Effect of NAMPT on the proliferation and apoptosis in odontoblast-like MDPC-23 cell.

This study aimed to evaluate the physiological role of NAMPT associated with MDPC-23 odontoblast cell proliferation. Cell viability was measured using the (DAPI) staining, caspase activation analysis and immunoblotting were performed. Visfatin promoted MDPC-23 odontoblast cell growth in a dose-dependent manner. Furthermore, the up-regulation of Visfatin promoted odontogenic differentiation and accelerated mineralization through an increase in representative odontoblastic biomarkers in MDPC-23 cells. However, FK-866 cell growth in a dose-dependent manner induced nuclear condensation and fragmentation. FK-866-treated cells showed H&E staining and increased apoptosis compared to control cells. The expression of anti-apoptotic factors components of the mitochondria-dependent intrinsic apoptotic pathway significantly decreased following FK-866 treatment. The expression of pro-apoptotic increased upon FK-866 treatment. In addition, FK-866 activated caspase-3 and PARP to induce cell death. In addition, after treating FK-866 for 72 h, the 3/7 activity of MDPC-23 cells increased in a concentration-dependent manner, and the IHC results also confirmed that Caspase-3 increased in a concentration-dependent. Therefore, the presence or absence of NAMPT expression in dentin cells was closely related to cell proliferation and formation of extracellular substrates.

25-Hydroxycholesterol induces odontoclastic differentiation through RANK-RANKL upregulation and NF-κB activation in odontoblast-like MDPC-23 cells: An in vitro study.

AIM: The physiological effects and cellular mechanism of 25-hydroxycholesterol (25-HC), which is an oxysterol synthesized from cholesterol by cholesterol-25-hydroxylase (CH25H) expressed under inflammatory conditions, are still largely unknown during odontoclastogenesis. This study aimed to evaluate 25-HC-induced odontoclastogenesis and its cellular mechanisms in odontoblast-like MDPC-23 cells. METHODOLOGY: To investigate 25-HC-induced odontoclastogenesis of MDPC-23 cells and its cellular mechanism, haemotoxylin and eosin staining, tartrate-resistant acid phosphatase (TRAP) staining, dentine resorption assay, zymography, reactive oxygen species (ROS) detection, immunocytochemistry, and nuclear translocation were performed. The experimental values are presented as mean ± standard deviation and were compared using analysis of variance, followed by post hoc multiple comparisons (Tukey's test) using SPSS software version 22 (IBM Corp.). A p-value <.05 was considered statistically significant. RESULTS: Lipopolysaccharide or receptor activator of nuclear factor-κB ligand (RANKL) induced the synthesis of 25-HC via the expression of CH25H in MDPC-23 cells (p < .01). Multinucleated giant cells with morphological characteristics and TRAP activity of the odontoclast were increased by 25-HC in MDPC-23 cells (p < .01). Moreover, 25-HC increased dentine resorption through the expression and activity of matrix metalloproteinases in MDPC-23 cells. It not only increased the expression of odontoclastogenic biomarkers but also translocated cytosolic nuclear factor-κB (NF-κB) to the nucleus in MDPC-23 cells. Additionally, 25-HC not only increased the production of ROS (p < .01), expression of inflammatory mediators (p < .01), pro-inflammatory cytokines, receptor activator of NF-κB (RANK), and RANKL but also suppressed the expression of osteoprotegerin (OPG) in MDPC-23 cells. In contrast, CDDO-Me, a chemical NF-κB inhibitor, decreased TRAP activity (p < .01) and downregulated the expression of the odontoclastogenic biomarkers, including RANK and RANKL, in MDPC-23 cells. CONCLUSION: 25-HC induced odontoclastogenesis by modulating the RANK-RANKL-OPG axis via NF-κB activation in MDPC-23 cells. Therefore, these findings provide that 25-HC derived from cholesterol metabolism may be involved in the pathophysiological etiological factors of internal tooth resorption.

GPR183 Regulates 7α,25-Dihydroxycholesterol-Induced Oxiapoptophagy in L929 Mouse Fibroblast Cell.

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.

Nicotinamide phosphoribosyltransferase regulates the cell differentiation and mineralization in cultured odontoblasts.

