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The aim of this study was to investigate whether experimental and commercial dental restorative materials with functional fillers can exert a protective anti-demineralizing effect on enamel that is not immediately adjacent to the restoration. Four experimental resin composites with bioactive glass and three commercial restorative materials were investigated. Enamel blocks were incubated in a lactic acid solution (pH = 4.0) at a standardized distance (5 mm) from cured specimens of restorative materials. The lactic acid solution was replenished every 4 days up to a total of 32 days. Surfaces of enamel blocks were periodically evaluated by Knoop microhardness measurements and scanning electron microscopy. The protective effect of restorative materials against acid was identified as enamel microhardness remaining unchanged for a certain number of 4-day acid addition cycles. Additionally, the pH of the immersion medium was measured. While enamel microhardness in the control group was maintained for 1 acid addition cycle (4 days), restorative materials postponed enamel softening for 2–5 cycles (8–20 days). The materials capable of exerting a stronger alkalizing effect provided longer-lasting enamel protection. The protective and alkalizing effects of experimental composites improved with higher amounts of bioactive glass and were better for conventional bioactive glass 45S5 compared to a fluoride-containing bioactive glass. Scanning electron micrographs evidenced the protective effect of restorative materials by showing a delayed appearance of an etching pattern on the enamel surface. A remotely-acting anti-demineralizing protective effect on enamel was identified in experimental composites functionalized with two types of bioactive glass, as well as in three commercial ion-releasing restorative materials.

In many blinding diseases of the retina, loss of function and thus severe visual impairment results from apoptotic cell death of damaged photoreceptors. In an attempt to survive, injured photoreceptors generate survival signals to induce intercellular protective mechanisms that eventually may rescue photoreceptors from entering an apoptotic death pathway. One such endogenous survival pathway is controlled by leukemia inhibitory factor (LIF), which is produced by a subset of Muller glia cells in response to photoreceptor injury. In the absence of LIF, survival components are not activated and photoreceptor degeneration is accelerated. Although LIF is a crucial factor for photoreceptor survival, the detailed mechanism of its induction in the retina has not been elucidated. Here, we show that administration of tumor necrosis factor-alpha (TNF) was sufficient to fully upregulate Lif expression in Muller cells in vitro and the retina in vivo. Increased Lif expression depended on p38 mitogen-activated protein kinase (MAPK) since inhibition of its activity abolished Lif expression in vitro and in vivo. Inhibition of p38 MAPK activity reduced the Lif expression also in the model of light-induced retinal degeneration and resulted in increased cell death in the light-exposed retina. Thus, expression of Lif in the injured retina and activation of the endogenous survival pathway involve signaling through p38 MAPK.

Aim To assess the distribution and deposition of aerosols during simulated periodontal therapy. Methods A manikin with simulated fluorescein salivation was treated by four experienced dentists applying two different periodontal treatment options, i.e. air-polishing with an airflow device or ultrasonic scaling in the upper and lower anterior front for 5 minutes, respectively. Aerosol deposition was quantitatively measured on 21 pre-defined locations with varying distances to the manikins mouth in triplicates using absorbent filter papers. Results The selected periodontal interventions resulted in different contamination levels around the patient’s mouth. The highest contamination could be measured on probes on the patient’s chest and forehead but also on the practitioner’s glove. With increasing distance to the working site contamination of the probes decreased with both devices. Air-polishing led to greater contamination than ultrasonic. Conclusion Both devices showed contamination of the nearby structures, less contamination was detected when using the ultrasonic. Affirming the value of wearing protective equipment we support the need for universal barrier precautions and effective routine infection control in dental practice.

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