Effect of bristle stiffness of manual toothbrushes on normal and demineralized human enamel-An in vitro profilometric study.

OBJECTIVE: To compare the brushing abrasion carried out by manual toothbrushes with different bristle types (hard and soft) on normal and demineralized human enamel. MATERIALS AND METHODS: Thirty enamel blocks (N = 30) were prepared and were randomly divided into three main groups: A, teeth kept in artificial saliva with no brushing (control, n = 2); B, teeth brushed with toothbrushes with hard bristles (n = 14); and C, teeth brushed with toothbrushes with soft bristles (n = 14). Seven teeth belonging to groups B and C were brushed normally, and the remaining seven were demineralized before brushing experiments with 6 wt.% citric acid (pH = 2.2) for 5 minutes. The brushing experiments were carried out twice a day for 2 mins for 7 days inside a toothbrush simulation machine. The changes in the surface of enamel (prebrushing and post-brushing) were evaluated using non-contact profilometry. The results were analysed statistically using Kruskal-Wallis test and the Wilcoxon signed rank test. RESULTS: For both normal and demineralized enamel, toothbrushes with soft bristles caused more abrasion. The results revealed significant differences (P = .055) in the surface roughness values between the four groups prebrushing. Within each group, the prebrushing and post-brushing surface roughness value differences were all statistically significant (P < .05). CONCLUSIONS: The results demonstrate that soft bristles caused more abrasion as compared with the hard bristles. These results could have an impact on the toothbrush recommendations for patients.

Antagonistic interactions between dexamethasone and fluoxetine modulate morphodynamics and expression of cytokines in astrocytes.

The "plasticity hypothesis" proposes that major depression is caused by morphological and biochemical modifications in neurons and astrocytes and those beneficial pharmacological effects of selective-serotonin-reuptake-inhibitors (SSRI) are at least partially associated with modifications of cellular communications between these cells. In this study we examined effects of the antidepressant fluoxetine on cultured astrocytes that were, in some cases, pretreated with dexamethasone, a cortisol analog known to trigger depressive disorder. Primary rat astrocytes were purified and treated with dexamethasone and the SSRI fluoxetine in physiological concentrations so that both drugs did not affect cell viability. Expression of interleukin-2 (IL-2) and glia-derived-neurotrophic-factor (GDNF) were analyzed and monitored and cell viability, apoptosis, cluster formation, particle-removing capacity and cell mobility were also monitored. Pre-studies without any drugs on mixed neuron-astrocyte co-cultures suggested that astrocytes interacted with neurons and other brain cells in vitro by actively assembling them into clusters. Treatment of purified astrocytes with dexamethasone significantly decreased their mobility compared to controls but had no effect on cluster formation. Dexamethasone-treated cells removed fewer extracellular particles derived from dead cells and cell debris. Both effects were abolished by simultaneous application of fluoxetine. Intracellular IL-2 increased, while GDNF amount expression was diminished following dexamethasone treatment. Simultaneous administration of fluoxetine reversed dexamethasone-triggered IL-2 elevation but had no effect on decreased GDNF concentration. These results suggest that mobility and growth factor equilibrium of astrocytes are affected by dexamethasone and by fluoxetine and that fluoxetine could reverse some changes induced by dexamethasone.