The aim of the present study was to investigate the physiological role of nicotinamide phosphoribosyltransferase (NAMPT) associated with odontogenic differentiation during tooth development in mice. Mouse dental papilla cell-23 (MDPC- 23) cells cultured in differentiation media were stimulated with the specific NAMPT inhibitor, FK866, and Visfatin (NAMPT) for up to 10 days. The cells were evaluated after 0, 4, 7, and 10 days. Cell viability was measured using the 3-(4,5-dimethylthiazol- 2-yl)-2,5-diphenyltetrazolium bromide assay. The mineralization assay was performed by staining MDPC-23 cells with Alizarin Red S solution. After cultivation, MDPC-23 cells were harvested for quantitative PCR or Western blotting. Analysis of variance was performed using StatView 5.0 software (SAS Institute Inc., Cary, NC, USA). Statistical significance was set at p < 0.05. The expression of NAMPT increased during the differentiation of murine odontoblast-like MDPC-23 cells. Furthermore, the up-regulation of NAMPT promoted odontogenic differentiation and accelerated mineralization through an increase in representative odontoblastic biomarkers, such as dentin sialophosphoprotein, dentin matrix protein-1, and alkaline phosphatase in MDPC-23 cells. However, treatment of the cells with the NAMPT inhibitor, FK866, attenuated odontogenic differentiation, as evidenced by the suppression of odontoblastic biomarkers. These data indicate that NAMPT regulated odontoblastic differentiation through the regulation of odontoblastic biomarkers. The increase in NAMPT expression in odontoblasts was closely related to the formation of the extracellular matrix and dentin via the Runx signaling pathway. Therefore, these data suggest that NAMPT is a critical regulator of odontoblast differentiation during tooth development.

Arctigenin induces caspase-dependent apoptosis in FaDu human pharyngeal carcinoma cells.

The present study was carried out to investigate the effect of Arctigenin on cell growth and the mechanism of cell death elicited by Arctigenin were examined in FaDu human pharyngeal carcinoma cells. To determine the apoptotic activity of Arctigenin in FaDu human pharyngeal carcinoma cells, cell viability assay, DAPI staining, caspase activation analysis, and immunoblotting were performed. Arctigenin inhibited the growth of cells in a dose-dependent manner and induced nuclear condensation and fragmentation. Arctigenin-treated cells showed caspase-3/7 activation and increased apoptosis versus control cells. FasL, a death ligand associated with extrinsic apoptotic signaling pathways, was up-regulated by Arctigenin treatment. Moreover, caspase-8, a part of the extrinsic apoptotic pathway, was activated by Arctigenin treatments. Expressions of anti-apoptotic factors such as Bcl-2 and Bcl-xL, components of the mitochondria-dependent intrinsic apoptosis pathway, significantly decreased following Arctigenin treatment. The expressions of pro-apoptotic factors such as BAX, BAD and caspase-9, and tumor suppressor -53 increased by Arctigenin treatments. In addition, Arctigenin activated caspase-3 and poly (ADP-ribose) polymerase (PARP) induced cell death. Arctigenin also inhibited the proliferation of FaDu cells by the suppression of p38, NF-κB, and Akt signaling pathways. These results suggest that Arctigenin may inhibit cell proliferation and induce apoptotic cell death in FaDu human pharyngeal carcinoma cells through both the mitochondria-mediated intrinsic pathway and the death receptor-mediated extrinsic pathway.

25-Hydroxycholesterol-Induced Oxiapoptophagy in L929 Mouse Fibroblast Cell Line.

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.

Radiological evaluation of the bone and soft tissue thicknesses of the palate for using a miniscrew-supported maxillary skeletal expander.

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.

Anatomical configuration of the inferior alveolar neurovascular bundle: a histomorphometric analysis.

PURPOSE: The inferior alveolar neurovascular bundle (NVB) is important in implant placement and many other surgeries in dentistry because it is a major supplier of sensation and blood to the mandible via the mandibular canal. The purposes of the present study were to determine the areas and diameters of the NVB, the inferior alveolar nerve (IAN), and the inferior alveolar artery (IAA), and to verify the buccolingual location of the mandibular canal. METHODS: The anatomical configuration of the NVB was examined by histomorphometrically analyzing 20 embalmed dentulous hemimandibles. The areas and maximum horizontal and vertical diameters of the NVB, IAN, and IAA were measured according to tooth region. The distances from the internal border of the mandibular canal to the outer surface of the buccal and lingual cortical plates were also measured. RESULTS: The areas of the vertically oval-shaped NVB and IAN appeared to be constant between the molar and premolar regions, which contain the mental branch, and decreased sharply in the lateral incisor after branching off of the mental branch via the mental canal. The mandibular canal was located close to the lingual cortical plate in the posterior tooth region before passing through the mental canal, immediately after which it was situated quite close to the buccal cortical plate, and then closer to the middle toward the anterior tooth region. CONCLUSIONS: The findings of this study provide useful anatomical information that should help to minimize the risk of injury to the NVB during surgical procedures in the mandibular region.

