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Temporomandibular arthritis will lengthen a rodent’s meal duration. We hypothesized that meal duration would also lengthen after tooth pulp exposure, suggesting that this behavior could be used to measure tooth nociception. To test this hypothesis, we placed rats in feeding units and subjected 4 anterior mandibular molars to pulp exposure, with and without pre-treatment with the analgesic buprenorphine-HCl. In the first study, male Sprague-Dawley rats were placed in computerized sound-attenuated feeding modules, the pulp of 4 molars on the mandible were exposed, and meal duration was measured for 13 days. In a second study, rats were injected with either the analgesic buprenorphine-HCl or saline every 12 hrs; injections were started one day before pulp exposure. Meal duration was determined before and after treatment. In the first study, pulp exposure significantly increased daily meal duration for 8 days. In the second study, pulp exposure lengthened daily meal duration, but the group that was treated with buprenorphine-HCl showed no significant difference compared with control rats without pulp exposure. Evidence supports that a lengthening in meal duration is a response to tooth nociception and that this nociception can be measured for over a week. [ABSTRACT FROM PUBLISHER]

In this study, we systematically investigated fiber demography, based on function and distribution, from the periphery to their destinations in the various central (sub) nuclei in the trigeminal brainstem nuclear sensory complex. Conventional and novel compelling information is provided, demonstrating that the ratio and somatotopy of types A and C sensory fibers at the site of a lesion can elucidate important puzzles in TNP disorders. For instance, we explain how of a major shift in the fibers’ direction and ratio at the level of the trigeminal root entry zone (REZ) influences the pathophysiology of pre- and typical trigeminal neuralgia. As a result, there is a high A/C ratio of oral and peri-oral fibers in the supero-medial region of the REZ, which is mostly susceptible to vascular compression. However, this A/C ratio varies considerably at lower proportions in other areas along the peripheral trigeminal pathway, where an injury (viral, vessel compression, or trauma) can lead to a broader spectrum of fiber involvement and, consequently, pain outcome. In summary, we explain how fiber demography can influence pain quality, location, temporal features, progress, and treatment prognosis of TNP in those patients who develop it. [ABSTRACT FROM PUBLISHER]

The functional impact of GABA (γ-aminobutyric acid)ergic neurons in nociceptive transmission of the spinal trigeminal nucleus is not fully established. Using both the glutamic acid decarboxylase (GAD)67-green fluorescence protein (GFP) knockin mouse and the tooth pulp stimulation model, we performed double-immunofluorescent histochemistry to determine the characteristics of GABAergic neuron activation in the spinal trigeminal nucleus. The number of Fos-positive GABAergic neuronal profiles was significantly increased 2 hrs after tooth pulp stimulation. The Fos/GFP double-labeled neurons were mainly present in superficial laminae of the spinal trigeminal subnucleus interpolaris-caudalis transition (Vi/Vc) and subnucleus caudalis (Vc) on the side ipsilateral to the stimulation. Subsequently, the number of double-labeled neurons decreased gradually and became comparable with that of the controls by 48 hrs. Our results provide direct morphological evidence that a subset of GABAergic neurons in the spinal trigeminal system was activated during tooth pulp stimulation. [ABSTRACT FROM AUTHOR]

The article discusses the author's involvement in studies of pain in the trigeminal system. Topics discussed include his research with Professor Denise Albe-Fessard at the University Rene Descartes in Paris, France, key findings made by the author in conjunction with Albe-Fessard and Jean Azerad, the role of the oralis in orofacial nociception, increased understanding of the trigeminal sensory complex, and a new trigeminal model that attracted attention from other researchers. His experience illustrates how scientific knowledge can be transmitted across disciplines.

An index of authors who have contributed to articles published in this issue is presented.

An index of authors who have contributed to articles published in this issue is presented.

