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Purpose: This report presents a unique case featuring real, ghost, and pseudo-ghost images on the panoramic radiograph of a patient wearing earrings. It also explains the formation of these images in an easy-to-understand manner. Material and Methods: One real image and two ghost images appeared on each side of a panoramic radiograph of a patient wearing earrings on both sides. Of the two ghost images on each side, one was considered a typical ghost image and the other was considered a ghost-like real image (pseudo-ghost image). The formation zones of the real, double, and ghost images were examined based on the path and angles of the X-ray beam from the Planmeca ProMax. To simulate the pseudo-ghost and typical ghost images on panoramic radiography, a radiopaque marker was affixed to the right mandibular condyle of a dry mandible, and the position of the mandible was adjusted accordingly. Results: The center of rotation of the Planmeca ProMax extended beyond the jaw area, and the area of double image formation also reached beyond the jaw. The radiopaque-marked mandibular condyle, situated in the outwardly extending area of double image formation, exhibited triple images consisting of real, double (pseudo-ghost), and ghost images. These findings helped to explain the image formation associated with the patient's earrings observed in the panoramic radiograph. Conclusion: Dentists must understand the characteristics and principles of the panoramic equipment they use and apply this understanding to taking and interpreting panoramic radiographs.
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BACKGROUND/AIM: 25-hydroxycholesterol (25-HC) plays important roles in lipid metabolism, inflammatory responses, and apoptosis, but its pathophysiological association with osteoporosis (OP) has not been verified in osteoblasts. Hence, we studied the pathophysiological linkage and underlying cellular mechanisms of 25-HC in human osteoblast-like MG-63 cells and an ovariectomy-induced osteoporotic mouse model. MATERIALS AND METHODS: To investigate the pathophysiological linkage between 25-HC-induced osteoblast oxiapoptophagy and OP, 25-HC ELISA assay, MTT assay, cell live/dead staining, hematoxylin and eosin staining, DAPI staining, flow cytometry analysis, western blot, caspase-3 staining, reactive oxygen species (ROS) assay, autophagy staining, immunocytochemistry, Micro-CT image analysis and immunocytochemistry were performed in MG-63 cells and ovariectomy-induced OP animals. RESULTS: The expression of cholesterol-25-hydroxylase (CH25H), an enzyme catalyzing the conversion of cholesterol to 25-HC, and the production of 25-HC were increased by lipopolysaccharide in MG-63 cells. Cytotoxicity was increased by 25-HC in MG-63 cells. Apoptosis with condensed chromatin and altered morphology was induced by 25-HC through cleavage of caspases-8, -9, and -3 in MG-63 cells. 25-HC induced oxidative stress in MG-63 cells via elevation of ROS production, cyclooxygenase-2, and inducible nitric oxide synthase. Furthermore, the expression of autophagy biomarkers, including beclin-1 and microtubule-associated protein 1A/1B-light chain 3, was elevated by 25-HC in MG-63 cells. In addition, p53 expression was increased, whereas Akt phosphorylation was suppressed in 25-HC-incubated MG-63 cells. The expression of CH25H, cleaved caspase-3, and beclin-1 were up-regulated in the femoral bone of ovariectomy-induced mouse osteoporotic animals. CONCLUSION: 25-HC plays a role in OP via the induction of oxiapoptophagic osteoblast death.
