The vasodilatory effect of a synthetic polymer-based root canal material on thoracic aorta.

AIM: To test the hypothesis that, Epiphany, either in its mixed form or as separate components, can alter the vascular reactivity of isolated rat thoracic aorta. The possible mechanism of its vascular action was also investigated. METHODOLOGY: The relaxant effect of the base, the catalyst and mixed Epiphany on isolated rat aortic rings pre-contracted with phenylephrine (PE) was tested. The aortic rings were then incubated with either nitric oxide synthase (NOS) inhibitor, cyclooxygenase (COX) inhibitor or K(+) channel inhibitors; after pre-contraction with PE, relaxations to the various compounds of Epiphany were examined. In another set of experiments, to investigate the Ca(2+)channel antagonistic effect of the Epiphany, the effect of these compounds in Ca(2+)-free solution on extracellular Ca(2+)(CaCl(2))-induced contraction in high-K(+) pre-challenged rings (in K(+)-depolarized rings) was examined to determine whether the direct inhibition of [Ca(2+)] influx increase accounted for the vasodilatory effects of these compounds. For comparison, L-type Ca(2+)channel blocker nifedipine (1 micromol L(-1)), instead of Epiphany compounds, was assayed in adjacent rat aortic rings in parallel. RESULTS: The catalyst and the mixture of Epiphany induced concentration-dependent relaxations. However, the base of Epiphany did not cause relaxation in rat aorta. The relaxation responses were not significantly altered by incubation of aorta with NOS, COX and potassium channel inhibitors. Whilst nifedipine, the catalyst and the mixture of Epiphany inhibited CaCl(2)-induced contractions (P < 0.05), the base of Epiphany did not inhibit CaCl(2)-induced contractions significantly (P > 0.05). CONCLUSION: Epiphany induced relaxation of rat aorta via a calcium antagonistic effect. Provided that the vasodilatory effect elicited by Epiphany can be reversed by the circulation, its haemorrhagic potential by virtue of permanent vascular dilatation can be ignored.

Dentin hypersensitivity: a randomized clinical comparison of three different agents in a short-term treatment period.

OBJECTIVE: Dentin hypersensitivity, or what patients may describe as "sensitive teeth," is defined as a short, sharp pain arising from exposed dentin in response to thermal, evaporative, tactile, electrical, osmotic or chemical stimuli. It is widely accepted that dentin hypersensitivity is an uncomfortable condition that also affects function and quality of life. This study determines the differences in efficiency of three desensitizing products when compared with a placebo. METHODS: A randomized controlled clinical trial was conducted to compare three different professional dentin desensitizer agents in 52 patients. The age and sex of the patients was recorded. Gluma Desensitizer (Heraeus Kulzer), UltraEZ (Ultradent Products, Inc) and Duraphat (Colgate Oral Pharmaceuticals, Inc, New York, NY, USA) were used as desensitizer agents and distilled water was used as the placebo. The baseline measurement of the dentin hypersensitivity was made by using a visual analog scale (VAS). Twenty-four hours and seven days after application of the desensitizer agents and placebo, a new VAS analysis was conducted for patients' sensitivity level. The desensitizer agents were compared in terms of mean values, and ANOVA was used for testing differences among the groups (p<0.05). RESULTS: The results showed that the mean pain scores of the placebo group were significantly higher than that of the study groups (p<0.05). The VAS analysis revealed a significant decrease in dentin hypersensitivity over time with the use of agents (p<0.05). No statistically significant difference was found among the three desensitizing agents (p>0.05). CONCLUSIONS: These three desensitizing agents, which contain different active ingredients, were effective in relieving dentin hypersensitivity. However, no superiority was found in dentin sensitivity relief among the agents.

Brain aluminium accumulation and oxidative stress in the presence of calcium silicate dental cements.

Mineral trioxide aggregate (MTA) is a calcium silicate dental cement used for various applications in dentistry. This study was undertaken to test whether the presence of three commercial brands of calcium silicate dental cements in the dental extraction socket of rats would affect the brain aluminium (Al) levels and oxidative stress parameters. Right upper incisor was extracted and polyethylene tubes filled with MTA Angelus, MTA Fillapex or Theracal LC, or left empty for the control group, were inserted into the extraction socket. Rats were killed 7, 30 or 60 days after operation. Brain tissues were obtained before killing. Al levels were measured by atomic absorption spectrometry. Thiobarbituric acid reactive substances (TBARS) levels, catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities were determined using spectrophotometry. A transient peak was observed in brain Al level of MTA Angelus group on day 7, while MTA Fillapex and Theracal LC groups reached highest brain Al level on day 60. Brain TBARS level, CAT, SOD and GPx activities transiently increased on day 7 and then returned to almost normal levels. This in vivo study for the first time indicated that initial washout may have occurred in MTA Angelus, while element leaching after the setting is complete may have taken place for MTA Fillapex and Theracal LC. Moreover, oxidative stress was induced and antioxidant enzymes were transiently upregulated. Further studies to search for oxidative neuronal damage should be done to completely understand the possible toxic effects of calcium silicate cements on the brain.