The purpose of this study was to verify the sensitive areas when the AI determines osteoporosis for the entire area of the panoramic radiograph. Panoramic radiographs of a total of 1,156 female patients(average age of 49.0±24.0 years) were used for this study. The panoramic radiographs were diagnosed as osteoporosis and the normal by Oral and Maxillofacial Radiology specialists. The VGG16 deep learning convolutional neural network(CNN) model was used to determine osteoporosis and the normal from testing 72 osteoporosis(average age of 73.7±8.0 years) and 93 normal(average age of 26.4±5.1 years). VGG16 conducted a gradient-weighted class activation mapping(Grad-CAM) visualization to indicate sensitive areas when determining osteoporosis. The accuracy of CNN in determining osteoporosis was 100%. Heatmap image from 72 panoamic radiographs of osteoporosis revealed that CNN was sensitive to the cervical vertebral in 70.8%(51/72), the cortical bone of the lower mandible in 72.2%(52/72), the cranial base area in 30.6%(22/72), the cancellous bone of the mandible in 33.3%(24/72), the cancellous bone of the maxilla in 20.8%(15/72), the zygoma in 8.3%(6/72), and the dental area in 5.6%(4/72). Consideration: it was found that the cervical vertebral area and the cortical bone of the lower mandible were sensitive areas when CNN determines osteoporosis in the entire area of panoramic radiographs.

Artificial intelligence, has been applied in interpreting osteoporosis on dental panoramic radiograph with high accuracy. The purpose of this study was to investigate the sensitive area of convolutional neural network(CNN), one of artificial intelligence, in interpreting osteoporosis on dental panoramic radiograph. Dental panoramic radiographs taken from 1,170 female (49.19 ±21.91 average age, 21 minimum age, and 84 maximum age) were selected for this study. Two oral maxillofacial radiologists agreed upon interpreting osteoporosis by interpreting mandibular inferior cortical changes. The region of interest included upper and lower jaws for training and testing CNN in interpreting osteoporosis. A filter which was set to look for image characteristics moved through the entire panoramic radiography to identify sensitive areas that distinguish normal groups and osteoporosis patients. In interpreting osteoporosis on panoramic radiograph, CNN responded sensitively at the cancellous bone of the upper and lower jaws while oral maxillofacial radiologists interpreted mandibular inferior cortical change.

Central odontogenic fibroma(COF) is a very rare benign tumor that accounts for 0.1-1.5% of all odontogenic tumors. Most COF develop in the molar-premolar region in the mandible and anterior to the first molar in the maxilla. Radiographically, the lesions appear as a unilocular or multilocular radiolucent image. Some maxillary lesions have cleft like depression in the palatal mucosa are found. This report presents a COF with external root resorption and palatal soft tissue depression on CBCT images. A 27-year-old man referred for evaluation of unilocular radiolucent lesion with external root resorption in the right anterior maxillary region. On clinical examination, the right anterior maxillary teeth responded positive to the cold stimulus and its response to the vitality test remained within the normal range. On radiographic examination, osteolytic lesion with external root resorption and palatal mucosa depression as a radiolucent shadow. After excisional biopsy, the lesion was diagnosed as COF in histopathologic examination. There was no recurrence at a follow-up 10 months.

During bone remodeling, there is requirement of differentiation of osteoblastic cells. Previously, we identified proteins differentially expressed in soft tissue during bone healing. Of these proteins, we focused the effect of LTF on differentiation of osteoblast. In order to analyze the osteogenic ability of LTF, we treated conditioned media collected from human LTF-stably transfected HEK293T cells into osteoblastic MC3T3-E1. The results showed that the activity and expression of alkaline phosphatase were increased in MC3T3-E1 cells treated with conditioned media containing LTF in dose- and time-dependent manner. At the same time, we observed the significant increase of the expression of osteoblastic genes, such as ALP, BSP, COL1A1, and OCN, and along with matrix mineralization genes, such as DMP1 and DMP2, in LTF conditioned media-treated groups. Moreover, the result of treating recombinant human LTF directly into osteoblastic MC3T3-E1 showed the same pattern of treating conditioned media containing LTF. Our study demonstrated that LTF constitutively enhances osteoblastic differentiation via induction of osteoblastic genes and activation of matrix mineralization in MC3T3-E1 cells.