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Osteoblastos , Osteoporose , Feminino , Camundongos , Animais , Humanos , Espécies Reativas de Oxigênio/metabolismo , Caspase 3/metabolismo , Proteína Beclina-1/metabolismo , Osteoblastos/metabolismo , Colesterol , Osteoporose/etiologia , Osteoporose/metabolismo , ApoptoseRESUMO
The aim of this study was to evaluate the anti-osteoporosis effects of Osmanthus fragrans leaf ethanol extract (OFLEE) in bone marrow-derived macrophages (BMM) and animals with osteoporosis. OFLEE not only suppressed tartrate-resistant acid phosphatase (TRAP)-positive cells with multiple nuclei but also decreased TRAP activity in BMM treated with macrophage colony stimulating factor (M-CSF) and receptor activator of nuclear factor-κB (NF-κB) ligand (RANKL). The formation of F-actin rings and the expression and activation of matrix metalloproteinases were decreased by OFLEE in BMM treated with M-CSF and RANKL. OFLEE suppressed M-CSF- and RANKL-induced osteoclastogenesis by inhibiting NF-κB phosphorylation, tumor necrosis factor receptor-associated factor 6, c-fos, the nuclear factor of activated T-cells, cytoplasmic 1, and cathepsin K in BMM. OFLEE downregulated reactive oxygen species, cyclooxygenase-2, inducible nitric oxide synthase, prostaglandin E2, tumor necrosis factor α, interleukin (IL)-1ß, IL-6, IL-17, and RANKL in BMM treated with M-CSF and RANKL. Oral administration of OFLEE suppressed osteoporotic bone loss without hepatotoxicity in ovariectomy-induced osteoporosis animals. Our findings suggest that OFLEE, with anti-inflammatory effects, prevents osteoporotic bone loss through the suppression of osteoclastic differentiation in BMM and animals with osteoporosis.
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The aim of this study was to evaluate cortical bone formation on the mandibular condyle using cone-beam computed tomography (CBCT) in asymptomatic adolescents and young adults and to evaluate the relationship between age and sex. CBCT images that can evaluate the shape of the mandibular condyle were selected from asymptomatic patients aged 13−25. The degree of cortication on the mandibular condyle (CMC) was evaluated using CBCT images reconstructed in the axial, sagittal, and coronal planes. CBCT data of 829 patients (413 males, 416 females) were selected and then the left and right images of all patients were acquired; consequently, a total of 1658 temporomandibular joint-related images were evaluated in this study. The degree of CMC was correlated with age in men and women (p < 0.05). The frequency of CMC 0 disappeared in woman aged 20 years and in men aged 21 years. Cortical bone formation of the mandibular condyle was completed at age 22 years in women and 24 years in men. The degrees of cortical bone formation of the mandibular condyle between men and women showed significant differences between the ages of 15−19 and 22 years. This difference can be interpreted as a different mandible growth period between the sexes.
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7α,25-dihydroxycholesterol (7α,25-DHC) is an oxysterol synthesized from 25-hydroxycholesterol by cytochrome P450 family 7 subfamily B member 1 (CYP7B1) and is a monooxygenase (oxysterol-7α-hydroxylase) expressed under inflammatory conditions in various cell types. In this study, we verified that 7α,25-DHC-induced oxiapoptophagy is mediated by apoptosis, oxidative stress, and autophagy in L929 mouse fibroblasts. MTT assays and live/dead cell staining revealed that cytotoxicity was increased by 7α,25-DHC in L929 cells. Consequentially, cells with condensed chromatin and altered morphology were enhanced in L929 cells incubated with 7α,25-DHC for 48 h. Furthermore, apoptotic population was increased by 7α,25-DHC exposure through the cascade activation of caspase-9, caspase-3, and poly (ADP-ribose) polymerase in the intrinsic pathway of apoptosis in these cells. 7α,25-DHC upregulated reactive oxygen species (ROS) in L929 cells. Expression of autophagy biomarkers, including beclin-1 and LC3, was significantly increased by 7α,25-DHC treatment in L929 cells. 7α,25-DHC inhibits the phosphorylation of Akt associated with autophagy and increases p53 expression in L929 cells. In addition, inhibition of G-protein-coupled receptor 183 (GPR183), a receptor of 7α,25-DHC, using GPR183 specific antagonist NIBR189 suppressed 7α,25-DHC-induced apoptosis, ROS production, and autophagy in L929 cells. Collectively, GPR183 regulates 7α,25-DHC-induced oxiapoptophagy in L929 cells.
