These results suggest that use of the NHF system can prevent hypoxia in dental patients under IVS. Further studies are necessary to determine the appropriate flow rate and indications for NHF in obese patients.

Introduction. A careful assessment of dental anxiety is necessary for its management. The Modified Dental Anxiety Scale (MDAS) is one of the most commonly used questionnaires to measure dental anxiety in the world. The reliability and validity of the Japanese version of MDAS have been demonstrated using undergraduates and a few patients with dental anxiety. The aim of the present study was to examine the reliability and validity of the Japanese version of the MDAS using a wide range of age samples in dental clinics. Methods. A total of 275 outpatients (145 men and 130 women; 21–87 years) from two dental clinics participated in the present study. Dental anxiety was assessed using the Japanese version of the MDAS and the Dental Fear Survey (DFS). The psychometric evaluation included exploratory factor analysis, and Cronbach’s α was used to evaluate for internal consistency. Criterion validity was assessed by correlating the MDAS and DFS scores using Spearman’s correlation coefficient. validity was evaluated by examining related factors’ differences in the MDAS score (e.g., sex and negative dental experiences). Results. Six patients (2.2%) reported high levels of dental anxiety (MDAS score ≥ 19). The internal consistency of the MDAS score was high (Cronbach’s α = 0.88). Dental anxiety was significantly higher among women (P=0.007), in patients with previous negative dental experiences (P<0.001), and among those with lower frequencies of dental visits (P<0.001). The MDAS score was significant and related to age (r = 0.48) and the DFS score (r = 0.87). Factor analysis revealed all items measured only one construct. Conclusions. The Japanese version of the MDAS score was found to be a reliable and valid measure of dental anxiety among dental outpatients. It could be useful for the Japanese dental practitioner to measure dental anxiety in a clinical setting.

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Recent evidence implicates endothelin in nociception, but it is unclear how endothelin activates trigeminal ganglion (TRG) neurons. In the present study, we investigated the expression of the endothelin receptors ETA and ETB and endothelin-induced responses in rat TRG neurons. Double-immunofluorescence studies demonstrated that ETA and ETB were expressed in TRG neurons and that 26% of ETA- or ETB-expressing neurons expressed both receptors. During whole-cell patch-clamp recording, endothelin-1 enhanced an induced current in response to capsaicin, a TRPV1 agonist, in approximately 20% of dissociated neurons. The enhancement was blocked by the PKC inhibitor chelerythrine and by the ETA antagonist BQ-123, but not by the ETB antagonist BQ-788. Ca(2+)-imaging showed that endothelin-1 increased the intracellular Ca(2+) concentration in more than 20% of the dissociated neurons. Importantly, unlike the effect of endothelin-1 on capsaicin-induced current, the Ca(2+) response was largely suppressed by BQ-788 but not by BQ-123. These results suggest that ETA-mediated TRPV1 hyperactivation via PKC activation and ETB-mediated Ca(2+) mobilization occurs in different subsets of TRG neurons. These endothelin-induced responses may contribute to the induction of orofacial pain. The ETB-mediated function in TRG neurons is a special feature in the trigeminal system because of no ETB expression in dorsal root ganglion neurons.

During dental treatments, intraoral appliances frequently induce traumatic ulcers in the oral mucosa. Such mucosal injury-induced mucositis leads to severe pain, resulting in poor quality of life and decreased cooperation in the therapy. To elucidate mucosal pain mechanisms, we developed a new rat model of intraoral wire-induced mucositis and investigated pain mechanisms using our proprietary assay system for conscious rats. A thick metal wire was installed in the rats between the inferior incisors for one day. In the mucosa of the mandibular labial fornix region, which was touched with a free end of the wire, traumatic ulcer and submucosal abscess were induced on day 1. The ulcer was quickly cured until next day and abscess formation was gradually disappeared until five days. Spontaneous nociceptive behavior was induced on day 1 only, and mechanical allodynia persisted over day 3. Antibiotic pretreatment did not affect pain induction. Spontaneous nociceptive behavior was sensitive to indomethacin (cyclooxygenase inhibitor), ONO-8711 (prostanoid receptor EP1 antagonist), SB-366791, and HC-030031 (TRPV1 and TRPA1 antagonists, respectively). Prostaglandin E2 and 15-deoxyΔ12,14-prostaglandin J2 were upregulated only on day 1. In contrast, mechanical allodynia was sensitive to FSLLRY-NH2 (protease-activated receptor PAR2 antagonist) and RN-1734 (TRPV4 antagonist). Neutrophil elastase, which is known as a biased agonist for PAR2, was upregulated on days 1 to 2. These results suggest that prostanoids and PAR2 activation elicit TRPV1- and TRPA1-mediated spontaneous pain and TRPV4-mediated mechanical allodynia, respectively, independently of bacterial infection, following oral mucosal trauma. The pathophysiological pain mechanism suggests effective analgesic approaches for dental patients suffering from mucosal trauma-induced pain.