NFI-C regulates osteoblast differentiation via control of osterix expression.

In bone marrow, bone marrow stromal cells (BMSCs) have the capacity to differentiate into osteoblasts and adipocytes. Age-related osteoporosis is associated with a reciprocal decrease of osteogenesis and an increase of adipogenesis in bone marrow. In this study, we demonstrate that disruption of nuclear factor I-C (NFI-C) impairs osteoblast differentiation and bone formation, and increases bone marrow adipocytes. Interestingly, NFI-C controls postnatal bone formation but does not influence prenatal bone development. We also found decreased NFI-C expression in osteogenic cells from human osteoporotic patients. Notably, transplantation of Nfic-overexpressing BMSCs stimulates osteoblast differentiation and new bone formation, but inhibits adipocyte differentiation by suppressing peroxisome proliferator-activated receptor gamma expression in Nfic(-/-) mice showing an age-related osteoporosis-like phenotype. Finally, NFI-C directly regulates Osterix expression but acts downstream of the bone morphogenetic protein-2-Runx2 pathway. These results suggest that NFI-C acts as a transcriptional switch in cell fate determination between osteoblast and adipocyte differentiation in BMSCs. Therefore, regulation of NFI-C expression in BMSCs could be a novel therapeutic approach for treating age-related osteoporosis.

Downregulation of adenomatous polyposis coli by microRNA-663 promotes odontogenic differentiation through activation of Wnt/beta-catenin signaling.

MicroRNAs (miRNAs) regulate cell differentiation by inhibiting mRNA translation or by inducing its degradation. However, the role of miRNAs in odontogenic differentiation is largely unknown. In this present study, we observed that the expression of miR-663 increased significantly during differentiation of MDPC-23 cells to odontoblasts. Furthermore, up-regulation of miR-663 expression promoted odontogenic differentiation and accelerated mineralization without proliferation in MDPC-23 cells. In addition, target gene prediction for miR-663 revealed that the mRNA of the adenomatous polyposis coli (APC) gene, which is associated with the Wnt/ß-catenin signaling pathway, has a miR-663 binding site in its 3'-untranslated region (3'UTR). Furthermore, APC expressional was suppressed significantly by miR-663, and this down-regulation of APC expression triggered activation of Wnt/ß-catenin signaling through accumulation of ß-catenin in the nucleus. Taken together, these findings suggest that miR-663 promotes differentiation of MDPC-23 cells to odontoblasts by targeting APC-mediated activation of Wnt/ß-catenin signaling. Therefore, miR-663 can be considered a critical regulator of odontoblast differentiation and can be utilized for developing miRNA-based therapeutic agents.

MicroRNA-205 suppresses the oral carcinoma oncogenic activity via down-regulation of Axin-2 in KB human oral cancer cell.

MicroRNA (miRNA) is a small noncoding RNA molecule, 19-25 nucleotides in length, which regulates several pathways including cell development, cell proliferation, carcinogenesis, apoptosis, etc. In this study, the over-expression of microRNA-205 (miR-205) increased the number of apoptotic cells by at least 4 times compared to the control. In addition, over-expressed miRNA in KB oral cancer cells triggered apoptosis via the caspase cascade, including the cleavage of caspase-9, caspase-7, caspase-3, and PARP. Flow cytometry showed that apoptotic cell death was increased significantly by 35.33% in KB oral cancer cells with over-expressed miR-205 compared to the control. The microarray data showed that axis inhibitor protein 2 (Axin2) was down-regulated in KB oral cancer cells transfected with miR-205. In addition, Axin2 was down-regulated by approximately 50% by over-expressed miR-205 at both the mRNA and protein levels. Interestingly, Axin2 was up-regulated in KB oral cancer compared to human normal oral keratinocytes. Furthermore, the cell cytotoxicity and apoptotic population of KB oral cancer cells were increased significantly after Axin2 siRNA transfection. These results suggest that Axin2 is might be as potential oncogene in KB oral cancer cells. The luciferase assay showed that over-expressed miR-205 in KB oral cancer cells suppressed AXIN2 expression through an interaction with its own binding site at AXIN2 3'UTR (64-92). These results suggest that miR-205 is a novel anti-oncogenic miRNA in KB oral cancer cells, and may have potential applications in oral cancer therapy.

