Hypoxia is one of the most common features of cancer. It is also associated with cancer progression and the acquisition of aggressiveness, which includes invasion and metastasis. Oral squamous cell carcinoma accounts for 90% of all oral cancers, and its 5-year survival rate is about 50%. Despite various attempts and trials, its prognosis has not improved. Among numerous adverse prognostic factors, hypoxia is suspected as one of the most important factors, as it increases the aggressiveness of oral cancer cells. We attempted to observe the effect of hypoxia on the expression of epithelial-mesenchymal transition markers in oral cancer cells. We analyzed and compared both the mRNA and protein expression levels of epithelial-mesenchymal markers using qRT-PCR and western blotting in both normoxic and hypoxic YD10B oral squamous cell carcinoma cells. Eighty-six genes were analyzed through real-time PCR using commercial microarray plates, performed in triplicate. Among the 86 genes, the expression of 24 were increased (≥ 2 fold) by hypoxia, while that of three genes was decreased (≥ 2 fold). Hypoxia significantly affects epithelial-mesenchymal transition-related genes. Further studies on the regulation of these genes may help to develop more efficient therapeutic modalities for oral cancer and to improve prognosis of oral cancer patients.
The purpose of this study was to identify the oral bacterial species in sequestra from patients with bisphosphonate-related osteonecrosis of the jaw (BRONJ). Fifteen patients with BRONJ (2 males and 13 females) were evaluated. Clinical features, radiographic findings, and bisphosphonate intake history were investigated. All patients were treated with surgical methods (curettage or sequestrectomy). Infected bone samples were collected from the affected BRONJ site. Ten bacterial species were selected for polymerase chain reaction (PCR) detection. Two to nine bacterial species were detected by PCR. Gram-negative species were predominant and all identified bacteria were anaerobes. Porphyromonas gingivalis, Tannerella forsythia, and Treponema denticola were detected at high levels. These are major pathogenic species in periodontal disease. Orthopantomographic radiographs showed generalized alveolar bone loss in most patients. These radiographic findings may provide evidence of chronic periodontitis as a pre-existing inflammatory disease. Most patients had experienced a predisposing dental procedure, such as tooth extraction. Sequestra (necrotic bone) infected with oral bacterial species may be an important risk factor for BRONJ. As such, prevention and management of BRONJ may rely on effective control of bacteria in the oral cavity.
Hydrogen peroxide (H2O2) is originally an endogenous small molecule which is reduced into water in cells. In order to know the H2O2-induced oxidative stress in RAW 264.7 cells, first of all, the optimum concentration of exogenous H2O2 which show reactive cellular responses was determined as 40 μM by MTT assay, and followed by 40 μM H2O2 application in RAW 264.7 cells for 30 min, 1, or 2 hours. The expressional changes of essential proteins for cellular proliferation, epigenetic modification, inflammation, apoptosis, survival, and protection were assessed by immunoprecipitation high performance liquid chromatography (IP-HPLC) using 51 antisera. 40 μM H2O2 treatment down-regulated proliferation-related proteins, Ki-67, PCNA, CDK4, cyclin D2, cMyc, and PLK4, induced histone methylation/ deacetylation and DNA methylation by increasing levels of HDAC10 and DMAP1 and by decreasing levels of DNMT1 and KDM4D, activated inflammatory reaction by increasing levels of MCP-1, COX-2, CD68, LTA4H, CXCR4, and lysozyme, and dramatically up-regulated cellular apoptosis-, survival-, and protection-related proteins, AIF, PARP-1, caspase 9, c-caspase 9, pAKT1/2/3, SOD-1, HO-1, NF-kB, NRF2, and GSTO1 in RAW 264.7 cells. These observations suggest exogenous 40 μM H2O2-induced oxidative stresses which resulted global cellular responses including not only antioxidant, inflammation, and apoptosis but also proliferation and epigenetic modification. Particularly, 40 μM H2O2-induced apoptosis was mainly derived from PARP-1/AIF signaling leading parthanatos, and 40 μM H2O2-induced suppression of cMyc/MAX/MAD network was relevant to reduction of RAW 264.7 cell proliferation. Accordingly, H2O2 appears to affect RAW 264.7 macrophages in several ways eliciting not only oxidative stresses but also genome-wide DNA damage.
The myxoma(odontogenic myxoma, myxofibroma) of the jaws is a benign, usually slow-growing infiltrative tumor of connectice tissue. This article describes a case history of the treatment of recurred odontogenic myxofibroma in the maxilla and further discusses the appropriate management of such cases with reference to the literature review. A 55-year-old male patient presented with a gingival swelling in the right side of maxilla. He had history of second time recurred disease. Microscopically, a high cellularity fibrous tumor with fibroblastic cells was observed. Tumor cells were composed of stellate and spindle shaped fibroblasts. Islands of odontogenic epithelium were seen in the specimen. The final diagnosis was made with odontogenic myxofibroma in consideration of twice-time recurrences and histological characteristics. Because of the high likelihood of recurrence, an accurate differential diagnosis of pathology at the time of initial visit is very important in determining treatment options, and immunohistochemical tests may be helpful. Also close following up is required.(155 words)