Periodontal inflammation increases the risk of tooth loss, particularly in cases where there is an associated loss of alveolar bone and periodontal ligament (PDL). Histological and morphometric evaluation of periodontal inflammation is difficult. Especially, the lengths of the periodontal ligament and interdental alveolar bone space have not been quan-tified. A quantitative imaging procedure applicable to an animal model would be an important clinical study. The purpose of this study was to quantify the loss of alveolar bone and perio-dontal ligament by evaluation with micro-computed tomo-graphy (micro-CT). Another purpose was to investigate diffe-rences in infections with systemic E. coli LPS and TNF-α on E. coli lipopolysaccharide (LPS) in loss of alveolar bone and periodontal ligament model on mice. This study showed that linear measurements of alveolar bone loss were repre-sented with an increasing trend of the periodontal ligament length and interdental alveolar process space. The effects of systemic E. coli LPS and TNF-α on an E. coli LPS-induced periodontitis mice model were investigated in this research. Loss of periodontal ligament and alveolar bone were eval-uated by micro-computed tomography (micro-CT) and cal-culated by the two- and three dimensional microstructure morphometric parameters. Also, there was a significantly increasing trend of the interdental alveolar process space in E. coli LPS and TNF-α on E. coli LPS compared to PBS. And E. coli LPS and TNF-α on E. coli LPS had a slightly increa-sing trend of the periodontal ligament length. The increa-sing trend of TNF-α on the LPS-induced mice model in this experiment supports the previous studies on the contribu-tion of periodontal diseases in the pathogenesis of systemic diseases. Also, our findings offer a unique model for the study of the role of LPS-induced TNF-α in systemic and chronic local inflammatory processes and inflammatory diseases. In this study, we performed rapidly quantification of the perio-dontal inflammatory processes and periodontal bone loss using micro-computed tomography (micro-CT) in mice.

Periodontal disease induces an increased incidence of tooth loss, particularly in cases with an associated loss of alveolar bone and periodontal ligaments. In this study, alveolar bone loss was detected by micro-computed tomography (CT) following exposure to E. coli lipopolysaccharide (LPS) in a streptozotocin (STZ)-induced diabetic mouse model. A 10 mg/ml dosage of E. coli LPS was applied between the first, second and third molars of the mice three times a week for 10 weeks. The loss of periodontal ligaments and alveolar processes was then evaluated by micro-CT using two and three dimensional microstructure morphometric parameters. In the diabetic mice, E. coli LPS induced the destruction of periodontal ligaments and loss of alveolar process spaces. The distances between periodontal ligaments were significantly widened in the STZ-LPS group compared with the untreated STZ group. The 10 mg/ml exposure to E. coli LPS in the STZ mice also resulted in a significant decrease in the alveolar bone volume fraction. The results of our study suggest that alveolar bone loss can be readily detected by volumetric micro-CT analysis as an increase in the distance between periodontal ligaments and in the alveolar process length.

Selenoprotein S (SelS) is widely expressed in diverse tissues where it localizes in the plasma membrane and endoplasmic reticulum. We studied the potential function of SelS in erythrocyte differentiation using K562 cells stably over-expressing SelS wild-type (WT) or one of two SelS point mutants, U188S or U188C. We found that in the K562 cells treated with 1μM Ara-C, SelS gradually declined over five days of treatment. On day 4, intracellular ROS levels were higher in cells expressing SelS-WT than in those expressing a SelS mutant. Moreover, the cell cycle patterns in cells expressing SelS-WT or U188C were similar to the controls. The expression and activation of SIRT1 were also reduced during K562 differentiation. Cells expressing SelS-WT showed elevated SIRT1 expression and activation (phosphorylation), as well as higher levels of FoxO3a expression. SIRT1 activation was diminished slightly in cells expressing SelS-WT after treatment with the ROS scavenger NAC (12 mM), but not in those expressing a SelS mutant. After four days of Ara-C treatment, SelS-WT-expressing cells showed elevated transcription of β-globin, y-globin, ε-globin, GATA-1 and zfpm-1, whereas cells expressing a SelS mutant did not. These results suggest that the suppression of SelS acts as a trigger for proerythrocyte differentiation via the ROS-mediated downregulation of SIRT1.

The mechanisms underlying the actions of the antioxidants upon reactive oxygen species (ROS) generation by NADPH oxidase complex have remained uncertain. In this study, we investigated NADPH oxidase activity and the role of antioxidant enzymes upon the generation of ROS during hypoxic stress. ROS generation was found to increase in the mouse kidney under hypoxic stress in a time-dependent manner. Moreover, we found in MCT cells that hypoxia-induced hydrogen peroxide production was decreased by NAC pretreatment. We further analyzed HIF-1α, PHD2 and VHL expression in the NAC-pretreated MCT cells and assessed the response of antioxidant enzymes at the transcriptional and translational levels. SOD3 and Prdx2 were significantly increased during hypoxia in the mouse kidney. We also confirmed in hypoxic Prdx2-l- and SOD3 transgenic mice that erythropoietin (EPO) is transcriptionally regulated by HIF-1α. In addition, although EPO protein was found to be expressed in a HIF-1α independent manner in three mouse lines, its activity differed markedly between normal and Prdx2-l-/SOD3 transgenic mice during hypoxic stress. In conclusion, our current results indicate that NADPH oxidase-mediated ROS generation is associated with hypoxic stress in the mouse kidney and that SOD3 and Prdx2 cooperate to regulate cellular redox reactions during hypoxia.