• Maxillofacial Plastic and Reconstructive Surgery
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• v.32 no.6
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• pp.592-596
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• 2010

The common local causes of active gingival bleeding are the vessel engorgement and erosion by severe inflammation and injury to hypervascularity lesion. Abnormal gingival bleeding is also associated with systemic bleeding disorders (liver disease, leukemia etc.). There are many conventional methods for gingival bleeding control, such as, direct pressure, packing, electrocoagulation, tight suture and application of hemostatic agents. If the continuous gingival bleeding is not stopped in spite of the all local application methods, the medical consultation should be obtained for systemic condition care and the major feeding arterial embolization. This is a case report of severe gingival bleeding and periodontitis control in a patient with liver cirrhosis and oral metastatic lesion of hepatocellular carcinoma. The bleeding lesion was placed in left buccal mucosa and gingiva of the left mandibular molars. The control methods were dental crown removal, primary endodontic drainage, gingival sulcus drainage and maxillary arterial embolization with medical consultation.

• Molecules and Cells
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• v.22 no.3
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• pp.291-299
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• 2006

Vitexin, a natural flavonoid compound identified as apigenin-8-C-${\beta}$-D-glucopyranoside, has been reported to exhibit antioxidative and anti-inflammatory properties. In this study, we investigated its effect on hypoxiainducible factor-$1{\alpha}$ (HIF-$1{\alpha}$) in rat pheochromacytoma (PC12), human osteosarcoma (HOS) and human hepatoma (HepG2) cells. Vitexin inhibited HIF-$1{\alpha}$ in PC12 cells, but not in HOS or HepG2 cells. In addition, it diminished the mRNA levels of hypoxia-inducible genes such as vascular endothelial growth factor (VEGF), smad3, aldolase A, enolase 1, and collagen type III in the PC12 cells. We found that vitexin inhibited the migration of PC12 cells as well as their invasion rates, and it also inhibited tube formation by human umbilical vein endothelium cells (HUVECs). Interestingly, vitexin inhibited the hypoxia-induced activation of c-jun N-terminal kinase (JNK), but not of extracellular-signal regulated protein kinase (ERK), implying that it acts in part via the JNK pathway. Overall, these results suggest the potential use of vitexin as a treatment for diseases such as cancer.