Local anesthesia known as the safe and essential procedure to control pain in dentistry may cause sensory changes such as paresthesia or altered taste at the affected sites after even successful local anesthesia. Although the prognosis of the nerve injuries after local anesthesia is favorable, it might cause prolonged problems such as dysesthesia. The lingual nerve is a single fascicle at the level of the lingual among 1/3 of patients and more movable during regeneration compared to the inferior alveolar nerve after the injury. As a result, the lingual nerve is more vulnerable and has poorer outcomes. More vigilant clinical considerations are required to the lingual nerve injury after local anesthesia. Generally, more than 80% of cases are spontaneously resolved within 2 weeks after the local anesthesia even without any specific treatment. However, the patient having long lasting abnormal sensations more than 2 weeks needs specialists' care for further assessment. In case of dysesthesia which is a symptom of neuropathic pain, immediate referral to specialists is mandatory. The exact mechanism, how to prevent its occurrence, or specific treatments of the nerve injury related to the local anesthesia have not been elucidated. To prepare clinical or medicolegal problems, many cautious considerations are given to the patients who complain sensory changes after local anesthesia.

Background: About 60% of patients with epilepsy showed a variety of complications after returning home. The purpose of this study is to get further information and to help in the anesthetic management of the disable patients with epilepsy. Methods: After searching the outpatient anesthesia list of Seoul National University Dental Hospital clinic of the disabled from September 2010 to March 2012, we found total 83 patient cases who were taking antiepileptic drugs. A nurse of anethesiology department called to the patient's home after general anesthesia and got surveys with questionnaires form filled with complications at home. We enrolled total of 51 patients who agreed to participate this survey. And we also reviewed pre-anesthesia evaluation sheet, anesthesia record, and recovery and discharge record. Results: 11 of 51 (21.6%) patients had seizure convulsion at home within 1 weeks. 33.4% of patients who had at least once seizure attack per week had a seizure attack within 3 days. And 50% of once a month frequency patients had a seizure attack within 1 week. 33% of 1 - 3 seizure attacks per year patient group had a convulsion within 1 week. But there was no seizure attack within 1 week in whom had no seizure attack history during more than 1 year. Conclusions: After dental treatment, patient taking anticonvulsant have so many complications-especially seizure, more than we respected. We need more research about handle these problems.

Background: Remifentanil, an ultra-short-acting mu-opioid receptor agonist, is unique from other opioids because of its esterase-based metabolism, minimal accumulation, and very rapid onset and offset of clinical action. Remifentanil can prevent the inflammatory response and can suppress inducible nitric oxide synthase expression in a septic mouse model. However, the effects of remifentanil on human keratinocyte and autophagy have yet to be fully elucidated during hypoxia-reoxygenation. Here we investigated whether remifentanil confers protective effect against hypoxia-reoxygenation in human keratinocyte and, if so, whether autophagy mediates this effect. Methods: The human keratinocytes were cultured under 1% oxygen tension. The cells were gassed with 94% $N_2$, and 5% $CO_2$ and incubated for 24 h at $37^{\circ}C$. To determine whether the administration of affects human keratinocytes hypoxia-reoxygenation injury, cells were then exposed to various concentrations of remifentanil (0.01, 0.1, 0.5 and 1 ng/ml) for 2 h. After remifentanil treatment, to simulate reoxygenation and recovery, the cells were reoxygenated for 12 h at $37^{\circ}C$. Control group did not receive remifentanil treatment. Normoxia group did not receive hypoxia and remifentanil treatment for 36 h. 3-MA group was treated 3-methyladenine (3-MA) for 1h before remifentanil treatment. Cell viability was measured using a quantitative colorimetric assay with MTT, showing the mitochondrial activity of living cells. Cells were stained with fluorescence and analyzed with Western blot analysis to find out any relations with activation of autophagy. Results: Prominent accumulation of autophagic specific staining MDC was observed around the nuclei in RPT group HaCaT cells. Similarly, AO staining, red fluorescent spots appeared in RPT group HaCaT cells, while the Normoxia, control and 3-MA groups showed mainly green cytoplasmic fluorescence. We here examined activation of autophagy related protein under H/R-induced cells by Western blotting analysis. Atg5, Beclin-1, LC3-II (microtubule-associated protein 1 light chain 3 form II) and p62 was elevated in RPT group cells. But they were decreased when autophagy was suppressed by 3-MA (Fig. 5). Conclusions: Although the findings of this study are limited to an in vitro interpretation, we suggest that remifentanil may have a beneficial effect in the recovery of wound from hypoxia-reoxygenation injury.

Background: Angiogenesis has been recognized an essential precondition for osteogenesis. Because reduction and disruption of the blood supply to tissue cause tissue hypoxia, pathological bone loss affected by hypoxia often can occur in various clinical conditions. The effects of propofol on the process of osteogenesis have received little direct attention. Therefore, we investigated the effect of propofol on the growth and function of osteoblasts under hypoxic condition. Methods: After propofol (3, 30, $300{\mu}M$) preconditioning for 2 hours, hFOB 1.19 human osteoblast cells were cultured under 1 % oxygen tension for 48 hours. Using real time PCR and western blot analysis, we analyzed the expression of, BMP-2, TGF-${\beta}1$, type I collagen, osteocalcin, HIF-1s and Akt. Cell viability was also determined by MTT assay. Results: Propofol preconditioning on hypoxic-cultured osteoblast promoted the expressions of BMP-2, TGF-${\beta}1$, type I collagen and osteocalcin and induced hypoxia-mediated HIF-1 activation and the expression of Akt protein. Propofol with $300{\mu}M$ significant decreased cell viability compared to control. Conclusions: Clinically relevant concentrations of propofol are not cytotoxic to hypoxic osteoblasts in vitro. Propofol preconditioning on hypoxic-cultured osteoblast stimulates proliferation and differentiation of osteoblast through induced expression of BMP-2, TGF-${\beta}1$, type I collagen and osteocalcin. Propofol might promote angiogenesis and bone regeneration under hypoxic condition.

Septic pulmonary embolism is a rare disease entity that consists of pulmonary infection and embolism predominantly arising from endocarditis and thrombophlebitis. We report a rare case of candidal septic pulmonary embolism secondary to odontogenic infection in a previously healthy and immunocompetent man, who had a submandibular abscess with dyspnea and fever. The patient was not responsive to prolonged broad spectrum antibiotics and surgical drainage, however, antifungal therapy was successful after Candida albicans was confirmed by his blood culture. Since proper identification and the resolution of the septic origin is as important as the diagnosis of septic pulmonary embolism, in a patient with odontogenic infection, who shows definite respiratory complications despite antimicrobial therapy with surgical drainage, various culture examinations should be adopted.

Difficulty in breathing can be very disconcerting to a patient who is conscious yet unable to breath normally. The common causes of acute respiratory distress include hyperventilation, vasodepressor syncope, asthma, heart failure, and hypoglycemia. In most of these situations, the patient does not exhibit respiratory distress unless an underlying medical disorder becomes acutely exacerbated. Examples of this include acute myocardial infarction, anaphylaxis, cerebrovascular accident, hyperglycemia, and hypoglycemia. A major factor that leads to the exacerbation of respiratory disorders is undue stress, either physiologic or psychologic. Psychologic stress in dentistry is the primary factor in the exacerbation of preexisting medical problems. Therefore, the most dental patient should be cared gently as the stress reduction protocol. This is a case report of acute respiratory distress with vasodepressor syncope during alginate impression taking of mandibular teeth in a long-standing temporomandibular joint dislocated 93-years-old pneumonic patient.