Comparative investigations of odontogenic cells in normally forming teeth and tumors may provide insights into the mechanisms of the differentiation process. The present study is devoted to late phenotypic markers of ameloblast and odontoblast cells, i.e., proteins involved in biomineralization. The in situ expression of amelogenins, keratins, collagens type III and IV, vimentin, fibronectin, osteonectin, and osteocalcin was performed on normal and tumor odontogenic human cells. The pattern of protein expression showed some similarities between ameloblasts and odontoblasts present in normally developing human teeth and cells present in neoplastic tissues of ameloblastic fibroma, ameloblastic fibro-odontomas, and complex odontomas. Amelogenins (for ameloblasts) and osteocalcin (for odontoblasts) were detected in cells with well-organized enamel and dentin, respectively. In contrast, "mixed" cells located in epithelial zones of mixed odontogenic tumors co-expressed amelogenins and osteocalcin, as shown by immunostaining. The presence of osteocalcin transcripts was also demonstrated by in situ hybridization in these cells. Keratins and vimentin were detected in the same epithelial zones. Tumor epithelial cells were associated with various amounts of polymorphic matrix (amelogenin- and osteocalcin-immunoreactive), depending on the types of mixed tumors. No osteocalcin labeling was found in epithelial tumors. This study confirms that the differentiation of normal and tumor odontogenic cells is accompanied by the expression of some common molecules. Furthermore, the gene products present in normal mesenchymal cells were also shown in odontogenic tumor epithelium. These data may be related to a tumor-specific overexpression of the corresponding genes transcribed at an undetectable level during normal development and/or to an epithelial-mesenchymal transition proposed to occur during normal root formation. A plausible explanation for the results is that the odontogenic tumor epithelial cells are recapitulating genetic programs expressed during normal odontogenesis, but the tumor cells demonstrate abnormal expression patterns for these genes. [ABSTRACT FROM AUTHOR]

The article presents abstracts on dental research topics including how the development of dental caries and the formation of dental plaque in rats are affected by the use of sugar substitutes, the discovery of immunoglobulins in dental plaque and histological perspectives on the teeth of children with Down's Syndrome.

An Author/Co-author index who have contributed to articles published in this issue is presented.

A list is presented of attendees of a joint meeting of the Continental European division of the Scandinavian Association for Dental Research, which was held September 12-15 of 1996 in Berlin, Germany.

Neuroplastic changes are known to occur in the CNS in response to injury of peripheral nerves. Previous investigation has demonstrated neuroplasticity in second-order neurons of the subnucleus oralis (SO) of the trigeminal (V) nuclear complex in association with aseptic injury to the tooth pulp. A question arises, therefore, as to whether similar changes occur in response to injury associated with inflammation induced by tooth pulp infection. The effects of tooth pulp infection on the mechanoreceptive fields (RFs) of SO neurons were examined in rats. Infection was established by exposure and removal of the coronal pulp of the mandibular first molar, which was left open to the oral environment for 7 (n = 5) or 28 (n = 6) days. Neurons in SO were then electrophysiologically characterized in chloralose/urethane-anesthetized rats. The RF and the response properties of 118 low-threshold mechanoreceptive (LTM) neurons from seven-day-old rats and 149 LTM neurons from 28-day-old rats were compared with those of 204 LTM neurons tested in 11 untreated (control) rats. Significant differences were noted in RF size and location when control, seven-day-old, and 28-day-old groups were compared. Radiographic examination revealed inconsistencies among examiners in the interpretation of periapical lesions < 2 mm in diameter and general agreement in the identification of periapical lesions < 2 mm in diameter. Histological examination of teeth with pulp exposure revealed superficial necrosis and inflammation without periapical extension in the seven-day-old animals and total pulp necrosis with periapical inflammation, abscess formation, and alveolar bone resorption in the 28-day-old animals. The results indicate that neuroplastic changes in LTM oralis neurons can develop subsequent to tooth pulp infection and that there may be a correlation between the incidence of these changes and the extension of the attending inflammation from the pulp to the dental supporting tissues. [ABSTRACT FROM AUTHOR]

Abstracts are presented for several articles, including "Wear Resistance and Increase of Wear Resistance with Time of Traditional and Light Curing Glass-Ionomers," "Fluoride release and uptake by five year old glass ionomer speciments," and "Putative Periodontal Pathogens in Interdental Supragingival Plaque of Young Periodontially Healthy Adults."

The article presents abstracts on dental topics which include assessing the quality of dental amalgam restorations, an examination of the behavior of various copper amalgam alloys and reasons for the failure or survival of dental amalgam restorations.