JPH203, an L-type amino acid transporter 1-selective compound, induces apoptosis of YD-38 human oral cancer cells.

Compared to most normal cells that express L-type amino acid transporter 2, L-type amino acid transporter 1 is highly expressed in cancer cells and presumed to support their elevated growth and proliferation. This study examined JPH203, a potent and selective L-type amino acid transporter 1 inhibitor, and its ability to suppress YD-38 human oral cancer cell growth. The YD-38 cells express L-type amino acid transporter 1 with its associating protein 4F2 heavy chain, but not L-type amino acid transporter 2. JPH203 and BCH, a non-selective L-type amino acid transporter inhibitor, completely inhibited l-leucine uptake in YD-38 cells. As expected, the intrinsic affinity of JPH203 to inhibit l-leucine uptake was far more efficient than BCH. Likewise, JPH203 and BCH inhibited YD-38 cell growth, with JPH203 being superior to BCH. JPH203 up-regulated the population of apoptotic YD-38 cells through the activation of apoptotic factors, including caspases and PARP. These results suggest that the inhibition of L-type amino acid transporter 1 activity via JPH203, which may act as a potential novel anti-oral-cancer agent, leads to apoptosis by inducing the intracellular depletion of the neutral amino acids essential for cancer cell growth in YD-38 human oral cancer cells.

Topographical relationship of the greater palatine artery and the palatal spine. Significance for periodontal surgery.

AIM: The aims of this study were to (1) identify the branching pattern and course of the greater palatine artery (GPA), (2) carry out a morphological analysis of the palatal bony prominence that divides the medial and lateral grooves and (3) characterize the topographical relationships between these two structures. METHODS: Thirty-six hemimaxillae were studied with the aid of a surgical microscope to elucidate the GPA. A further 25 dry skulls were examined to establish the morphology of the palatal spine. RESULTS: The most common GPA branching pattern was type I (41.7%, 15 sides), which gave off the medial and canine branches after the bony prominence. The distances from the CEJ to the lateral branch of the GPA were 9.04 ± 2.93 mm (canine), 11.12 ± 1.89 mm (first premolar), 13.51 ± 2.08 mm (second premolar), 13.76 ± 2.86 mm (first molar) and 13.91 ± 2.20 mm (second molar). The palatal spine was frequently observed as the bony prominence (66.3%, 57 sides), and was located at 6.49 ± 1.76 mm from the greater palatine foramen, with a length of 10.42 ± 2.45 mm. There was no a correlation between the bony prominence shape and the GPA branching pattern. CONCLUSIONS: These results could provide the reference data regarding the topography of the GPA for periodontal surgery.

Histomorphologic approach for the modiolus with reference to reconstructive and aesthetic surgery.

The modiolus is strongly associated with facial expression, beauty, and aging, and so it is often viewed as the main facial landmark, both functionally and aesthetically. This study examined the modiolus and the surrounding structures histomorphologically with the aim of providing useful information for reconstructive and aesthetic surgery. Nineteen embalmed cadavers (38 hemifaces; 8 males and 11 females; mean age at death, 66.9 years) were examined in this study. For macroscopic observations, the modiolus and facial artery in the perioral region of 28 hemifaces were revealed by meticulous dissection. The modiolus and its surrounding structures were then prepared from 12 hemifaces for routine histology and stained with hematoxylin-eosin and Masson trichrome. A tendinous tissue nodule in the modiolus was found in 21.4% of cases (ie, 6 hemifaces). The facial artery passed approximately 1 mm lateral to the lateral border of the modiolus. In the central region of modiolus, which was an area of convergence of muscle fibers, the tendinous structure appeared as dense irregular collagenous connective tissue. Particularly in the middle layer between the skin and the oral mucosa, it appeared as a dense, compact, and prominent shape horizontally. The finding of the existence of a tendinous structure in the central region of the modiolus, which could act as an anchor for the converging facial muscles, is expected to provide critical information in the field of facial plastic surgery.

Histomorphometric analysis of the palatal mucosa associated with periodontal plastic surgery on cadavers.

