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Bilobalide isolated from the leaves of Ginkgo biloba has several pharmacological activities such as neuroprotective, anti-inflammatory, and anticonvulsant. However, the effect of bilobalide on cancer has not been clearly established. The main purpose of this study was to investigate the effect of bilobalide on cell growth and apoptosis induction in FaDu human pharyngeal squamous cell carcinoma. This was examined by 3-[4,5-dimethylthiazol-2-yl]-2,5- diphenyltetrazolium bromide assay, nuclear 4′,6-diamidino-2-phenylindole dihydrochloride staining, DNA fragmentation analysis, and immunoblotting. Bilobalide inhibited the growth of FaDu cells in dose- and time-dependent manners. Treatment with bilobalide resulted in nuclear condensation and DNA fragmentation in FaDu cells. Furthermore, it promoted the proteolytic cleavage of procaspase-3/-7/-8/-9 with increase in the amount of cleaved caspase-3/-7/-8/-9. Bilobalide-induced apoptosis in FaDu cells was mediated by the expression of Fas and the activation of caspase-8, caspase-3, and poly (ADP-ribose) polymerase. Immunoblotting revealed that the antiapoptotic mitochondrial protein Bcl-2 was downregulated, but the proapoptotic protein Bax was upregulated by bilobalide in FaDu cells. Bilobalide significantly increased Bax/Bcl-2 ratio. These results suggest that bilobalide inhibits cell proliferation and induces apoptosis in FaDu human pharyngeal squamous cell carcinoma via both the death receptor-mediated extrinsic apoptotic pathway and the mitochondrial-mediated intrinsic apoptotic pathway.

Purpose: This study examines the properties and potential commercial value of the pine cones extract when used as bioactive and cosmetics ingredients. Methods: Pine cones were extracted with hot water (WE), 70% ethanol (EE), and supercritical fluid extraction (SFE) to examine their antioxidant properties on the basis of their total polyphenol content, 2,2-diphenyl-1-picrylhydrazyl (DPPH) radical scavenging activity, and gas chromatography-mass spectrometry (GC-MS) analysis. The antibacterial properties of the pine cone extract were also studied on 2 types of bacteria. In addition, this study examined the nitric oxide (NO) inhibition effect using RAW 264.7 cells, in which the inflammatory reaction was induced by lipopolysaccharides (LPS), and cell migration activity in the HeCaT cells. Results: The extract obtained with SFE exhibited high antioxidative ability even at low concentration (0.125%). The antimicrobial activity of the of SFE pine cone extract was 12.1±1.04 mm for Staphylococcus aureus (S. aureus ) and 11.8±0.45 mm for Staphylococcus epidermidis (S. epidermidis ). Cytotoxicity evaluation showed cell viability above 80% in all extracts. During the antiinflammatory test, the nitric oxide expression level was low, and it was confirmed by the antiinflammatory effect. The results of the stability test showed that emulsions containing SFE extract were very stable. The pH and high temperature (40℃) of each emulsion containing SFE extract did not considerably change for 30 days. Conclusion: These findings suggest that SFE extract is a possible cosmeceutical material with potent skin regeneration and antiinflammatory properties.

Purpose The purpose of this study was to evaluate the effects of the growth factor within platelet-rich fibrin (PRF) in proliferation and differentiation of osteoblast and to observe the effectiveness of PRF. Materials and methods The colorimetric MTT assay, cell live and dead assay, alkaline phosphatase staining and activity assay, alizarine red S, and von Kossa staining were performed. Finally, the alterations of biomarkers associated with bone formation were verified at the mRNA level by quantitative polymerase chain reaction (PCR) and quantitative real-time PCR. In in vivo study, 6 adult mongrel dogs were used. The defect was performed and divided into 3 groups: (1) defect left unfilled, (2) defect filled with only 0.25-g Bio-Oss, and (3) defect filled with 0.25-g Bio-Oss mixed with PRF. Results MTT and cell live and dead assay showed that PRF did not affect the cell viability in MG-63 cells. The alkaline phosphatase activity, calcification, and mineralization were gradually increased in the MG-63 cells treated with PRF. Furthermore, the mRNA levels of biomarker gene in the MG-63 cells treated with PRF were significantly higher than those of control. In in vivo study, both radiographical and histological evaluations showed that the new bone formations were significantly increased in the defecting bone region transplanted with Bio-Oss and PRF compared with Bio-Oss only at 2 weeks after transplantation. Conclusion PRF can promote the bone regeneration without any complications.

