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Background/aim: The first objective of this study was to identify predictive factors for oral and maxillofacial fractures at the initial response to the patient. The second objective was to determine the factors influencing the incidence of treatment duration of more than 1 month using the information shown in the medical record., Materials and Methods: Hospital records from 2011 to 2019 were reviewed to identify patients who had sustained oral and maxillofacial injuries by falling or falling from a height. Patterns and types of oral and maxillofacial injury, injury severity, and background of the injury were collected from the hospital records. The variables independently associated with a treatment duration of more than 1 month were determined by logistic regression analysis., Results: In total, 282 patients (150 men, 132 women; median age, 17.5 years) were selected for analysis. Maxillofacial fractures were observed in 20.9% of patients (59/282); among these, mandibular fractures were the most common (47/59). Logistic regression analysis showed that age (odds ratio [OR], 1.026), nighttime occurrence (OR, 2.192), and upper face injury (OR, 20.704) were independent predictive factors for having a maxillofacial fracture. Additionally, the number of injured teeth (OR, 1.515) and the use of intermaxillary fixation (OR, 16.091) were independent predictors of treatment duration of more than 1 month., Conclusions: These results may be useful in the initial management of maxillofacial injuries in terms of better-informing patients injured by falling their expected treatment duration and managing the psychological impacts of a long treatment duration., (© 2023 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Deep skin wounds with periosteal defects, frequently caused by traffic accidents or radical dissection, are refractory. Transplant surgery is frequently performed, but patients are subjected to stress for long operation periods, the sacrifice of donor regions, or several complications, such as flap necrosis or intractable ulcers. Even if the defects are covered, a scar composed of fibrous tissue remains in the body, which can cause itching, dysesthesia, or repeated ulcers because of the lack of distribution of peripheral nerves or hair follicles. Thus, treatments with the aim of regenerating lost tissue for deep wounds with periosteal defects are needed. Here, we show that the use of gelatin sponges (GS), which have been used as haemostatic materials in clinical practice, allowed the regeneration of heterogeneous tissues, including periosteum, skin, and skin appendages, when used as scaffolds in deep wounds with periosteal defects in rats. Bone marrow transplantation in rats revealed the mechanism by which the microenvironment provided by GS enabled bone marrow-derived cells (BMDCs) to form a vascular niche, followed by regeneration of the periosteum, skin, or skin appendages such as hair follicles by local cells. Our findings demonstrated that vascular niche formation provided by BMDCs is crucial for heterogeneous tissue regeneration., (© 2022. The Author(s).)

In oral surgery, tissue loss may occur in some cases, resulting in bone exposure and subsequent wound infection and possible scar formation during secondary healing. In this study, Terudermis ® Artificial Dermis (AD-T), a dermal defect graft made from processed bovine dermis collagen and gelatin sponge (GS) were used as dressings on 100-mm 2 wounds with exposed bone on the heads of rats. For the control group, the wound was left exposed. The wound-healing efficacy of the treatment was compared macroscopically and histologically among the three groups at 1, 2, and 4 weeks after surgery. Complete wound healing was achieved faster in the AD-T group than in the GS group, and osteoblasts appeared on the bone surface, indicating accelerated bone remodeling. Furthermore, in the AD-T group, there was an increased production of newly formed blood vessels, fibroblasts and osteoblasts positive for anti-cortactin antibodies, which are believed to contribute to wound healing. Our findings suggest that AD-T is better than GS as a wound dressing material.

Aim: Prevention of medication-related osteonecrosis of the jaw (MRONJ) in patients with osteoporosis requires the cooperation of physicians and dentists. We investigated the knowledge, experience, and behaviour related to medical and dental cooperation for MRONJ prevention in patients with osteoporosis between physicians and dentists practising in the Shiga prefecture., Materials and Methods: We conducted a cross-sectional study to investigate the cooperation between practising physicians and dentists for preventing osteonecrosis of the jaw (ONJ) in patients with osteoporosis using 2 separate questionnaires from July 28, 2018, to February 3, 2019., Results: Of 461 dentists who were sent the questionnaires at their dental clinics, 307 (67%) responded via fax. Of 846 physicians who were sent the questionnaire at their clinics, 378 (45%) responded via fax. Of these, 268 (32%) were finally analysed because 110 (13%) physicians had never treated patients with osteoporosis; 50% dentists and 24% physicians were familiar with the MRONJ position paper in Japan, and 39% dentists and 9% physicians had encountered MRONJ in their clinical practice. A total of 30% physicians had requested oral health care by a dentist before administering bone-modifying agents (BMA) therapy. The knowledge and experience of MRONJ differed between physicians and dentists., Conclusion: The behaviour of physicians and dentists was insufficient to enable medical and dental cooperation for the prevention of MRONJ in patients with osteoporosis. The lack of cooperation between physicians and dentists during osteoporosis treatment in the Shiga prefecture in Japan is documented in this study., Competing Interests: Conflict of interest None disclosed., (Copyright © 2020 The Authors. Published by Elsevier Inc. All rights reserved.)