PURPOSE: The palatal mucosa is a major donor site for connective tissue in the field of periodontal plastic surgery, since it satisfies both the esthetic and functional demands of patients. The purpose of this study was to use histomorphometric analysis to measure the thicknesses of the palatal mucosa and the lamina propria including the epithelium on cadavers. METHODS: Thirty-four hemimaxillae of cadavers were examined (13 male and 4 female, mean age 57.2 years). Each maxilla was processed for histological sectioning and subsequently for histomorphometric analysis. The thicknesses of the palatal mucosa and the lamina propria including the epithelium were measured at three points starting from the alveolar crest, at intervals of 4 mm, with the aid of Adobe Photoshop. RESULTS: The thickness of the palatal mucosa at the alveolar crest and at 4 and 8 mm below the alveolar crest were 2.51 ± 0.83 (mean ± SD), 2.92 ± 0.80, and 3.62 ± 0.99 mm, respectively, and thus increasing from the alveolar crest toward the midpalatal suture. Conversely, the thicknesses of the lamina propria including the epithelium at these same positions were 2.06 ± 0.70, 1.54 ± 0.48, and 1.28 ± 0.46 mm, respectively, thus decreasing toward the midpalatal suture. CONCLUSIONS: The present results indicate that clinicians need to be particularly careful when harvesting palatal mucosa that is destined to be used as autogenous donor material for connective tissue in periodontal plastic surgery.

Anticancer activity of Saussurea lappa extract by apoptotic pathway in KB human oral cancer cells.

CONTEXT: Saussurea lappa Dence (Compositae) is used as a traditional herbal medicine to treat abdominal pain and tenesmus in East Asia. Current studies have shown that S. lappa has anticancer activity in divergent of cancer cells. However, the effects of S. lappa on oral cancer and its mechanisms of action have yet to be elucidated. OBJECTIVE: To explore its potential chemotherapeutic effects and mechanism of cell growth inhibition on human oral cancer cells. MATERIALS AND METHODS: The dried roots of S. lappa were used in this study. Cell viability of KB cells was evaluated by 3-[4, 5-dimethylthiazol-2-yl]-2, 5-diphenyltetrazolium bromide assay after treatment with 30 µg/ml of methanol extract from the dried roots of S. lappa. To understand whether its effect on cell death is related with apoptosis pathway, we performed DNA fragmentation assay, western blot, caspase activity assay and fluorescence-activated cell sorting (FACS) analysis. RESULTS: Treatment of S. lappa extract onto KB cells reduced cell viability significantly with an IC50 value of 30 µg/ml. The formation of a DNA ladder was observed starting at the 24 h treatment. In western blotting analysis, the S. lappa extract induced the proteolytic processing of caspase-3, -9 and poly (ADP-ribose) polymerase, a significant increase of Bax and marked reduction of Bcl-2. We also confirmed the activation of caspase-3/-7 in living KB cells by fluorescence microscopy. CONCLUSION: These results suggested that S. lappa extract inhibited cell proliferation through the apoptosis pathway in KB human oral cancer cells.

7α,25-Dihydroxycholesterol-Induced Oxiapoptophagic Chondrocyte Death via the Modulation of p53-Akt-mTOR Axis in Osteoarthritis Pathogenesis.

This study aimed to exploring the pathophysiological mechanism of 7α,25-dihydroxycholesterol (7α,25-DHC) in osteoarthritis (OA) pathogenesis. 7α,25-DHC accelerated the proteoglycan loss in ex vivo organ-cultured articular cartilage explant. It was mediated by the decreasing extracellular matrix major components, including aggrecan and type II collagen, and the increasing expression and activation of degenerative enzymes, including matrix metalloproteinase (MMP)-3 and -13, in chondrocytes cultured with 7α,25-DHC. Furthermore, 7α,25-DHC promoted caspase dependent chondrocytes death via extrinsic and intrinsic pathways of apoptosis. Moreover, 7α,25-DHC upregulated the expression of inflammatory factors, including inducible nitric oxide synthase, cyclooxygenase-2, nitric oxide, and prostaglandin E2, via the production of reactive oxygen species via increase of oxidative stress in chondrocytes. In addition, 7α,25-DHC upregulated the expression of autophagy biomarker, including beclin-1 and microtubule-associated protein 1A/1B-light chain 3 via the modulation of p53-Akt-mTOR axis in chondrocytes. The expression of CYP7B1, caspase-3, and beclin-1 was elevated in the degenerative articular cartilage of mouse knee joint with OA. Taken together, our findings suggest that 7α,25-DHC is a pathophysiological risk factor of OA pathogenesis that is mediated a chondrocytes death via oxiapoptophagy, which is a mixed mode of apoptosis, oxidative stress, and autophagy.