Purpose The purpose of this study was to evaluate a new graft material, biphasic calcium phosphate, composed of 60% hydroxyapatite and 40% β-Tricalcium phosphate and deproteinized bovine bone mineral, which is established as a predictable graft material for maxillary sinus augmentation. Materials and methods Maxillary sinus augmentation was performed with different bone materials. Bone biopsies were performed on tissue harvested from the future implant bed using a trephine bur at 6 months after maxillary sinus augmentation. Resonance frequency analysis was performed immediately and at 6 months after the implant placement. Microcomputed tomography and histomorphometric analysis were performed in all patients. Results Fifty-six patients (60 sinuses) were included in the study. At 6 months postoperative, 31 biopsies were performed on tissues harvested from the calcium phosphate, and 29 biopsies on tissues from the bovine bone grafts. There was no implant failure during the 21-month mean follow-up period. The overall implant stability quotient values were higher than 60, and gradually increased for 6 months. Higher new bone volume fraction and new bone surface density were observed in the calcium phosphate group compared with the bovine bone group. In contrast, residual bone graft volume in the bovine bone group was higher than that in the calcium phosphate group. Nevertheless, there was no significant difference between groups in the microcomputed tomography and histomorphometric parameters. Conclusion Within the study's limitations, both graft materials demonstrated similar biocompatibility and osteoconductivity in the maxillary sinus augmentation.

Background/purpose: The classification and treatment of odontogenic keratocyst (OKC) are controversial. The objective of this study was to present the efficiency of decompression followed by enucleation by clinical and histomorphometric evaluation for the treatment of OKC. Materials and methods: Thirty four OKCs of 27 patients who underwent decompression followed by enucleation were included in this study. Clinical and histomorphometric analysis were performed. Results: The average decreasing rate was 59% in maximum diameter, 66% in the amount of the volume for the average of period of the decompression was 9.8 months. The mean of increasing rate of the thickness of the epithelial lining was 921.16%. There were no recurrences for a mean follow-up period of 5.8 years. The thin and friable cyst wall of the OKC was changed to thickened, hard type. Conclusion: The decompression was found to be effective and reliable as a treatment of the OKC to decrease the recurrence tendency, even for Gorlin-Goltz syndrome. Keywords: Epithelial thickness, Jaw cysts, Keratocysts, Odontogenic tumors

This study investigates the potential of propolis-embedded zeolite nanocomposites for dental implant application. Propolis-embedded zeolite nanocomposites were fabricated by complexation of propolis and zeolites. Then, they were pelleted with Poly(L-lactide) (PLA)/poly(e-caprolactone) (PCL) polymer for the fabrication of a dental implant. The chemical properties of propolis were not changed during the fabrication of propolis-embedded zeolite nanocomposites in attenuated total reflection-fourier transform infra-red (ATR FT-IR) spectroscopy measurements. Propolis was continuously released from propolis-embedded zeolite nanocomposites over one month. PLA/PCL pellets containing propolis-embedded zeolite nanocomposites showed longer sustained release behavior compared to propolis-embedded zeolite nanocomposites. Propolis-embedded zeolite nanocomposite powder showed similar antibacterial activity against C. albicans in an agar plate and formed an inhibition zone as well as chlorohexidine (CHX) powder. Eluted propolis solution from PLA/PCL pellets also maintained antibacterial activity as well as CHX solution. Furthermore, eluted propolis solution from PLA/PCL pellets showed significant antibacterial efficacy against C. albicans, S. mutans and S. sobrinus. Dental implants fabricated from PLA/PCl polymer and propolis-embedded zeolite nanocomposites also have antibacterial efficacy and negligible cytotoxicity against normal cells. We suggest that PLA/PCl pellets containing propolis-embedded zeolite nanocomposites are promising candidates for dental implants.