Background/aim: Because bicyclists and motorcyclists with oral and maxillofacial injuries often suffer from disabilities requiring long-term treatment, reducing the severity of such injuries is a valuable objective for improving these people's quality of life (QOL). The aims of this study were, first, to present the prevalence and patterns of oral and maxillofacial injuries of bicyclists and motorcyclists and to compare the features of these injuries and, second, to determine the factors contributing to long-term hospitalization for these patients and to propose effective preventive measures., Material and Methods: This was a single-center retrospective analysis. Hospital records from 2011 through 2018 were reviewed for all patients who had sustained oral and maxillofacial injuries in bicycle or motorcycle collisions and had presented at a university hospital which was the only hospital in the region attended 24 hours per day by oral and maxillofacial surgeons. Characteristics of the oral and maxillofacial injuries, injury severity, and factors influencing the length of hospitalization were examined., Results: Records of 130 patients (82 bicyclists and 48 motorcyclists) with a mean age of 28.0 years were analyzed. Thirty-three patients (25.4%) had maxillofacial fractures, with 41 fracture lines while 103 patients (79.2%) had dental injuries and 57 patients (43.8%) had soft-tissue injuries. The distribution and prevalence of oral and maxillofacial injuries were similar for bicyclists and motorcyclists. However, motorcyclists had significantly higher Abbreviated Injury Scale (AIS) scores for facial injuries and the maximum AIS score than did bicyclists. According to a multiple regression analysis, the number of fracture lines and the requirement for intermaxillary fixation were independent factors influencing long-term hospitalization (standard regression coefficients: 6.795 and 6.715, respectively; P < .001)., Conclusions: The number of fracture lines and the use of intermaxillary fixation were independent factors influencing long-term hospitalization of both bicyclists and motorcyclists with oral and maxillofacial injuries., (© 2020 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Purpose: The investigators characterized the occurrence of maxillofacial injuries in cyclists and biomechanically analyzed the mechanisms of mandible fractures., Methods: We retrospectively analyzed injury data and performed biomechanical analyses with finite element models. Hospital records from 2011 through 2019 were reviewed to identify patients who had sustained oral and maxillofacial injuries while riding a bicycle. Patients with maxillofacial fractures were compared to those without. Logistic regression analysis was performed to identify which variables were independently associated with the occurrence of maxillofacial fractures. To reconstruct the injury scenario (one in which a person falls from a bicycle and contacts the road surface with their face), computer simulations using The Total Human Model for Safety model were performed., Results: The hospital records of 94 patients (62 men, 32 women; 26.1 ± 17.3 years of age) who sustained oral and maxillofacial injuries while riding a bicycle were reviewed. Twenty patients (21.3%) sustained maxillofacial fractures; mandible fractures were most common (16 patients). Patients with maxillofacial fractures were significantly older and had higher severity injuries; however, logistic regression analysis showed that only age was an independent predictor of the occurrence of maxillofacial fracture (odds ratio, 1.03; P = .025). In simulations, higher von Mises stresses were found in the mandible when the cyclist fell with the neck extended and the body horizontal, and consequently, the center of mandibular body strikes the road surface. Contact forces were approximately 8 kN. High tensile stresses occurred laterally and high compressive stresses occurred medially in the mandibular ramus, which indicated that the mandibular ramus deformed in the transverse plane., Conclusion: Biomechanical analyses show that mandible fractures can occur when a cyclist falls from a bicycle and their lower face strikes the road's surface., (Copyright © 2020 American Association of Oral and Maxillofacial Surgeons. Published by Elsevier Inc. All rights reserved.)