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Oxisteróis , Receptores Acoplados a Proteínas G , Animais , Apoptose/genética , Apoptose/fisiologia , Autofagia/genética , Autofagia/fisiologia , Fibroblastos/metabolismo , Hidroxicolesteróis/metabolismo , Camundongos , Oxisteróis/metabolismo , Espécies Reativas de Oxigênio/metabolismo , Receptores Acoplados a Proteínas G/metabolismoRESUMO
Background: Demethoxycurcumin (DMC) is a curcumin analog with antitumor properties. However, its effects have not been investigated in human head and neck squamous cell carcinoma (HNSCC). The aim of the present study was to verify the antitumor effect and cellular signaling pathways of DMC in FaDu HNSCC cells. Methods: 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), cell Live/Dead staining, hematoxylin and eosin staining, DAPI staining, FACS, western blotting, caspase-3 activity assay, and nuclear translocation were performed to verify apoptosis and the cellular signaling pathway of DMC in FaDu cells. Results: DMC increased FaDu cell death, with cells presenting altered morphology and condensed nuclei. DMC increased significantly the apoptotic population of FaDu cells. Sequentially, DMC increased the expression of cleaved caspase-3 and PARP through the up-regulation of pro-apoptotic factors such as FasL, cleaved caspase-8, Bax, Bad, and cleaved caspase-9 and the suppression of anti-apoptotic factors including Bcl-xL and Bcl-2 in FaDu cells. Furthermore, DMC not only suppressed the phosphorylation of NF-κB, but also inhibited the translocation of NF-κB from cytosol to nucleus of FaDu cells. Conclusions: Present study demonstrates that DMC-induced cell death is mediated caspase-dependently by death receptor-mediated extrinsic and mitochondria-dependent intrinsic apoptosis through the inhibition of NF-κB translocation from the cytosol to the nucleus of FaDu cells. DMC is a curcuminoid with antitumor properties that modulates the NF-κB cellular signaling pathway in FaDu cells. Taken together, this study suggests that DMC has a considerable chemotherapeutic potential for HNSCC.
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SUMMARY: The aim of this study was to determine the morphologic characteristics of the lingual foramen and lateral lingual foramen using cone-beam CT in elderly Korean. Cone-beam CT images were obtained from 80 Korean older than 50 years (mean age, 65.2 years). The prevalence of the lingual and lateral lingual foramina at the lingual aspect of the mandible was determined. The diameter and height to the upper margin of the foramina from the mandibular inferior margin, and the bone height to the alveolar crest from the mandibular inferior margin were measured. In addition, the location of the lateral lingual foramen, the direction of its canal, and the presence of communication with the mandibular canal were evaluated. All of elderly Korean possessed at least one lingual foramen, with two or three foramina occurring in 77.5 % of Korean. A lateral lingual foramen was observed in 91.3 % of Korean, with the prevalence being highest at the second premolar in dentulous cases (21.6 %; 33/153). The very high frequencies of these foramina were attributable to high frequencies of relatively small-diameter inferior lingual foramen and lateral lingual foramen in the incisor region. The prevalence of a large-diameter (≥1 mm) superior lingual foramen was high, at 31.0 %. A large-diameter lateral lingual foramen in the premolar region occurred at a frequency of 17.0 %; communication with the mandibular canal was observed in 70.0 % of these cases. These quantitative data on the lingual and lateral lingual foramina of the mandible provide valuable information that could help to avoid surgical complications during implant placement in elderly Korean.
RESUMEN: El objetivo de este estudio fue determinar las características morfológicas del foramen lingual y del foramen lingual lateral mediante TC de haz cónico en adultos mayores coreanos. Se obtuvieron imágenes de TC de haz cónico de 80 coreanos mayores de 50 años (edad media, 65,2 años). Se determinó la prevalencia de los forámenes linguales y linguales laterales en la cara lingual de la mandíbula. Se midió el diámetro y la altura hasta el margen superior de los forámenes desde el margen inferior mandibular, y la altura ósea hasta la cresta alveolar desde el margen inferior mandibular. Además, se evaluó la ubicación del foramen lingual lateral, la dirección de su canal y la presencia de comunicación con el canal mandibular. Todos los adultos mayores coreanos tenían al menos un foramen lingual, con dos o tres forámenes en el 77,5 %. Se observó un foramen lingual lateral en el 91,3 %, siendo la prevalencia más alta en el segundo premolar en casos dentados (21,6 %; 33/ 153). Las mayores frecuencias de estos forámenes se atribuyeron a altas frecuencias de foramen lingual inferior y foramen lingual lateral de diámetro relativamente pequeño en la región de los incisivos. La prevalencia de un foramen lingual superior de gran diámetro (≥1 mm) fue alta, del 31,0 %. Un foramen lingual lateral de gran diámetro en la región premolar ocurrió con una frecuencia del 17,0 %; se observó comunicación con el canal mandibular en el 70,0 % de estos casos. Estos datos cuantitativos sobre los forámenes linguales y linguales laterales de la mandíbula proporcionan información valiosa que podría ayudar a evitar complicaciones quirúrgicas durante la colocación de implantes en adultos mayores coreanos.