Background/aim MicroRNAs (miRNAs) are closely associated with a number of cellular processes, including cell development, differentiation, proliferation, carcinogenesis, and apoptosis. The aim of the present study was to elucidate the molecular mechanisms underlying the tumor suppressor activity of miRNA-203 (miR-203) in YD-38 human oral cancer cells. Materials and methods Polymerase chain reaction analysis, MTT assay, DNA fragmentation assay, fluorescence-activated cell-sorting analysis, gene array, immunoblotting, and luciferase assay were carried out in YD-38 cells. Results miR-203 expression was significantly down-regulated in YD-38 cells compared to expression levels in normal human oral keratinocytes. miR-203 decreased the viability of YD-38 cells in a time- and dose-dependent manner. In addition, over-expression of miR-203 significantly increased not only DNA segmentation, but also the apoptotic population of YD-38 cells. These results indicate that miR-203 overexpression induces apoptosis in YD-38 cells. Target gene array analysis revealed that the expression of the polycomb complex protein gene Bmi-1, a representative oncogene, was significantly down-regulated by miR-203 in YD-38 cells. Moreover, both mRNA and protein levels of Bmi-1 were significantly reduced in YD-38 cells transfected with miR-203. These results indicate that Bmi-1 is a target gene of miR-203. A luciferase reporter assay confirmed that miR-203 suppressed Bmi-1 expression by directly targeting the 3'-untranslated region. Conclusion miR-203 induces apoptosis in YD-38 cells by directly targeting Bmi-1, which suggests its possible application as an anti-cancer therapeutic.

The fracture of dental implants is a rare occurrence in clinical settings. Possible causes of implant fracture include design or production flaws, overloaded occlusion force, implant location, metal fatigue, and bone resorption around the implant. This study reports on the successful removal and reimplantation of fractured implants.

The inferior alveolar nerve block is the most common method of local anesthesia for intraoral surgery at the posterior mandibular region. However, unexpected complications may occur when administering the local anesthesia. One of these uncommon complications is the fracture of the needle. If the injection needle is broken during the surgery, it should be removed immediately. However, this is one of the most difficult procedures. In this report, we present two cases of needle fracture during the procedure, and its successful removal under general/local anesthesia administration.

Metformin (1,1-dimethylbiguanide hydrochloride), derived from French lilac (Galega officinalis), is a first-line drug prescribed for patients with type 2 diabetes. It has been reported to have anti-cancer effects in a variety of cancer cells. However, effects of metformin on oral cancer cells have not been clearly established. The main goal of this study was to investigate the effect of metformin on cell growth and apoptosis induction in oral cancer cells derived from Korean patients. The effect of metformin on cell growth and apoptosis induction in oral cancer cells was examined by inhibition of cell growth, DNA fragmentation analysis and immunoblotting in YD-38 human oral cancer cells derived from Korean patients. Treatment with metformin induced inhibition of cell growth depending on the metformin treatment time and concentration in YD-38 human oral cancer cells. Treatment with metformin induced nuclear fragmentation in YD-38 human oral cancer cells. Metformin promoted proteolytic cleavage of procaspase-3 with an increase in the amount of cleaved caspase-3. Cleaved PARP was increased by metformin in YD-38 human oral cancer cells. Treatment of YD-38 human oral cancer cells with metformin increased the level of Bax, but it decreased the level of Bcl-2. These results suggest that metformin can induce suppression of cell growth and cell apoptosis in YD-38 human oral cancer cells derived from Korean patients.

Background/aim The present study aimed to investigate the apoptotic effects of phenformin, a therapeutic agent for diabetes, on head and neck squamous cell carcinoma (HNSCC). Materials and methods Cytotoxicity was measured by the MTT and live/dead cell assay. Phenformin-induced apoptotic FaDu cell death and its associated cellular signaling pathways were investigated by hematoxylin and eosin staining, 4',6-diamidino-2-phenylindole staining, caspase-3 activity assay, fluorescence-activated cell sorting analysis, and western blotting. Results Phenformin promoted death of and apoptotic processes in FaDu cells, including morphological alterations and nuclear condensation. Furthermore, treatment with phenformin increased caspase-3 activity and apoptotic populations via the caspase cascade through cleavage of capspase-8, -9, and -3 and poly(ADP-ribose) polymerase in FaDu cells. Moreover, phosphorylation levels of mitogen-activated protein kinases, nuclear factor-κB, and AKT were down-regulated in FaDu cells by phenformin. Conclusion Phenformin induced death of FaDu cells via caspase-dependent extrinsic and intrinsic apoptosis pathways and is a promising novel therapeutic agent for HNSCC.