Malaris muscle, the lateral muscular band of orbicularis oculi muscle.

Little is currently known about the variations in the muscular band around the orbicularis oculi muscle (OOc) region, and so the aim of the current study was to describe in anatomic terms the morphologic patterns of the lateral muscular bands of the OOc. Sixty-one hemifaces from embalmed Korean adult cadavers (34 males, 27 females; age range, 45-85 years; mean age, 62.6 years; 28 bilateral and 5 unilateral) were dissected to reveal the anatomic features of the region around the OOc. The lateral muscular band originating from the superficial temporal fascia lateral to the OOc was observed in 54.1% of cases. It terminated at the zygomatic arch region in 17 cases (type A, 27.9%), at the cheek region in 11 cases (type B, 18%), and at the angle of the mouth in 5 cases (type C, 8.2%). When the linear length from the lateral canthus to the tragion was set as 100, the length from the lateral canthus to the lateral edge of OOc was 34.0 (male, 34.1; female, 33.7), and the length between the lateral edge of OOc and the lateral muscular bands of OOc was 6.4 (male, 6.5; female, 6.2). The results of this study suggest that the lateral muscular bands of the OOc may play a significant role in facial animation and dimple formation. In addition, these data provide an index of suggested regions to be injected in patients with periorbital rhytides.

Histomorphometric analysis of the sinus lateral wall and Schneiderian membrane: A cadaveric study.

OBJECTIVES: Sinus augmentation is frequently used to maintain implant stability when there is severe alveolar bone loss. The aim of this study was to determine the thicknesses and histologic features of the sinus lateral wall and Schneiderian membrane in embalmed cadavers. DESIGN: This study included 35 hemimaxillae from 25 cadavers (19 males and 6 females with a mean age at death of 59 years). Specimens obtained from the first premolar to the second molar were embedded in paraffin, stained with hematoxylin-eosin, and observed under a light microscope. The thicknesses of the lateral wall and Schneiderian membrane were measured according to tooth site and measurement level, and their histologic features were evaluated. RESULTS: The mean thicknesses of the lateral wall were 2.22, 2.17, 2.64, and 2.64 mm at the first premolar, second premolar, first molar, and second molar, respectively, and 2.79, 2.24, and 2.12 mm at 0, 2, and 8 mm from the sinus floor. The mean thickness of the Schneiderian membrane did not differ significantly between at the sinus floor (0.41 mm) and 2 mm above the floor (0.38 mm). The lateral wall consisted of the outer cortical plate, trabecular bone in the center, and the inner cortical plate near the Schneiderian membrane, being the inner cortical plate the more porous. CONCLUSIONS: These histomorphometric results for the sinus lateral wall and Schneiderian membrane are expected to provide relevant information for use in sinus augmentation procedures.

Morphology of the temporalis muscle focusing on the tendinous attachment onto the coronoid process.

The temporalis muscle is usually described as a single layer originating at the temporal line, converging to a tendon, and inserting onto a narrow site of the coronoid process. However, recent studies have shown that the temporalis muscle can be divided into two or three separate segments and the distal attachment continues inferiorly beyond the coronoid process. Therefore, the aims of this study were to analyze the morphology of the temporalis muscle focusing on the tendinous attachment onto the coronoid process and to provide educational values. The temporalis muscle was carefully dissected in 26 cadavers and classified based on the muscle fascicle direction. Each divided part was sketched and measured based on bony landmarks to elucidate its tendinous insertion site onto the coronoid process, and the results obtained were reviewed through the literature. The temporalis muscle ends at two distinct terminal tendons with wider insertion sites than usually presented in textbooks and atlases and separates into two parts that combine to act as a single structural unit. The superficial part is a large fan-shaped muscle commonly recognized as the temporalis muscle. This converges infero-medially to form the superficial tendon and the lateral boundary of the retromolar triangle. Meanwhile, the deep part is a narrow vertically oriented rectangular muscle that converges postero-laterally to form the deep tendon and the medial boundary of the retromolar triangle. These results indicate that understanding the temporalis muscle's insertion site onto the coronoid process will be useful clinically with educational values during surgical procedures.