The manual technique employed in this study produced cleaner root canal walls than the rotary ProFile technique.

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Aims:  Enterococcus faecalis is associated with a significant number of refractory endodontic infections. Previous studies report a prevalence of Ent. faecalis ranging from 24% up to 77% in teeth with failed endodontic treatment. The origin of the micro‐organism remains unclear, as enterococci do not belong to the normal oral microflora. The aim of this study was to determine whether these enterococci were of endogenous or exogenous origin. Methods and Results:  Fifty consecutive patients with apical periodontitis in need of endodontic orthograde re‐treatment were included. Samples were collected from root canals, saliva and faeces and subjected to microbiological culturing. The genetic relationship between Ent. faecalis from root canals and isolates from the different host sources was determined using pulsed‐field gel electrophoresis. In 16% (8/50) of the patients, enterococci were collected from the root canal samples. The genetic analysis showed that the isolates from the root canals were not related to those from the normal gastrointestinal microflora. None of these patients had enterococci in their saliva samples. Conclusions:  Endodontic infections with Ent. faecalis are probably not derived from the patient’s own normal microflora, which indicates that these infections ent. faecalis are of exogenous origin. Significance and Impact of the Study:  This is the first study to genetically compare endodontic infectious Ent. faecalis isolates with isolates from the hosts’ own normal microflora.

The vanilloid receptor VR1 and the vanilloid receptor-like protein VRL-1 are associated with polymodal nociceptors, and may be important for pain processing in normal and injured teeth. Using immunohistochemistry, we have studied the distribution of these receptors in rat pulpal or gingival trigeminal ganglion neurons that were identified through retrograde labeling with fluoro-gold. Twenty-one percent to 34% of tooth pulp-innervating neurons were VRl-positive, while 32%-51% were VRL-1-immunoreactive. However, double-labeling experiments revealed that VR1 and VRL-1 rarely co-existed in the same cells, but rather seemed to be confined to separate subpopulations. Among the gingival neurons, about 25% were VR1-positive and about 41% were VRL-1-immunoreactive. A lesion of the inferior alveolar nerve, which supplies mandibular teeth and gingiva, resulted in a marked down-regulation of VR1 in the affected trigeminal ganglion cells. A down-regulation of VRL-l was also indicated. The results suggest that both VR1 and VRL-1 could have significant roles in pulpal and gingival nociceptive transduction.

The purpose of the present investigation was to find neurophysiological correlates of pain perception. The magnitude and time course of perceived pain was successfully related to the neural discharge evoked by rapid cooling of the tooth surface in 6 dental patients whose lower incisors were to be extracted for prosthodontic reasons. Two cavities were prepared on the facial surface of human lower incisors. The cavities were deepened using hand driven instruments until the pulp was visible through a thin layer of dentin. A metal tube was placed in contact with amalgam on each cavity bottom and fixed in place by composite filling material. The tubes were connected to standard equipment for electrophysiological recordings by a flexible circuit. The magnitude of perceived pain was assessed by a cross-modality matching to finger span in combination with sensory verbal pain descriptors and magnitude estimation. The striking agreement between the integrated nerve activity, probably of the A delta type and pain perception, is of great importance from the methodological point of view since it strongly argues in favor of the appropriateness of the techniques applied here to elucidate the neural substrate of some types of nociception and also to evaluate various means of relieving such pain.