In the present study, we demonstrated the anti-catabolic effects of formononetin, a phytoestrogen derived from herbal plants, against interleukin-1β (IL-1β)-induced severe catabolic effects in primary rat chondrocytes and articular cartilage. Formononetin did not affect the viability of primary rat chondrocytes in both short- (24 h) and long-term (21 days) treatment periods. Furthermore, formononetin effectively antagonized the IL-1β-induced catabolic effects including the decrease in proteoglycan content, suppression of pericellular matrix formation, and loss of proteoglycan through the decreased expression of cartilage-degrading enzymes like matrix metalloproteinase (MMP)-13, MMP-1, and MMP-3 in primary rat chondrocytes. Moreover, catabolic oxidative stress mediators like nitric oxide, inducible nitric oxide synthase, cyclooxygenase-2, and prostaglandin E2 were significantly downregulated by formononetin in primary rat chondrocytes treated with IL-1β. Sequentially, the upregulation of pro-inflammatory cytokines (like IL-1α, IL-1β, IL-6, and tumor necrosis factor α), chemokines (like fractalkine, monocyte chemoattractant protein-1, and macrophage inflammatory protein-3α), and vascular endothelial growth factor were significantly downregulated by formononetin in primary rat chondrocytes treated with IL-1β. These data suggest that formononetin may suppress IL-1β-induced severe catabolic effects and osteoarthritic condition. Furthermore, formononetin may be a promising candidate for the treatment and prevention of osteoarthritis.

Morin, a flavonoid isolated from various medicinal herbal plants, has an anti-inflammatory effect. This study aimed to elucidate the anticatabolic effects and cellular mechanism of morin against interleukin-1β (IL-1β) in rat primary chondrocytes. Morin at 10–100 μM did not affect the viability of rat primary chondrocytes. Treatment with morin for 21 days ameliorated the IL-1β-induced decrease in extracellular matrix. Furthermore, treatment with morin attenuated IL-1β-induced proteoglycan loss in the articular cartilage through suppression of catabolic factors, such as matrix metalloproteinases, inflammatory mediators, and pro-inflammatory cytokines. These data indicated that morin exerted anticatabolic effects that can prevent and reduce progressive degeneration of the articular cartilage, and thus may be a potential candidate treatment for osteoarthritis.

In the present study, we investigated the anti-catabolic effects of coumestrol, a phytoestrogen derived from herbal plants, against interleukin-1β-induced cartilage degeneration in primary rat chondrocytes and articular cartilage. Coumestrol did not affect the viability of human normal oral keratinocytes and primary rat chondrocytes treated for 24 h and 21 days, respectively. Although coumestrol did not significantly increase the proteoglycan contents in long-term culture, it abolished the interleukin-1β-induced loss of proteoglycans in primary rat chondrocytes and knee articular cartilage. Furthermore, coumestrol suppressed the expression of matrix-degrading enzymes such as matrix metalloproteinase-13, −3, and −1 in primary rat chondrocytes stimulated with interleukin-1β. Moreover, the expression of catabolic factors such as nitric oxide synthase, cyclooxygenase-2, prostaglandin E2, and inflammatory cytokines in interleukin-1β-stimulated primary rat chondrocytes was suppressed by coumestrol. In summary, these results indicate that coumestrol counteracts the catabolic effects induced by interleukin-1β through the suppression of inflammation. Therefore, based on its biological activity and safety profile, coumestrol could be used as a potential anti-catabolic biomaterial for osteoarthritis.

Nevoid basal cell carcinoma syndrome (NBCCS), also known as Gorlin syndrome, is characterized by various embryological deformities and carcinoma formation. It is caused by PTCHI gene mutations and is autosomal dominantly inherited. Some of the main symptoms of NBCCS are multiple basal cell carcinomas, multiple keratocystic odontogenic tumors (KCOTs) of the mandible, hyperkeratosis of the palmar and plantar, skeletal deformity, calcification of the falx cerebri, and facial defomity. Recurrent KCOT is the main symptom of NBCCS and is present in approximately 90% of patients. In NBCCS, KCOTs typically occur in multiples. KCOTs can be detected in patients under the age of 10, and new and recurring cysts develop until approximately the age of 30. The postoperation recurrence rate is approximately 60%. This case report presents a 14-year-old female patient with a chief complaint of a cyst found in the maxilla and mandible. The patient was diagnosed with NBCCS, and following treatment of marsupialization and enucleation, the clinical results were satisfactory.