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Humanos , Masculino , Feminino , Pessoa de Meia-Idade , Idoso , Língua/anatomia & histologia , Língua/diagnóstico por imagem , Mandíbula/anatomia & histologia , Mandíbula/diagnóstico por imagem , Tomografia Computadorizada de Feixe CônicoRESUMO
PURPOSE: The purpose of this study was to determine the palatal bone and soft tissue thicknesses using a miniscrew-supported maxillary skeletal expander (MSE) in Class III malocclusion. METHODS: The thicknesses of the palatal bone and soft tissue were measured in cone-beam computed tomography images obtained from 58 patients. All 20 points were crossing points between five levels, which were defined at 3 mm intervals relative to the line connecting the central fossae of the first molar (Level 0), and 2 mm and 4 mm lateral to the anteroposterior reference line (AP line). RESULTS: The palatal bone was significantly thicker in males than females in the anterior palate up to Level 0, while there was no significant sex-related difference in the posterior palate. There was a tendency for the thickness to decrease in the posterior direction, except in females at 2 mm lateral to the AP line. The palatal soft tissue was significantly thicker in males than females in all positions. At 2 mm lateral to the AP line, the palatal soft tissue thickness decreased in the posterior direction. A 4 mm lateral to the AP line, it initially decreased in the posterior direction, and then increasing again at Level - 6 (6 mm posterior of Level 0). As the lateral distance from the AP line increased, the palatal bone thickness decreased while the palatal soft tissue thickness increased. CONCLUSIONS: These findings provide quantitative data on the palatal bone and soft tissue thicknesses for the miniscrew-supported MSE in the posterior palate.
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Má Oclusão Classe III de Angle/cirurgia , Maxila/anormalidades , Técnica de Expansão Palatina/instrumentação , Palato Duro/anatomia & histologia , Palato Mole/anatomia & histologia , Adolescente , Adulto , Parafusos Ósseos , Tomografia Computadorizada de Feixe Cônico , Feminino , Humanos , Imageamento Tridimensional , Masculino , Maxila/diagnóstico por imagem , Maxila/cirurgia , Palato Duro/diagnóstico por imagem , Palato Duro/cirurgia , Palato Mole/diagnóstico por imagem , Palato Mole/cirurgia , Estudos Retrospectivos , Adulto JovemRESUMO
25-hydroxycholesterol (25-HC) is an oxysterol synthesized from cholesterol by cholesterol-25-hydroxylase during cholesterol metabolism. The aim of this study was to verify whether 25-HC induces oxiapoptophagy in fibroblasts. 25-HC not only decreased the survival of L929 cells, but also increased the number of cells with condensed chromatin and altered morphology. Fluorescence-activated cell sorting results showed that there was a dose-dependent increase in the apoptotic populations of L929 cells upon treatment with 25-HC. 25-HC-induced apoptotic cell death was mediated by the death receptor-dependent extrinsic and mitochondria-dependent intrinsic apoptosis pathway, through the cascade activation of caspases including caspase-8, -9, and -3 in L929 cells. There was an increase in the levels of reactive oxygen species and inflammatory mediators such as inducible nitric oxide synthase, cyclooxygenase-2, nitric oxide, and prostaglandin E2 in L929 cells treated with 25-HC. Moreover, 25-HC caused an increase in the expression of beclin-1 and microtubule-associated protein 1A/1B-light chain 3, an autophagy biomarker, in L929 cells. There was a significant decrease in the phosphorylation of protein kinase B (Akt) in L929 cells treated with 25-HC. Taken together, 25-HC induced oxiapoptophagy through the modulation of Akt and p53 cellular signaling pathways in L929 cells.