Background: Ezrin, ERK, STAT3, and AKT are proteins that are overexpressed in various types of cancer, although their expressions in tongue cancer has received less focus. This study aimed to address associations between the expression levels of these proteins and with characteristics of the tumor and patient survival., Methods: We performed immunohistochemical staining of ezrin, ERK, STAT3, and AKT in tumors from patients with tongue carcinoma in situ (CIS, n = 17) and tongue squamous cell carcinoma (SCC, n = 46). Statistical differences between the SCC versus the CIS cohorts were estimated by calculations of bivariate odds ratios of low versus high expression of the proteins. Fisher's exact tests were used to appraise interassociations between the proteins, as well as expression levels versus patient and tumor characteristics. Survival based on Kaplan-Meier statistics in combination log-rank tests were used to address potential effects of the patient and tumor characteristics versus 5-year survival rate., Results: The relative high: low expression of all four proteins in the two cohorts differed, and particularly ERK was markedly overexpressed in the SCC versus the CIS cohort (odds ratio = 45.3, p < .01). The relative high: low expression each protein versus patient and tumor characteristics; showed associations between AKT expression and T stage (p = .002) plus node metastases (p = .12), and between ERK expression and drinking (p = .01) and smoking history (p = .01). There was no significant difference observed between ERK and the three other molecules, nor any significant difference between the degree of expression of each protein and the 5-year disease-specific survival rate., Conclusion: Ezrin, ERK, STAT3, and AKT appear to be involved in the progress from carcinoma in situ in the tongue into squamous cell carcinoma. ERK in particular is overexpressed, suggesting that ERK may be a novel therapeutic target for preventing tongue cancer., (© 2020 The Authors. Clinical and Experimental Dental Research published by John Wiley & Sons Ltd.)

To screen for additional treatment targets against tongue cancer, we evaluated the contributions of extracellular signal-related kinase (ERK), AKT and ezrin in cancer development. Immunohistochemical staining showed that ERK and ezrin expressions were significantly higher in invasive squamous cell carcinoma than in carcinoma in situ. To investigate the roles of ERK and ezrin in cancer development, we used the non-woven silica fibre sheet Cellbed TM with a structure resembling the loose connective tissue morphology in a novel 3D culture system. We confirmed that the 3D system using Cellbed TM accurately mimicked cancer cell morphology in vivo. Furthermore, cell projections were much more apparent in 3D-cultured tongue cancer cell lines than in 2D cultures. Typically, under conventional 2D culture conditions, F-actin and cortactin are colocalized in the form of puncta within cells. However, in the 3D-cultured cells, colocalization was mainly observed at the cell margins, including the projections. Projections containing F-actin and cortactin colocalization were predicted to be invadopodia. Although suppressing ezrin expression with small interfering RNA transfection caused no marked changes in morphology, cell projection formation was decreased, and the tumour thickness in vertical sections after 3D culture was markedly decreased after suppressing ERK activity because both the invasion ability and proliferation were inhibited. An association between cortactin activation as well as ERK activity and invadopodia formation was detected. Our novel 3D culture systems using Cellbed™ are simple and useful for in vitro studies before conducting animal experiments. ERK contributes to tongue cancer development by increasing both cancer cell proliferation and migration via cortactin activation.

Oral surgical procedures occasionally require removal of the periosteum due to lesions, and these raw bone surfaces are prone not only to infection but also to scar formation during secondary healing. The objective of this study was to identify successful methods for reconstruction using periosteal defect dressings. We created 1-cm 2 defects in the skin and cranial periosteum of 10-week-old male Wistar rats under isoflurane anesthesia. The animals were assigned to three defect treatment groups: (1) polyglycolic acid sheets with fibrin glue dressing (PGA-FG), (2) Spongel® gelatin sponge dressing (GS), and (3) open wound (control). Postoperative wound healing was histologically evaluated at 2, 4, and 6 weeks. The moist conditions maintained by the GS and PGA-FG treatments protected the bone surface from the destructive effects of drying and infection. Complete wound healing was observed in the GS group but not for all animals in the PGA-FG and control groups. Histologically, osteoblast proliferation on bone surfaces and complete epithelialization with adnexa were observed in the GS group at 6 weeks after surgery. In contrast, PGA sheets that had not been absorbed inhibited osteoblast proliferation and delayed wound healing in the PGA-FG group. Wound surface dressings maintain a moist environment that promotes wound healing, but PGA materials may not be suitable for cases involving exposed periosteum or bone surfaces due to the observed scar formation and foreign-body reaction.