Implant displacement into the maxillary sinus often results from features specific to the posterior maxillary teeth, including poor bone quality and insufficient remaining bone. This study reviews implants displaced into the maxillary sinus, the causes and complications of displacement, and how to remove them, according to when the displacement occurs.The PubMed, Ovid (MEDLINE), and EMBASE databases were searched using the keywords "displacement," "implant," "maxillary sinus," and "removal" for articles published between January 2000 and July 2013.Twenty-two journal articles were selected; these discussed 49 displaced implants. Most of the implants were displaced into the maxillary sinus during implantation, but resulted in a low incidence of complications, such as maxillary sinusitis. The displaced implants were removed using the Caldwell-Luc approach or a transoral or transnasal endoscopic approach.Implants displaced into the maxillary sinus have various causes according to when they are displaced. As displaced implants can cause several complications, transnasal endoscopy is recommended to remove them; however, the implants should be examined thoroughly before selecting the removal method.

This analysis examined the types of retreatment in failed sinus bone grafts due to the development of maxillary sinusitis. Reoperation was performed in 7 patients. The types of reoperation included infection management, reconstruction of the sinus roof using a pedicled buccal fat pad and collagen membrane, oroantral fistula closure, sinus bone graft using an autogenous bone graft, and implant placement. In one case, sinusitis developed 14 months after the reoperation, but it was managed by incision, drainage, and administration of antibiotics. All sinus bone grafts that were performed during the retreatments were successful.

Objectives: If teeth are missing, super-eruption of teeth in the opposing arch can occur in the area and can change the occlusal plane. When missing teeth are replaced with implants, the oral surgeon must determine whether or not the super-erupted teeth need to be treated in order to normalize the occlusal plane. In this study, we evaluated the clinical prognosis of dentition after implant placement and prosthetic treatment were completed in an occlusal plane altered by super-erupted teeth in the opposing arch without additional treatment of the super-erupted teeth. Materials and Methods: Twenty-two patients (9 males, 13 females) were treated with implants and prosthetics without addressing the super-erupted opposing dentition from April 2004 to August 2012 at Seoul National University Bundang Hospital. A total of 33 implants were placed. Values of crestal bone loss, survival rates, and surgical and prosthetic complications for an average of 29.6 months after prosthetic loading were recorded. Results: In one case, the cover screw was exposed after implant surgery. The mean crestal bone loss was 0.09±0.30 mm. Of the 33 implants, 31 survived, a survival rate of 93.94%. A prosthetic complication occurred in one case but functioned well after correction. Conclusion: Favorable clinical results from prosthetic complications, crestal bone loss, and implant survival rates were exhibited in implants next to a super-erupted opposing tooth.

MicroRNAs (miRNAs) are closely associated with a number of cellular processes, including cell development, differentiation, proliferation, carcinogenesis, and apoptosis. The aim of the present study was to elucidate the molecular mechanisms underlying the tumor suppressor activity of miRNA-203 (miR-203) in YD-38 human oral cancer cells.Polymerase chain reaction analysis, MTT assay, DNA fragmentation assay, fluorescence-activated cell-sorting analysis, gene array, immunoblotting, and luciferase assay were carried out in YD-38 cells.miR-203 expression was significantly down-regulated in YD-38 cells compared to expression levels in normal human oral keratinocytes. miR-203 decreased the viability of YD-38 cells in a time- and dose-dependent manner. In addition, over-expression of miR-203 significantly increased not only DNA segmentation, but also the apoptotic population of YD-38 cells. These results indicate that miR-203 overexpression induces apoptosis in YD-38 cells. Target gene array analysis revealed that the expression of the polycomb complex protein gene Bmi-1, a representative oncogene, was significantly down-regulated by miR-203 in YD-38 cells. Moreover, both mRNA and protein levels of Bmi-1 were significantly reduced in YD-38 cells transfected with miR-203. These results indicate that Bmi-1 is a target gene of miR-203. A luciferase reporter assay confirmed that miR-203 suppressed Bmi-1 expression by directly targeting the 3'-untranslated region.miR-203 induces apoptosis in YD-38 cells by directly targeting Bmi-1, which suggests its possible application as an anti-cancer therapeutic.