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Autofagia/efeitos dos fármacos , Fibroblastos/efeitos dos fármacos , Fibroblastos/metabolismo , Hidroxicolesteróis/farmacologia , Estresse Oxidativo/efeitos dos fármacos , Animais , Apoptose/efeitos dos fármacos , Morte Celular/efeitos dos fármacos , Linhagem Celular , Sobrevivência Celular/efeitos dos fármacos , Hidroxicolesteróis/química , Mediadores da Inflamação/metabolismo , Camundongos , Mitocôndrias , Estrutura Molecular , Espécies Reativas de Oxigênio/metabolismoRESUMO
BACKGROUND/PURPOSE: Due to the pneumatization of the maxillary sinus, the sinus floor augmentation is often performed to implant placement in the maxillary posterior region. The aim was to perform radiographic and histomorphometric evaluation after placement of mixed allografts (cortical freeze-dried bone allograft [FDBA] 50%:cancellous FDBA 50%) during sinus floor augmentation. MATERIALS AND METHODS: In 37 patients, anorganic bovine bone (ABB, sitesâ¯=â¯16), mineralized cancellous bone allograft (MCBA, sitesâ¯=â¯15), and mixed allografts (Mixed AG, sitesâ¯=â¯20) were placed during sinus floor elevation via the lateral approach (LSFE), at total 51 sites with residual alveolar bone height (RBH)â¯<â¯5â¯mm. Cone-beam computed tomography images were obtained before LSFE (T0), after surgery (T1), and 6 months after surgery (T2) for radiographic analysis. After a 6-month healing period, core biopsies were harvested and histomorphometric analysis was performed. RESULTS: The mean augmented bone height (ABH) of ABB, MCBA, and mixed AG groups after surgery was similar (13.86⯱â¯4.19â¯mm, 13.99⯱â¯4.07â¯mm, and 14.20⯱â¯3.12â¯mm, respectively; Pâ¯>â¯0.05). The mean ABH of ABB, MCBA, and mixed AG groups after 6 months was similar (13.72⯱â¯4.55â¯mm, 11.83⯱â¯3.31â¯mm, and 12.53⯱â¯2.97â¯mm, respectively; Pâ¯>â¯0.05). In the ABB, MCBA, and mixed AG groups, the proportion of newly formed bone (NB) was similar (36.13⯱â¯10.01%, 39.26⯱â¯10.72%, and 31.27⯱â¯18.31%, respectively; Pâ¯>â¯0.05). CONCLUSION: This result demonstrated that mixed AG led to sufficient bone augmentation and histologically comparable NB formation as compared to ABB and MCBA for sinus floor augmentation.
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The aim of the present study was to investigate the pathophysiological etiology of osteoarthritis that is mediated by the apoptosis of chondrocytes exposed to 25-hydroxycholesterol (25-HC), an oxysterol synthesized by the expression of cholesterol-25-hydroxylase (CH25H) under inflammatory conditions. Interleukin-1ß induced the apoptosis of chondrocytes in a dose- dependent manner. Furthermore, the production of 25-HC increased in the chondrocytes treated with interleukin-1ß through the expression of CH25H. 25-HC decreased the viability of chondrocytes. Chondrocytes with condensed nucleus and apoptotic populations increased by 25-HC. Moreover, the activity and expression of caspase-3 were increased by the death ligand-mediated extrinsic and mitochondria-dependent intrinsic apoptotic pathways in the chondrocytes treated with 25-HC. Finally, 25-HC induced not only caspase-dependent apoptosis, but also induced proteoglycan loss in articular cartilage ex vivo cultured rat knee joints. These data indicate that 25-HC may act as a metabolic pathophysiological factor in osteoarthritis that is mediated by progressive chondrocyte death in the articular cartilage with inflammatory condition.
