Incidence of microcracks in maxillary first premolars after instrumentation with three different mechanized file systems: a comparative ex vivo study.

OBJECTIVES: The objective of this study is to determine the potential for microcracks in the radicular dentin of first maxillary premolars using three different mechanized endodontic instrumentation systems. METHODS: Eighty extracted maxillary first premolars with two root canals and no externally visible microcracks were selected. Root canal instrumentation was performed with either the ProTaper file system, the WaveOne primary file, or the self-adjusting file (SAF). Teeth with intact roots served as controls. The roots were cut into segments and examined with an intensive, small-diameter light source that was applied diagonally to the entire periphery of the root slice under ×20 magnification; the presence of microcracks and fractures was recorded. Pearson's chi-square method was used for statistical analysis, and significance was set at p < 0.05. RESULTS: Microcracks were present in 30 and 20 % of roots treated with the ProTaper and WaveOne systems, respectively, while no microcracks were present in the roots treated with the SAF (p = 0.008 and p = 0.035, respectively). Intact teeth presented with cracks in 5 % of the roots. The intensive, small-diameter light source revealed microcracks that could not be detected when using the microscope's light alone. CONCLUSIONS: Within the limitations of this study, it could be concluded that mechanized root canal instrumentation with the ProTaper and WaveOne systems in maxillary first premolars causes microcracks in the radicular dentin, while the use of the SAF file causes no such microcracks. CLINICAL RELEVANCE: Rotary and reciprocating files with large tapers may cause microcracks in the radicular dentin of maxillary first premolars. Less aggressive methods should be considered for these teeth.

EGL-36 Shaw channels regulate C. elegans egg-laying muscle activity.

The C. elegans egl-36 gene encodes a Shaw-type potassium channel that regulates egg-laying behavior. Gain of function [egl-36(gf)] and dominant negative [egl-36(dn)] mutations in egl-36 cause reciprocal defects in egg laying. An egl-36::gfp reporter is expressed in the egg-laying muscles and in a few other tissues. Expression of an egl-36(gf) cDNA in the egg-laying muscles causes behavioral defects similar to those observed in egl-36(gf) mutants. Gain of function EGL-36 subunits form channels that are active at more negative potentials than wild-type channels. The egl-36(gf) alleles correspond to missense mutations in an amino terminal subunit assembly domain (E138K) and in the S6 transmembrane domain (P435S), neither of which were previously implicated in the voltage dependence of channel activation. Altogether, these results suggest that EGL-36 channels regulate the excitability of the egg-laying muscles.

Modulation of serotonin-controlled behaviors by Go in Caenorhabditis elegans.

Seven transmembrane receptors and their associated heterotrimeric guanine nucleotide-binding proteins (G proteins) have been proposed to play a key role in modulating the activities of neurons and muscles. The physiological function of the Caenorhabditis elegans G protein Go has been genetically characterized. Mutations in the goa-1 gene, which encodes an alpha subunit of Go (G alpha o), cause behavioral defects similar to those observed in mutants that lack the neurotransmitter serotonin (5-HT), and goa-1 mutants are partially resistant to exogenous 5-HT. Mutant animals that lack G alpha o and transgenic animals that overexpress G alpha o [goa-1(xs) animals] have reciprocal defects in locomotion, feeding, and egg laying behaviors. In normal animals, all of these behaviors are regulated by 5-HT. These results demonstrate that the level of Go activity is a critical determinant of several C. elegans behaviors and suggest that Go mediates many of the behavioral effects of 5-HT.