The purpose of this study is to clarify the effect of cast structure on the accuracy of digital light processing （DLP）. We created 3D model data of the maxillary edentulous jaw with five spheres and used it as the reference model data. The reference model data was edited to prepare full arch model data and half arch model data. Three types of full arch model data were prepared: a hollow type with a thickness of 3 mm, a hollow type with a thickness of 5 mm, and a solid type. On the other hand, one type of half arch model data was prepared: a hollow type with a thickness of 3 mm. Experimental casts were manufactured from the data of prepared models, using a 3D printer with DLP method, and the error of the casts was evaluated by measuring the distance between the center points of the spheres on the casts.
The error level of hollow casts was significantly higher than the error level of solid casts. （p <0.05, Kruskal-Wallis test）. Moreover, when comparing the full arch cast with the half arch cast, the error of the full arch cast was significantly higher （p <0.05, Mann-Whitney test）. The results of this study suggest that the structure of the model affects the accuracy of DLP.
Squamous cell carcinoma（ SCC） is the most common cancer that develops in the oral cavity. Epithelial-mesenchymal transition（ EMT） is known to play an important role in the process of metastasis of SCC cells. In our previous study, we demonstrated that transforming growth factor-β1 （TGF-β1） induces EMT in the human oral SCC（ hOSCC） cell line HSC-4. However, the molecular mechanisms of the metastasis after an EMT-induced cancer are poorly understood. Moreover, tumorassociated macrophages（ TAMs）, which coexist with the cancer tissues, are known to participate in permeation metastasis. However, it still remains uncertain whether TAMs affect the metastatic activity of hOSCC cells. We found that the expression of CXCL14, which is known to suppress the progression of colon, and breast cancers, was upregulated in HSC-4 cells by TGF-β1 stimulation. The Smad3 inhibitor, SIS3, suppressed the TGF-β1-induced expression of CXCL14. Interestingly, the CXCL14 suppressed the migratory and proliferative activities in HSC-4 cells. Moreover, the expression of CXCL14 in HSC-4 cells was downregulated by cocultivation with differentiated macrophages derived from monocytic THP-1 cells, but not by cocultivation with non-differentiated monocytic THP-1 cells. On the other hand, we found that expression levels of CCL20 in the differentiated macrophages derived from THP-1 cells was higher than that in non-differentiated monocytic THP-1 cells. In addition, CCL20 suppressed TGF-β1-induced expression of CXCL14. Intriguingly, the MAPK/ERK kinase （MEK） inhibitor U0126, PI3K inhibitor LY294002, or NF-κB kinase-2（ IKK-2） inhibitor TPCA-1 abrogated the CCL20-promoted inhibition of TGF-β1-induced expression of CXCL14. Moreover, CCL20 decreased the migratory activity of HSC-4 cells. Taken together, these results suggest that CCL20 derived from TAMs abrogated the TGF-β1-induced expression of the cancer progression suppressor CXCL14 in HSC-4 cells in PI3K-, MEK1/2-, and NF- κB-dependent manners, resulting in the activation of metastatic activity in HSC-4 cells.
Objective: There are rare cases that post in root canal dentin was debonded from root canal treated with sodium hypochlorite. The purpose of this study was to clarify the effect of ascorbic acid on the bond of resin abutment to root canal dentin on tooth. Materials and Methods: Post-cavities were formed in the bovine root canal and treated with sodium hypochlorite. Half of specimens were applied to sodium ascorbic acid, and a chemical and dual cured bonding system, and filled with composite resin for abutment. After storage in water at 37°C for 7 days, the root was cut from the coronal to the apical to a thickness of about 1 mm. Two-thirds of the samples obtained from one tooth were measured for bond strength by push out test, and the remaining one-third of the specimens were dye penetration for observing the bond interface and fracture region. Results: No significant difference in bond strength between with and without ascorbic acid treatment was observed regardless of bonding systems. However, some specimens without ascorbic acid treatment in the chemical and dual cured-bonding agents had observed gaps at the bonding interface and adhesive fractures comparison for those with ascorbic acid treatment. Conclusion: In the limitation of this study, there was no difference in bond strength of endodontically treated roots with or without ascorbic acid treatment, but the ascorbic treatment resulted in a decrease in the gap at the adhesive interface and an increase in the rate of mixed fracture or cohesive fracture.
Transforming growth factor-beta （TGF-β） is known to be an important factor for osteogenic differentiation of mesenchymal stem cells （MSCs）. We previously reported that TGF-β1 promoted the human MSC （hMSC） cell line UE7T-13 in an extracellular signal-regulated kinase （ERK）1/2-dependent manner. In addition, ascorbate, dexamethasone （Dex）, and β-glycerophosphate （β-Gp） are widely used for inducing osteogenic differentiation of osteoblast progenitor cells by activating the ERK1/2-mediated signaling pathway. Conversely, lipopolysaccharide （LPS） generally suppresses osteoblastic activity in MSCs. However, the molecular mechanisms underlying the LPSpromoted suppression of osteoblastic differentiation of hMSCs remains to be clarified. This study aimed to 1） identify key molecules that relay intracellular signals for the LPS-induced inhibition of osteogenic activity in hMSCs, and 2） investigate how TGF-β1 affects the LPS-induced inhibition of osteoblastic differentiation of hMSCs. Here, we demonstrated that LPS suppresses ascorbate-, Dex-, and β-Gp-induced osteogenic activity, but not ascorbate-, Dex-, β-Gp-, and TGF-β1-induced osteogenic activity in UE7T-13 cells. In addition, LPS suppressed ascorbate-, Dex-, and β-Gp-induced ERK activation, and partially suppressed the ascorbate-, Dex-, β-Gp-, and TGF-β1-induced ERK1/2 activation in UE7T-13 cells in a nuclear factor kappa-B （NF-κB）-dependent manner. These results suggested that TGF-β1 abrogated the LPS-induced activation of the NF- κB-mediated signaling pathway that relays the suppressive effect on the osteogenic activity of hMSCs partially by the ERK1/2-mediated signal. However, the network would be complexed, and the further research is needed to confirm this.
The present findings partially clarify the molecular mechanisms underlying the development of apical periodontitis-induced suppression of ossification around the tooth root apex, and may aid in identifying therapeutic targets for this condition.
Tooth gemination is generally defined as a tooth in which one tooth germ separates into two during development. We report here a case of a malformed tooth that was considered to be a geminated tooth of the paramolar or a fused tooth between the paramolars in the maxillary molar region. A 43-year-old male was referred to department of oral surgery for extraction of a supernumerary tooth in the right maxillary molar region. Oral examination revealed a malformed tooth considered paramolar having two cusps on the buccal side of the space between the second and third molars. Conventional radiography did not elucidate the structure of the malformed tooth, but cone-beam computed tomography （CT） images revealed that the tooth having two cusps was flat in the bucco-lingual direction. Micro-CT images of the extracted tooth revealed a single fused root and root canal with separated crowns suggestive of a malformed tooth that was considered to be a geminated tooth of the paramolar or a fused tooth between the paramolars. Micro-CT also detected an enamel pearl without dental pulp cavity in the buccal tooth cervix of the malformed tooth. This case is an interesting and rare example of a suspected a geminated tooth of the paramolar or a fused tooth between the paramolars in the maxillary molar region. Cone-beam CT and micro-CT images were useful in the diagnosis for the anatomical structure of this malformed tooth.