Adhesion between fiber post and root dentin: evaluation of post surface conditioning for bond strength improvement.

AIM: The aim of this paper was to evaluate two surface conditioning methods associated with the application of adhesive on the post surface for improving the bond to resin cement. METHODS: Sixty single-rooted bovine teeth were sectioned at 16 mm in length, prepared (9 mm depth), embedded in a PVC cylinder using acrylic resin, and allocated into 3 groups (N.=20) according to post surface treatment: cleaning with ethanol (control group); etching with hydrogen peroxide; etching with hydrofluoric acid. Ten posts for each group were silanized and other 10 posts were silanized and received an adhesive agent. The posts were cemented with self-adhesive resin cement (RelyX U100 resin cement). All teeth were sectioned perpendicularly to the long axis (2 mm thickness per slice), submitted to push out bond strength testing and the type of failure was recorded. The obtained data were submitted to two-way ANOVA and Turkey´s test, with the level of significance set at 5%. RESULTS: Neither the hydrofluoric acid or hydrogen peroxide post surface treatment, nor the adhesive application, had an influence on bond strength values. The main type of failure was adhesive between cement and dentin. CONCLUSION: Etching and the application of an adhesive on the post surface did not presented a significant influence on the bond strength results for the fiber post resin cement-root dentin assembly. The cement appears to adhere very well to the fiber post surface rather than the dentin surface.

Complexes trans-[RuCl(2)(nic)(4)] and trans-[RuCl(2)(i-nic)(4)] as free radical scavengers.

This study evaluates the action of the new ruthenium complexes trans-RuCl(2)(nic)(4)] (I) and trans-[RuCl(2)(i-nic)(4)] (II) as free radical scavengers. In our experiments, both compounds acted as scavengers of superoxide anion (O(2)*(-)), hydroxyl radicals (HO*) and nitrogen monoxide (formally known as 'nitric oxide'; NO*). In addition, complexes I and II potentiated the release of NO* from S-nitroso-N-acetyl-DL-penicilamine (SNAP), a NO* donor. Complex II, but not I, also decreased the nitrite levels in culture media of activated macrophages. A hypsochromic shift of lambda(max) and a significant change in half-wave potential (E(1/2)) was observed when NO* was added to the Complex II. Thiobarbituric reactive substance (TBARS) levels were significantly reduced in rats treated for 1 week with Complex II plus tert-butylhydroperoxide, when compared to rats treated only with tert-butylhydroperoxide. None of the complexes showed cytotoxicity. These findings support the suggestion that the new ruthenium complexes, especially trans-[RuCl(2)(i-nic)(4)] or its derivatives, might provide potential therapeutic benefits in disorders where reactive nitrogen (RNS) or oxygen (ROS) species are involved.

Synthesis, potentiometric titration, electrochemical investigation and biological properties of trans-[RuCl2(dinic)4] (dinic = 3,5-pyridinecarboxylic acid).

This work discusses both the synthesis of trans-[RuCl2(dinic)4], dinic = 3,5-pyridinecarboxylic acid, and its main characteristics including potentiometric titration, spectroscopic and electrochemical properties, and some biological properties. The complex was synthesized using ruthenium blue solution as the precursor in a synthetic route. The complex was characterized using electronic spectroscopy, vibrational FT-IR spectroscopy, and Raman spectroscopy, as well as 1H and 13C NMR. The results indicated that the complex exhibits a trans-geometry. Cyclic voltammetry carried out in water:acetone 1:1 solution revealed a quasi-reversible process centered on the Ru(II) atom, as well as a dependence of the redox potential, E1/2, on pH. An analysis of the electronic spectra revealed that the MLCT (metal ligand charge transfer) band underwent a hypsochromic shift as the pH increased. Spectroelectrochemical analysis indicated that the visible region band progressively faded out upon oxidation. The equilibrium constants for the eight protons of the complex were determined by potentiometric titration. The complex neither inhibits the activity of nitrogen monoxide synthase nor acts as a scavenger for nitrogen monoxide. Nevertheless, the complex shows antinociceptive properties and acts as a scavenger for hydroxyl radicals.

Antinociceptive properties and nitric oxide synthase inhibitory action of new ruthenium complexes.

This study evaluates the actions of the new ruthenium complexes trans-[RuCl2(nic)4] (Complex I) and trans-[RuCl2(i-nic)4] (Complex II) as antinociceptives, and their interaction with nitric oxide isoenzymes and with acetylcholine-induced relaxation of rat and rabbit aorta. Complex II inhibited, in a graded manner, neuronal and inducible nitric oxide (NO) synthase, and was about two fold more effective in inhibiting the neuronal NO synthase than the inducible form of the enzyme. Complex I was inactive. Both complexes failed to interfere with constitutive endothelial nitric oxide synthase because they did not change the mean arterial blood pressure of rats. The vasorelaxant effect of acetylcholine was markedly antagonised by the Complexes I and II in rings of both rat and rabbit aorta. Complexes I and II, given intraperitoneally, like N(omega)-nitro-L-arginine methyl ester (L-NAME) and N(G)-nitro-L-arginine (L-NOARG), inhibited, in a graded manner, both phases of the pain response induced by formalin. The actions of L-NAME, L-NOARG and Complex II, but not that of Complex I, were largely reversed by L-arginine. Both complexes failed to affect the motor response of animals in the rota-rod test and had no effect in the hot-plate assay. Together, these findings provide indications that the new ruthenium complexes, especially Complex II and its derivatives, might be of potential therapeutic benefit in the management of pain disorders.