Background Socket sealing surgery is performed for the preservation of the form and volume of the soft tissue by covering the resulting socket with autogenous soft tissue graft or membrane barriers. This procedure is usually necessary to improve the esthetic results of the maxillary anterior or premolar areas. Methods This study retrospectively investigated cases involving the open membrane technique or socket sealing surgery with a palatal gingival graft or collagen membrane where implant placement and bone grafting were performed immediately after tooth extraction. From January 2005 to December 2008, socket sealing surgery was performed in 24 patients, and 25 implants were placed. Results All implants were successful in the follow-up period. In the palatal gingival graft group, the mean marginal bone loss was 1.17 mm during the mean follow-up period of 81.0 months. In the collagen membrane group, the mean marginal bone loss was 1.23 mm during the mean follow-up period of 76.9 months. There was no significant difference between the two groups. Conclusions Consequently, socket sealing surgery is effective at minimizing the loss of soft tissue and alveolar bone. Electronic supplementary material The online version of this article (10.1186/s40902-017-0137-x) contains supplementary material, which is available to authorized users.

In the present study, we investigated berberine‑induced apoptosis and the signaling pathways underlying its activity in FaDu head and neck squamous cell carcinoma cells. Berberine did not affect the viability of primary human normal oral keratinocytes. In contrast, the cytotoxicity of berberine was significantly increased in FaDu cells stimulated with berberine for 24 h. Furthermore, berberine increased nuclear condensation and apoptosis rates in FaDu cells than those in untreated control cells. Berberine also induced the upregulation of apoptotic ligands, such as FasL and TNF-related apoptosis-inducing ligand, and triggered the activation of caspase-8, -7 and -3, and poly(ADP ribose) polymerase, characteristic of death receptor-dependent extrinsic apoptosis. Moreover, berberine activated the mitochondria‑dependent apoptotic signaling pathway by upregulating pro-apoptotic factors, such as Bax, Bad, Apaf-1, and the active form of caspase-9, and downregulating anti-apoptotic factors, such as Bcl-2 and Bcl-xL. In addition, berberine increased the expression of the tumor suppressor p53 in FaDu cells. The pan-caspase inhibitor Z-VAD-fmk suppressed the activation of caspase-3 and prevented cytotoxicity in FaDu cells treated with berberine. Interestingly, berberine suppressed cell migration through downregulation of vascular endothelial growth factor (VEGF), matrix metalloproteinase (MMP)-2, and MMP-9. Moreover, the phosphorylation of extracellular signal-regulated kinase (ERK1/2) and p38, components of the mitogen-activated protein kinase pathway that are associated with the expression of MMP and VEGF, was suppressed in FaDu cells treated with berberine for 24 h. Therefore, these data suggested that berberine exerted anticancer effects in FaDu cells through induction of apoptosis and suppression of migration. Berberine may have potential applications as a chemotherapeutic agent for the management of head and neck squamous carcinoma.

We report generation and characterization of pain-related behavior in a minimally invasive facet joint degeneration (FJD) animal model in rats. FJD was produced by a non-open percutaneous puncture-induced injury on the right lumbar FJs at three consecutive levels. Pressure hyperalgesia in the lower back was assessed by measuring the vocalization response to pressure from a force transducer. After hyperalgesia was established, pathological changes in lumbar FJs and alterations of intervertebral foramen size were assessed by histological and imaging analyses. To investigate treatment options for lumber FJ osteoarthritis-induced pain, animals with established hyperalgesia were administered with analgesic drugs, such as morphine, a selective COX-2 inhibitor, a non-steroidal anti-inflammatory drug (NSAID) (ketorolac), or pregabalin. Effects were assessed by behavioral pain responses. One week after percutaneous puncture-induced injury of the lumbar FJs, ipsilateral primary pressure hyperalgesia developed and was maintained for at least 12 weeks without foraminal stenosis. Animals showed decreased spontaneous activity, but no secondary hyperalgesia in the hind paws. Histopathological and microfocus X-ray computed tomography analyses demonstrated that the percutaneous puncture injury resulted in osteoarthritis-like structural changes in the FJs cartilage and subchondral bone. Pressure hyperalgesia was completely reversed by morphine. The administration of celecoxib produced moderate pain reduction with no statistical significance while the administration of ketorolac and pregabalin produced no analgesic effect on FJ osteoarthritis-induced back pain. Our animal model of non-open percutanous puncture-induced injury of the lumbar FJs in rats shows similar characteristics of low back pain produced by human facet arthropathy.