Purpose: Sevoflurane increases reactive oxygen species (ROS), which mediate cardioprotection against myocardial ischemia-reperfusion injury. Emerging evidence suggests that autophagy is involved in cardioprotection. We examined whether reactive oxygen species mediate sevoflurane preconditioning through autophagy., Methods: Isolated guinea pigs hearts were subjected to 30 min ischemia followed by 120 min reperfusion (control). Anesthetic preconditioning was elicited with 2 % sevoflurane for 10 min before ischemia (SEVO). The ROS-scavenger, N-(2-mercaptopropionyl) glycine (MPG, 1 mmol/l), was administered starting 30 min before ischemia to sevoflurane-treated (SEVO + MPG) or non-sevoflurane-treated (MPG) hearts. Infarct size was determined by triphenyltetrazolium chloride stain. Tissue samples were obtained after reperfusion to determine autophagy-related protein (microtubule-associated protein light chain I and II: LC3-I, -II) and 5' AMP-activated protein kinase (AMPK) expression using Western blot analysis. Electron microscopy was used to detect autophagosomes., Results: Infarct size was significantly reduced and there were more abundant autophagosomes in SEVO compared with control. Western blot analysis revealed that the ratio of LC3-II/I and phosphorylation of AMPK were significantly increased in SEVO. These effects were abolished by MPG., Conclusions: Sevoflurane induces cardioprotection through ROS-mediated upregulation of autophagy.

Purpose: Necroptosis has been proposed as a mode of cell death that is a caspase-independent programmed necrosis. We investigated whether necroptosis is involved in myocardial ischemia-reperfusion injury in isolated guinea pig hearts and, if so, whether simultaneous inhibition of necroptosis and apoptosis confers enhanced cardioprotection., Methods: Isolated perfused guinea pig hearts were subjected to 30 min ischemia and 4 h reperfusion (control = CTL, n = 8). Necrostatin-1 (necroptosis inhibitor, 10 μM), Z-VAD (apoptosis inhibitor, 0.1 μM) and both inhibitors were administered starting 5 min before ischemia and during the initial 30 min of reperfusion (Nec, Z-VAD, Nec + Z-VAD; n = 8 each). Contractile recovery was monitored by left ventricular developed (LVDP) and end-diastolic (LVEDP) pressure. Infarct size was determined by triphenyltetrazolium chloride staining. Tissue samples were obtained after 4 h reperfusion to determine expression of receptor-interacting protein 1 (RIP1) and activated caspase 3 by Western blot analysis., Results: After reperfusion, Nec + Z-VAD had higher LVDP and lower LVEDP compared with CTL. Infarct size was reduced in Nec and Z-VAD compared with CTL. Combination of necroptosis and apoptosis inhibition further reduced infarct size. Expression of activated caspase 3 was not increased in Z-VAD and Nec + Z-VAD compared with Nec and CTL. Expression of RIP1 was preserved in Z-VAD and Nec + Z-VAD compared with CTL, suggesting RIP1-mediated necrosis is involved in myocardial ischemia-reperfusion injury., Conclusion: Necroptosis is involved in myocardial ischemia-reperfusion injury, and simultaneous inhibition of necroptosis and apoptosis enhances the cardioprotective effect. These findings may provide a novel, additive strategy for cardioprotection in acute myocardial infarction.

Sevoflurane preconditioning against myocardial ischemia-reperfusion injury is lost if the ischemic insult is too long. Emerging evidence suggests that induction of autophagy may also confer cardioprotection against ischemia-reperfusion injury. We examined whether induction of autophagy prolongs sevoflurane preconditioning protection during a longer ischemic insult. Isolated guinea pigs hearts were subjected to 30 or 45 min ischemia, followed by 120 min reperfusion (control). Anesthetic preconditioning was elicited with 2% sevoflurane for 10 min prior to ischemia (SEVO-30, SEVO-45). Chloramphenicol (autophagy upregulator, 300 µM) was administered starting 20 min before ischemia and throughout reperfusion in SEVO-45 (SEVO-45+CAP). To inhibit autophagy, 3-methyladenine (10 μM) was administered during sevoflurane administration in SEVO-45+CAP. Infarct size was determined by triphenyltetrazolium chloride stain. Tissue samples were obtained before ischemia to determine autophagy-related protein (microtubule-associated protein light chain I and II: LC3-I, II), Akt and glycogen synthase kinase 3β (GSK3β) expression using Western blot analysis. The effect of autophagy on calcium-induced mitochondrial permeability transition pore (MPTP) opening in isolated calcein-loaded mitochondria was assessed. Electron microscopy was used to detect autophagosomes. Infarct size was significantly reduced in SEVO-30, but not in SEVO-45. Chloramphenicol restored sevoflurane preconditioning lost by 45 min ischemia. There were more abundant autophagozomes and LC3-II expression was significantly increased in SEVO-45+CAP. Induction of autophagy before ischemia enhanced GSK3β phosphorylation and inhibition of calcium-induced MPTP opening. These effects were abolished by 3-methyladenine. Pre-ischemic induction of autophagy restores sevoflurane preconditioning lost by longer ischemic insult. This effect is associated with enhanced inhibition of MPTP by autophagy., (Copyright © 2013 Elsevier B.V. All rights reserved.)

