin (30micrometer significantly inhibited the amplitude and frequency of 0.1 mM [Mg2+o-induced [Ca2+]i spikes. These data together suggest that apigenin inhibits glutamate-induced calcium signaling in cultured rat hippocampal neurons.