Purpose: The aim of the present study is to assess the importance of proper treatment timing for dental emergency patients by characterizing current patient care in the emergency room. Materials and Methods: A retrospective chart review of 3,211 patients who visited the Chosun University Hospital’s dental emergency department (Gwangju, Korea) was conducted from January 1, 2011 to May 31, 2014. Information regarding age, gender, onset date, main causes, and diagnoses were collected and analyzed. The main causes were divided into six categories: assault, household/play, sports, traffic, work, and others. Result: Emergency visits were more common for men (69%), and the ratio of males to females was 2.2:1 On average, the major cause was household/play (49.8%), followed by others (18.9%), traffic (16.6%), assault (9.1%), sports (2.9%), and work (2.6%). The most frequent diagnosis on average was dental trauma with 82.4%, followed by infection (10.7%), others (4.7%), and bleeding (2.2%). Conclusion: The main reasons for visits to the dental emergency department are dental trauma, dental infection, bleeding, and others. The most frequent reason for dental emergency patients to visit the emergency department was dental trauma (82.4%).

The purpose of this study was to compare different internal fixation techniques with resorbable or titanium fixation system used in sagittal split ramus osteotomy (SSRO) for mandibular setback. Synthetic polyurethane hemimandible replicas were used. The distal segment was repositioned in a 5-mm setback position. The hemimandibles were divided into the following eight groups: resorbable miniplate (A), titanium miniplate (B), resorbable hybrid; resorbable miniplate and bicortical screw (C), titanium hybrid; titanium miniplate and bicortical screw (D), resorbable mixed hybrid; resorbable bicortical screw and titanium miniplate (E), titanium mixed hybrid; titanium bicortical screw and resorbable miniplate (F), three resorbable bicortical screws (G) and three titanium bicortical screws (H). The compression loads were applied on the incisal edge. The compression loads (N) at 5- and 10-mm displacement were analyzed (P < 0.05). Miniplate groups (A and B) were significantly weaker than the other groups (C ∼ H). Group (H) had greatest biomechanical stability. There was no significant difference between group (D) and group (H) at 10-mm displacement. Group (G) showed a lower load than group (H) and group (D). There was no significant difference between the hybrid and mixed hybrid groups. It was concluded that additional placement of a bicortical screw, either titanium or resorbable with a miniplate may provide significantly better stabilization.

We investigated Licochalcone-A (Lico-A)-induced apoptosis and the pathway underlying its activity in a pharyngeal squamous carcinoma FaDu cell line. Lico-A purified from root of Glycyrrhiza inflata had cytotoxic effects, significantly increasing cell death in FaDu cells. Using a cell viability assay, we determined that the IC50 value of Lico-A in FaDu cells was approximately 100 µM. Chromatin condensation was observed in FaDu cells treated with Lico-A for 24 h. Consistent with this finding, the number of apoptotic cells increased in a time-dependent manner when FaDu cells were treated with Lico-A. TRAIL was significantly up-regulated in Lico-A-treated FaDu cells in a dose-dependent manner. Apoptotic factors such as caspases and PARP polymerase were subsequently activated in a caspase-dependent manner. In addition, levels of pro-apoptotic factors increased significantly in response to Lico-A treatment, while levels of anti-apoptotic factors decreased. Lico-A-induced TRAIL expression was mediated in part by a MAPK signaling pathway involving ERK1/2 and p38. Lastly, in an in vivo xenograft mouse model, Lico-A treatment effectively suppressed the growth of FaDu cell xenografts by activating caspase-3, without affecting the body weight of mice. Taken together, these data suggest that Lico-A has potential chemopreventive effects and should therefore be developed as a chemotherapeutic agent for pharyngeal squamous carcinoma.

