Articaine is more effective than lidocaine or mepivacaine in rat sensory nerve conduction block in vitro.

The reasons for the relatively high failure rate after inferior alveolar nerve block in dentistry are not fully understood. Therefore, the effectiveness of different anesthetic solutions (2% and 4% lidocaine, 3% mepivacine, 2% and 4% articaine) in depressing the compound action potential amplitude of the sensory fibers in the rat sural nerve was examined under strictly controlled conditions in vitro. After application of an anesthetic solution and stimulation of the nerve with a supramaximal electrical stimulus, a complete disappearance of the compound action potential of the C fibers, but not of the A fibers, was observed in all the experimental groups. Both 2% and 4% articaine more effectively depressed the compound action potential of the A fibers than did other anesthetic solutions. These results are discussed in the light of recent clinical reports finding no differences in the effectiveness between 4% articaine and 2% lidocaine regarding the inferior alveolar nerve block.

Sensitivity of sensory axons to lidocaine nerve block in rats.

The aim of the present study was to test the sensitivity of different classes of sensory axons to lidocaine 2 and 4% nerve block. The basic approach was to examine changes in compound action potential (CAP) of A and C axons of the rat sural nerve induced by 2 or 4% lidocaine nerve block in vitro. CAP in control sural nerves (n = 6 for each experimental group) before nerve block was induced, consisted of the early component (A axons: 0.3 +/- 0.02 ms) and the late component (C axons: 12.2 +/- 1.14 ms) with peak voltage amplitudes 4.4 +/- 1.4 mV and 0.04 +/- 0.02 mV, respectively. Lidocaine 2% nerve block completely abolished the amplitude of CAP of C axons and depressed the amplitude of CAP of A axons to about 20 % of control level. Doubled concentration of lidocaine significantly decreased time taken to develop maximal depression of CAP and significantly increased excitation threshold of sensory A axons, but not of sensory C axons. However, 4% lidocaine did not affect the maximal depression of CAP of sensory A axons. These results support the view, that C axons are more sensitive to lidocaine nerve block than A axons. In addition, our results suggest a population of sensory A axons which is non-sensitive to 2% and 4% lidocaine.

Effect of 10% carbamide peroxide bleaching gel on enamel microhardness, microstructure, and mineral content.

The effect of 10% carbamide peroxide on human enamel subsurface layers was examined. Microhardness, microstructure, and mineral content were studied in such a manner that control and test side were located on the same tooth. Longitudinally sectioned samples were obtained from six teeth and Vickers microhardness of the enamel was measured. Enamel microstructure was analyzed using a scanning electron microscope and subjected to electron probe microanalysis for chemical analysis of calcium (Ca) and phosphorus (P). The concentration of Ca in the bleaching gel was measured spectrophotometrically and the concentration of P was measured photometrically. Results showed that a bleaching gel of 10% carbamide peroxide did not significantly affect the microhardness of the enamel. Scanning electron microscopic analysis showed local changes in enamel microstructure similar to those of initial caries. Electron probe microanalysis showed lowered concentrations of Ca and P; in addition the Ca:P ratio was lowered. There was some Ca and P in the bleaching gel after use. It is concluded that 10% carbamide peroxide causes local microstructural and chemical changes in enamel that are likely not clinically significant.

Failure of inferior alveolar nerve block in endodontics.

Analgesia is essential for successful completion of modern dental procedures. Standard inferior alveolar nerve block (IANB) is the primary method used to achieve mandibular analgesia. Difficulty experienced in obtaining satisfactory analgesia after IANB, especially of an acutely inflamed mandibular molar, remains a common clinical problem. Even when a proper technique is employed, clinical studies show that IANB fails in approximately 30% to 45% of cases. The reasons for failure are not fully understood. Anatomical considerations and abnormal physiological responses in the presence of inflammation as explanations for IANB failure are discussed in this paper.