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BACKGROUND/AIM: Oxysterol plays important physiological roles in diverse biological processes including apoptosis. However, the mechanisms underlying oxysterol-induced apoptosis remain unknown. 25-hydroxycholesterol (25-HC) is an oxysterol synthesized by cholesterol 25-hydroxylase from cholesterol during sterol metabolism. The aim of present study was to investigate 25-HC-induced apoptosis and associated signalling pathways in FaDu cells, which is originated form human head and neck squamous cell carcinoma cells. MATERIALS AND METHODS: 25-HC-induced apoptosis was investigated by cell cytotoxicity assay using MTT, cell viability assay using cell LIVE/DEAD cell viability assay, haematoxylin & eosin staining, nuclear staining, fluorescence-activated cell sorting, western blotting using specific antibodies associated with extrinsic and intrinsic apoptosis pathways, and caspase-3/-7 activity assay in FaDu cells. RESULTS: 25-HC dose-dependently decreased the viability of FaDu cells and up-regulated apoptotic events, such as alteration in morphology, and nuclear condensation. Flow cytometric analysis showed an increase in apoptotic population upon 25-HC treatment, suggesting that 25-HC induces apoptosis in FaDu cells. Moreover, 25-HC-induced apoptosis in FaDu cells was dependent on the activation of caspases by Fas antigen ligand-triggered death receptor-mediated extrinsic pathway and mitochondria-dependent intrinsic pathway via mitogen activated protein kinases. CONCLUSION: Cholesterol-derived oxysterol, 25-HC has potential anti-cancer function in FaDu cells and may have potential properties for the discovery of anti-cancer agents.
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Apoptose/efeitos dos fármacos , Hidroxicolesteróis/uso terapêutico , Carcinoma de Células Escamosas de Cabeça e Pescoço/tratamento farmacológico , Linhagem Celular Tumoral , Humanos , Hidroxicolesteróis/farmacologia , Carcinoma de Células Escamosas de Cabeça e Pescoço/patologiaRESUMO
Formononetin, a phytoestrogen extracted from various herbal plants, has been investigated as an anticancer agent against diverse types of cancer. The aim of the present study was to investigate the induction of apoptotic cell death by formononetin in the FaDu pharyngeal squamous cell carcinoma cell line. Formononetin significantly increased FaDu cell death, with an estimated IC50 value of 50 µM; however, it did not affect the viability of normal L929 mouse fibroblasts used as normal control at 525 µM. Typical characteristics of apoptosis, such as morphological alterations, chromatin condensation, DNA fragmentation and the size of the apoptotic cell population, were increased in FaDu cells treated with formononetin for 24 h. Furthermore, formononetininduced FaDu cell death involved the death receptormediated extrinsic and the mitochondriadependent intrinsic apoptotic pathways by activating the caspase cascade. The chemotherapeutic effects of formononetin were mediated by the suppression of mitogenactivated protein kinases, including extracellular signalregulated kinase 1/2 and p38, and nuclear factorκB phosphorylation in FaDu cells. Finally, the oral administration of formononetin decelerated tumor growth through the expression of cleaved caspase3 in a FaDu cell xenograft animal model. Taken together, these findings indicate that formononetin holds promise as a chemotherapeutic agent and may be of value in the treatment of human head and neck squamous cell carcinoma.
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Carcinoma de Células Escamosas/tratamento farmacológico , Neoplasias de Cabeça e Pescoço/tratamento farmacológico , Isoflavonas/administração & dosagem , Proteínas Quinases Ativadas por Mitógeno/metabolismo , NF-kappa B/metabolismo , Administração Oral , Animais , Carcinoma de Células Escamosas/metabolismo , Linhagem Celular Tumoral , Sobrevivência Celular/efeitos dos fármacos , Regulação para Baixo , Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos , Neoplasias de Cabeça e Pescoço/metabolismo , Humanos , Isoflavonas/farmacologia , Camundongos , Fosforilação/efeitos dos fármacos , Ensaios Antitumorais Modelo de XenoenxertoRESUMO
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-1ß (IL-1ß) 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-1ß-induced decrease in extracellular matrix. Furthermore, treatment with morin attenuated IL-1ß-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.
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Condrócitos/metabolismo , Condrócitos/patologia , Flavonoides/farmacologia , Inflamação/metabolismo , Inflamação/patologia , Interleucina-1beta/toxicidade , Animais , Cartilagem Articular/efeitos dos fármacos , Cartilagem Articular/metabolismo , Cartilagem Articular/patologia , Sobrevivência Celular/efeitos dos fármacos , Células Cultivadas , Condrócitos/efeitos dos fármacos , Citocinas/metabolismo , Matriz Extracelular/metabolismo , Flavonoides/química , Mediadores da Inflamação/metabolismo , Metaloproteinases da Matriz/metabolismo , Proteoglicanas/metabolismo , Ratos Sprague-DawleyRESUMO
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.