Objective: The purposes of this study were to investigate whether sevoflurane (SEVO) enhances moderate-dose ethanol (EtOH) preconditioning and whether this additional cardioprotection is associated with glycogen synthase kinase-3β (GSK-3β), protein kinase B (Akt), mammalian target of rapamycin (mTOR), 70-kDa ribosomal s6 kinase-1 (p70s6K), and/or mitochondrial permeability transition pore (MPTP) opening., Design: In vitro study using an isolated heart Langendorff preparation., Setting: University research laboratory., Participants: Male guinea pigs (n = 170)., Interventions: Isolated perfused guinea pig hearts underwent 30-minute ischemia and 120-minute reperfusion (control). The EtOH group received 5% EtOH in the drinking water for 8 weeks. Anesthetic preconditioning was elicited by a 10-minute exposure to 2% SEVO in EtOH (EtOH + SEVO group) or non-EtOH (SEVO group) hearts. The inhibition of GSK-3β phosphorylation and mTOR was achieved with LY294002 and rapamycin, respectively. GSK-3β, Akt, mTOR, and p70s6K expressions were determined by western blot. Calcium-induced MPTP opening was assessed in isolated calcein-loaded mitochondria., Measurements and Main Results: After ischemia-reperfusion, the EtOH, SEVO, and EtOH + SEVO groups had higher left ventricular developed pressure recovery and lower end-diastolic pressure versus the control group. Infarct size was smaller in the EtOH and SEVO groups versus control and even smaller in the EtOH + SEVO group. Phosphorylation of GSK-3β and Akt, but not mTOR and p70s6K, was increased in the EtOH and SEVO groups. Phosphorylation of GSK-3β, but not mTOR and p70s6K, was further increased in the EtOH + SEVO group. The EtOH and SEVO groups exhibited a smaller calcium-induced MPTP opening, and the EtOH + SEVO presented an even smaller MPTP opening., Conclusions: SEVO and chronic EtOH preconditioning offer additive cardioprotection. This effect is associated with an increased GSK-3β phosphorylation and an inhibition of MPTP opening., (Copyright © 2013 Elsevier Inc. All rights reserved.)

Keratocystic odontogenic tumor (KCOT) is a relatively rare benign neoplasm of odontogenic origin. The squamous epithelium of KCOT usually does not contain melanocytes, however, pigmented KCOT has been documented, albeit extremely rarely. In the present study, we described an additional case of pigmented KCOT and review the clinicopathological features of this extremely rare lesion. A 23-year-old Japanese female presented with a relatively well-circumscribed round unilocular radiolucency that impacted the third molar in her right mandibula. Surgical resection was performed subsequent to a clinical diagnosis of KCOT. Histopathological study of the resected mandibular cyst showed that it was covered by a parakeratinized stratified squamous epithelium, which had slightly enlarged hyperchromatic nuclei. On the luminal surface, a wavy layer of parakeratin was observed. In addition, dendritic melanocytes without atypia were observed in approximately half of the squamous epithelium. Immunohistochemical analyses revealed that these melanocytes were positive for S-100 protein, Melan-A and HMB-45. Therefore, a diagnosis of pigmented KCOT was made. Review of the clinicopathological features of the previously reported cases of pigmented KCOT as well as the present case revealed that: i) this lesion occurs mostly in young persons (average age, 18 years) and shows female predominance; ii) most cases are solitary and involve the mandibula; and iii) the reported incidence is 0.36-10.6% and this difference may be associated with ethnicity. Thus, we described the ninth reported case of pigmented KCOT. The mechanism by which melanocytes appear and the difference in ethnic prevalence remain unclear. Additional clinicopathological studies are needed to clarify these issues.