The neurotrophin-inducible gene VGF plays an important role in the maintenance of organismal energy balance and in the mediation of hippocampal synaptic activity. The regulatory mechanism of VGF transcription is not fully understood. The neuron-restrictive silencer factor (NRSF) binds with the neuron-restrictive silencer element (NRSE), thereby suppressing the transcription of NRSE-containing genes. In this study, we show that the NRSE sequence of the VGF gene critically regulates the repression of VGF expression in NMB cells. Sequence analysis also establishes the presence of two putative NRSEs (NRSE-1 and NRSE-2) in the promoter region of the VGF gene. In reporter gene experiments, a more than eight-fold increase in the promoter activity was observed when both NRSE-1 and NRSE-2 were deleted. Deletion of NRSE-2 alone did not affect the promoter activity, thus indicating that NRSE-1 could be solely responsible for the repression of VGF gene expression. Mutations in the NRSE-1 sequence increased promoter activity. However, no change in activity was observed when NRSE-1 was coexpressed with dominant-negative NRSF, thereby suggesting that endogenous NRSF interacts with NRSE-1. Binding of NRSF to NRSE in a sequence-specific manner was confirmed with chromatin immunoprecipitation assays, respectively. Furthermore, the overexpressed NRSF in PC12 cells significantly suppressed the VGF gene expression by interacting with the NRSE located in the VGF promoter region. Our results indicate that NRSF plays an important role as a repressor of VGF gene regulation in NMB cells through a mechanism that is dependent on VGF-NRSE.

PURPOSE The purpose of this study was to evaluate the ability of new bone formation of deproteinized bovine bone (Bio-Oss) and mineralized allogenic bone (Tutoplast). MATERIALS AND METHODS Sixty rats were divided into control and experimental groups (groups 1 and 2): control group, unfilled control; group 1, Bio-Oss; group 2, Tutoplast, respectively. The animals were killed after 6 and 12 weeks, and newly formed bone was analyzed histomorphometrically. RESULTS In the control group, some new bone formed in the rim of the defect area. In the group 1, newly formed bone was thinner than the adjacent normal bone, and Bio-Oss particles were observed. In the group 2, showed a pattern of gradual fusion with adjacent bone, as well as particles in some areas, similar to the Bio-Oss-treated group. In the 12-week groups, the amount of new bone formation was significantly higher in the experimental groups than in the control group, and it was significantly higher in group 2 than in group 1. CONCLUSION Although Tutoplast and Bio-Oss graft materials seem to be useful for bone grafts, Tutoplast showed more active new bone formation than Bio-Oss.

In the present study, we examined the anticancer properties of berberine in KB oral cancer cells with a specific focus on its cellular mechanism. Berberine did not affect the cell viability of the primary human normal oral keratinocytes that were used as a control. However, the viability of KB cells was found to decrease significantly in the presence of berberine in a dose-dependent manner. Furthermore, in KB cells, berberine induced the fragmentation of genomic DNA, changes in cell morphology, and nuclear condensation. In addition, caspase-3 and -7 activation, and an increase in apoptosis were observed. Berberine was also found to upregulate significantly the expression of the death receptor ligand, FasL. In turn, this upregulation triggered the activation of pro-apoptotic factors such as caspase-8, -9 and -3 and poly(ADP-ribose) polymerase (PARP). Furthermore, pro-apoptotic factors such as Bax, Bad and Apaf-1 were also significantly upregulated by berberine. Anti-apoptotic factors such as Bcl-2 and Bcl-xL were downregulated. Z-VAD-FMK, a cell-permeable pan-caspase inhibitor, suppressed the activation of caspase-3 and PARP. These results clearly indicate that berberine-induced cell death of KB oral cancer cells was mediated by both extrinsic death receptor-dependent and intrinsic mitochondrial-dependent apoptotic signaling pathways. In addition, berberine-induced upregulation of FasL was shown to be mediated by the p38 MAPK signaling pathway. We also found that berberine-induced migration suppression was mediated by downregulation of MMP-2 and MMP-9 through phosphorylation of p38 MAPK. In summary, berberine has the potential to be used as a chemotherapeutic agent, with limited side-effects, for the management of oral cancer.