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Antineoplásicos/farmacologia , Neoplasias de Cabeça e Pescoço/tratamento farmacológico , Fenformin/farmacologia , Carcinoma de Células Escamosas de Cabeça e Pescoço/tratamento farmacológico , Apoptose/efeitos dos fármacos , Caspase 3/metabolismo , Caspase 7/metabolismo , Linhagem Celular Tumoral , Sobrevivência Celular/efeitos dos fármacos , Proteína Ligante Fas/metabolismo , HumanosRESUMO
PURPOSE: The purpose of this study was to evaluate a new graft material, biphasic calcium phosphate, composed of 60% hydroxyapatite and 40% ß-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.
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Materiais Biocompatíveis/administração & dosagem , Substitutos Ósseos/administração & dosagem , Transplante Ósseo/métodos , Implantação Dentária Endóssea/normas , Hidroxiapatitas/administração & dosagem , Seio Maxilar/cirurgia , Minerais/administração & dosagem , Levantamento do Assoalho do Seio Maxilar/métodos , Adulto , Idoso , Animais , Produtos Biológicos/administração & dosagem , Regeneração Óssea , Bovinos , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Estudos Prospectivos , Microtomografia por Raio-XRESUMO
The aim of the present study was to investigate biochanin-A-induced anticancer effects and their cellular signaling pathway in FaDu pharyngeal squamous carcinoma cells. Biochanin-A induced cell death through increased cytotoxicity of FaDu cells in a dose- and time-dependent manner. The number of cells with nucleus condensation and the apoptotic population were increased in the FaDu cells stimulated with biochanin-A for 24 h. Furthermore, extrinsic apoptotic factors such as FasL and their downstream target caspase-8 were increased and activated in the FaDu cells treated with biochanin-A in a dose-dependent manner. Moreover, biochanin-A decreased the expression of intrinsic anti-apoptotic factors such as Bcl-2 and Bcl-xL, and increased the level and activation of intrinsic apoptotic factors such as Bad and caspase-9. Finally, biochanin-A induced the activation of caspase-3 and Poly(ADP ribose) polymerase (PARP) in FaDu cells. Our results suggest that biochanin-A-induced apoptosis was mediated by death receptor mediated-extrinsic and mitochondria-dependent intrinsic apoptotic signaling pathways. Biochanin-A also inhibited wound healing migration and proliferation of FaDu cells via the downregulation and inactivation of matrix metalloproteinase-2 and -9 that are mediated by the suppression of p38, mitogen activated protein kinase (MAPK), NF-κB and Akt cellular signaling pathways. Therefore, these data suggest that the biochanin-A may act as a potential chemotherapeutic compound to treat head and neck cancer.
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Antineoplásicos/farmacologia , Proteínas Reguladoras de Apoptose/metabolismo , Carcinoma de Células Escamosas/metabolismo , Genisteína/farmacologia , Neoplasias Faríngeas/metabolismo , Apoptose , Carcinoma de Células Escamosas/tratamento farmacológico , Linhagem Celular Tumoral , Movimento Celular/efeitos dos fármacos , Proliferação de Células/efeitos dos fármacos , Sobrevivência Celular/efeitos dos fármacos , Relação Dose-Resposta a Droga , Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos , Redes Reguladoras de Genes/efeitos dos fármacos , Humanos , Neoplasias Faríngeas/tratamento farmacológico , Fatores de TempoRESUMO
Multiple keratocystic odontogenic tumors (KCOT) occurred in a young child is challenging problem in the field of pediatric dentistry, and might have been related to nevoid basal cell carcinoma syndrome (NBCCS). Because of high recurrence rate of KCOTs, complete surgical resection is generally accepted as definitive treatment. However, complete surgical resection could induce negative effect on the development of permanent teeth and growth of jaw. Herein, we reported successful treatment case of young KCOT patient with NBCCS. Although multiple KCOTs occurred continually, the majority of the lesions healed well by decompression and important anatomical structures and permanent teeth were successfully preserved. The purpose of this paper is to report more conservative treatment of multiple keratocystic odontogenic tumors (KCOTs) by repeated decompressions with later peripheral ostectomy during a 7-year follow-up.
