RESUMO
OBJECTIVE: The aim of the study is to evaluate the effect of extrinsic pigmentation on the dimensional stability, hardness, detail reproduction, and color of a silicone after thermocycling. MATERIALS AND METHODS: Sixty samples of MDX4-4210 silicone (Dow Corning Corporation Medical Products) with intrinsic pink pigment (H-109-P, Factor II) and intrinsic opacifier (TiO) were fabricated. Two groups were created: Group 1-only intrinsic pigmentation (H-109P, Factor II + TiO) (Control); and Group 2-intrinsic (H-109P, Factor II + TiO) and extrinsic (Tan FE - 215, Factor II) pigmentation. The following tests were performed for each group: dimensional stability, Shore A hardness, detail reproduction, and color. Readings for the tests were taken before and after thermocycling (2,000 cycles). For dimensional stability and hardness, two-way analysis of variance (ANOVA) was used. One-way ANOVA was used for the color test. In case of significant statistical difference, the Tukey test was applied (p <0.05). All samples achieved the same detail reproduction score, therefore, no statistical evaluation was performed. RESULTS: For the dimensional stability test, comparing the initial time with the final time, there was a significant contraction in both groups after thermocycling. For the hardness test, comparing the time points, only group 1 showed a significant reduction in hardness after thermocycling. Groups 1 and 2 scored 2 for the detail reproduction test, before and after thermocycling. Comparing group 1 with group 2, there was no significant difference for color change. CONCLUSION: Based on the tests performed, extrinsic pigmentation did not show a negative effect on silicone, and therefore it can be indicated. The results of the dimensional, hardness, detail reproduction and color evaluations of the MDX4-4210 silicone were clinically acceptable in all cases in the groups with and without extrinsic pigmentation.
RESUMO
Chronic consumption of hyperpalatable and hypercaloric foods has been pointed out as a factor associated with cognitive decline and memory impairment in obesity. In this context, the integration between peripheral and central inflammation may play a significant role in the negative effects of an obesogenic environment on memory. However, little is known about how obesity-related peripheral inflammation affects specific neurotransmission systems involved with memory regulation. Here, we test the hypothesis that chronic exposure to a highly palatable diet may cause neuroinflammation, glutamatergic dysfunction, and memory impairment. For that, we exposed C57BL/6J mice to a high sugar and butter diet (HSB) for 12 weeks, and we investigated its effects on behavior, glial reactivity, blood-brain barrier permeability, pro-inflammatory features, glutamatergic alterations, plasticity, and fractalkine-CX3CR1 axis. Our results revealed that HSB diet induced a decrease in memory reconsolidation and extinction, as well as an increase in hippocampal glutamate levels. Although our data indicated a peripheral pro-inflammatory profile, we did not observe hippocampal neuroinflammatory features. Furthermore, we also observed that the HSB diet increased hippocampal fractalkine levels, a key chemokine associated with neuroprotection and inflammatory regulation. Then, we hypothesized that the elevation on glutamate levels may saturate synaptic communication, partially limiting plasticity, whereas fractalkine levels increase as a strategy to decrease glutamatergic damage.