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ABSTRACT: Peripheral odontoma is rare, and only two cases of congenital peripheral odontoma have been reported. Congenital oral fibroma is also rare. We describe a unique case of congenital peripheral developing odontoma accompanied by congenital teratomatous fibroma in an infant. Both tumors were difficult to detect on radiography. Two small masses were seen in the median anterior portion of the palatal mucosa of a 9-month-old boy. The masses had been present since birth and were surgically removed at age 28 months, when one of the masses had grown to a diameter of 8 mm. Histopathologic examination showed a fibrous lesion and a tooth germ-like rounded lesion composed of dental papilla, enamel organ, dentin, and cementum. Although congenital odontoma is rare, it should be considered when selecting appropriate treatment, as early radiographic detection is difficult. (J Oral Sci 55, 89-91, 2013).
Journal of Oral Science 01/2013; 55(1):89-91.
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ABSTRACT: J Oral Pathol Med (2012) Background: The product of the Wilms' tumor gene, WT1 protein, is a tumor antigen for various kinds of cancer, and WT1 peptide-based cancer immunotherapy is widely anticipated as a new possibility for cancer treatment. The aim of this study was to investigate the expression of WT1 from quantitative and morphological perspectives in oral squamous cell carcinoma (OSCC), the most widespread malignant neoplasm of the oral cavity. Methods: Six OSCC cell lines and tissue sections from 29 OSCC patients were analyzed. To detect WT1 expression, reverse transcription-polymerase chain reaction analysis (RT-PCR), real-time PCR, Western blots, and immunofluorescence flow cytometry for WT1 were performed on the cell lines, and immunohistochemistry and fluorescence in situ hybridization (FISH) were performed on the tissue sections. Results: WT1 mRNA was found overexpressed in one of the six OSCC cell lines, with expression levels higher than that seen in human leukemia cell line (K562). Immunohistochemical analysis of tissue sections showed overexpression of WT1 protein in two patients, concentrated mainly in the cytoplasm of the outer one to three cell layers of the cancer nests. This was consistent with the expression of WT1 mRNA observed by FISH. Meanwhile, WT1 was not detected on normal oral epithelium. WT1 protein was detected on actively proliferating cancer nests and even on elongated epithelial ridge where new droplet-cancer-nests were being formed and starting infiltration toward subepithelial layer. Conclusions: The results suggest that WT1 plays an important role in the pathogenesis of some types of OSCC, particularly in proliferation of the cancer cells.
Journal of Oral Pathology and Medicine 06/2012; · 1.63 Impact Factor
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ABSTRACT: The periodontal ligament (PDL) is a fibrous connective tissue located between the tooth root and the alveolar bone. We previously demonstrated that a single cell-derived culture of primarily cultured PDL fibroblasts has the potential to construct an endothelial cell (EC) marker-positive blood vessel-like structure, suggesting that the fibroblastic lineage cells in ligament tissue could act as the endothelial progenitor cells (EPCs), which regenerate to construct a vascular system around the damaged ligament tissue. Moreover, we showed that EPC-like fibroblasts expressed not only EC markers but also smooth muscle cell (SMC) markers. Generally, an interaction between ECs and SMCs regulates blood vessel development and remodeling, and is required for the formation of a mature and functional vascular network. However, the mechanism underlying the SMC differentiation of the ligament-derived EPC-like fibroblasts remains to be clarified. In this study, we showed that suppression of fibroblast growth factor 1 (FGF-1)-induced extracellular signal-regulated kinase 1/2 (ERK1/2) signaling with the MAPK/ERK kinase (MEK) inhibitor U0126 completely abolished the FGF-1-induced proliferation of the ligament-derived EPC-like fibroblasts. In addition, U0126 treatment of FGF-1-stimulated ligament-derived EPC-like fibroblasts significantly induced the SMC differentiation of the cells. Thus, FGF-1-induced ERK1/2 signaling not only promoted the proliferation of the ligament-derived EPC-like fibroblasts, but also suppressed the SMC differentiation of the cells, suggesting that FGF-1 controls the construction of a vascular network around the ligament tissue by regulating the proliferation and SMC differentiation of the EPC-like cells through ERK-mediated signaling.
International Journal of Molecular Medicine 11/2011; 29(3):357-64. · 1.98 Impact Factor
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ABSTRACT: An in vitro cell culture system of dental epithelium is useful for the investigations of cellular differentiation and function of ameloblast in amelogenesis and of regenerative therapy in human tooth. However, there have been no immortalized human dental epithelial ameloblastic-lineage cell lines, which proliferate indefinitely and additionally produce enamel matrix proteins.
We transfected two retroviral constructs of human telomerase reverse transcriptase (hTERT) cDNA and mouse cyclin-dependent kinase 4 (cdk4) cDNA into the primary ameloblastoma cells and isolated immortalized human dental epithelial cell lines of HAM1, HAM2 and HAM3. The three cell lines were examined by electron microscopy, assay of senescence-associated β-galactosidase activity, mRNA expression and immuno-reactivity of dental epithelial marker cell molecules and enamel matrix proteins.
They showed undifferentiated phenotypes in monolayer culture and did not have any β-galactosidase activity. The transcripts of dental epithelial cell markers of Msx2, Jagged1, Notch1, Sp3, Sp6, keratin 14 and keratin 18 were confirmed. In addition, mRNA and protein expression of ameloblastin and enamelin were also detected in three cell lines. All cells in the three cell lines were keratin 14- and 18-positive and some elongated cells were Jagged1-positive. Msx2-positive nuclei were noted in only HAM2 cells.
We established three cell lines by transfection of hTERT and cdk4 cDNAs, which were characterized as dental epithelial progenitor cells containing ameloblast-lineage cell phenotype.
Journal of Oral Pathology and Medicine 10/2010; 40(3):227-34. · 1.63 Impact Factor