Assuntos
Síndrome do Nevo Basocelular/cirurgia , Descompressão Cirúrgica/métodos , Neoplasias Mandibulares/cirurgia , Neoplasias Primárias Múltiplas/cirurgia , Tumores Odontogênicos/cirurgia , Síndrome do Nevo Basocelular/patologia , Criança , Feminino , Humanos , Neoplasias Mandibulares/patologia , Recidiva Local de Neoplasia/patologia , Recidiva Local de Neoplasia/cirurgia , Neoplasias Primárias Múltiplas/patologia , Tumores Odontogênicos/patologia , Osteotomia , Radiografia Panorâmica , Reoperação , Extração DentáriaRESUMO
OBJECTIVES: The aim of this study was to identify the detailed anatomic morphology of the retromolar canal using histologic sections and cone-beam computed tomography (CBCT) images. MATERIALS AND METHODS: Twenty-two sides of the mandible obtained from cadavers and CBCT images of 72 patients (144 sides) were analyzed. All mandibles were prepared using conventional methods of tissue processing, stained with hematoxylin-eosin, and measured to elucidate the composition and dimensions of the retromolar canal with the aid of a light microscope. In addition, the prevalence, course, opening position, and distance of the retromolar canal from the second molar were measured on CBCT images. RESULTS: The retromolar neurovascular bundle in the retromolar canal originated from the inferior alveolar neurovascular bundle, and the mean areas of the neurovascular bundle and each artery and nerve contained within it were 0.59, 0.07, and 0.05mm2, respectively. The mean horizontal and vertical diameters of the neurovascular bundle were 0.82 and 0.90mm, respectively. The retromolar canal was detected more often on CBCT images (43.1%, 31 out of 72 patients). It mainly arose vertically (71.0%) from the mandibular canal and opened in the middle portion (57.9%) of the retromolar triangle at a mean distance of 13.13mm from the second molar. CONCLUSIONS: The retromolar canal is a normal anatomic structure that is relatively common and contains both a relatively large artery and a nerve. Clinicians need to pay closer attention to vascular problems as well as nerve damage when they are performing surgical procedures in the retromolar area.
Assuntos
Tomografia Computadorizada de Feixe Cônico , Mandíbula/anatomia & histologia , Mandíbula/diagnóstico por imagem , Dente Molar/anatomia & histologia , Dente Molar/diagnóstico por imagem , Adulto , Idoso , Cadáver , Feminino , Humanos , Masculino , Pessoa de Meia-IdadeRESUMO
The aim of the present study was to investigate licochalcone-E (Lico-E)-induced apoptosis and the associated apoptotic signaling pathway in FaDu cells, a human pharyngeal squamous carcinoma cell line. Treatment with Lico-E exhibited significant cytotoxicity on FaDu cells in a concentration-dependent manner. The IC50 value of Lico-E in FaDu cells was ~50 µM. Treatment with Lico-E increased the number of dead FaDu cells. Furthermore, chromatin condensation, which is associated with apoptotic cell death, was observed in FaDu cells treated with Lico-E for 24 h. By contrast, Lico-E did not produce cytotoxicity or increase the number of dead cells when applied to human normal oral keratinocytes (hNOKs). Furthermore, chromatin condensation was not observed in hNOKs treated with Lico-E. Treatment with Lico-E increased the expression of Fas ligand and the cleaved form of caspase-8 in FaDu cells. Furthermore, treatment with Lico-E increased the expression of pro-apoptotic factors, including apoptosis regulator BAX, Bcl-2-associated agonist of cell death, apoptotic protease-activating factor 1, caspase-9 and tumor suppressor p53, while decreasing the expression of anti-apoptotic factors, including apoptosis regulator Bcl-2 and Bcl-2-like protein 1 in FaDu cells. The expression of cleaved caspases-3 and poly (ADP-ribose) polymerase was significantly upregulated following treatment with Lico-E in FaDu cells, while Lico-E-induced apoptotic FaDu cell death was partially suppressed by treatment with Z-VAD-FMK, a pan caspase inhibitor. Therefore, Lico-E-induced oral cancer (OC) cell-specific apoptosis is mediated by the death receptor-dependent extrinsic and mitochondrial-dependent intrinsic apoptotic signaling pathways. In conclusion, these data suggested that Lico-E exhibits potential chemopreventive effects and warrants further developed as a chemotherapeutic agent against OC.