Comparison of biofilm on titanium and zirconia surfaces: in vivo study / 대한치과보철학회지

PURPOSE: This study was conducted to compare in vivo biofilm formation on titanium surface and zirconia surface. MATERIALS AND METHODS: For biofilm formation on titanium and zirconia in oral cavity, after producing oral appliances using acrylic resin and orthodontic wire tailored to 9 subjects, we made titanium and zirconia specimens (6 mm x 6 mm x 2 mm), fixed them on oral appliances and maintained them in oral cavity of test subjects for 24 and 72 hours. Test subjects who have equipped two pairs of specimens maintained oral hygiene not by using toothpaste but only by tooth brushing. After 24 and 72 hours, we removed and observed specimens through scanning electron microscopy (SEM). RESULTS: Biofilm formation showed large deviation depending on individuals. For formation comparison between titanium and zirconia for 24 hours, zirconia showed less biofilm formation than titanium. Biofilm formation showed large deviation depending on individuals. As for formation comparison between zirconia and titanium, the degree of biofilm formation in zirconia was less than it was in titanium after a lapse of 24 hours. The result of biofilm formation in 72 hours trial show that zirconia has an inclination to formate less biofilm than it was in titanium. CONCLUSION: Based on the above results, we can conclude that early biofilm formation in oral cavity was influenced by difference of abutment materials.

Effect of ursodeoxycholic acid on experimental hepatic porphyria induced by griseofulvin

Griseofulvin(GF) has become the drug of choice as an antifungal agent for patients who suffer from many kinds of fungal infection. In order to clarify hepatic injury by griseofulvin(GF) overload and the effect of UDCA on GF-induced hepatic injury, the authors carried out biochemical, histologic, and ultrastructural studies of liver following treatment with griseofulvin and ursodeoxycholic acid(UDCA) in mice. Urine porphobilinogen excretion in the group treated with GF alone was significantly increased and reached the highest level in the 4th week and declined thereafter. Biochemical studies of the liver function showed no remarkable changes of serum bilirubin levels throughout the experimental period in all groups, except for SGPT and alkaline phosphatase activities which were significantly elevated and reached the highest level in the second week. Then they slightly decreased in GF treated groups(GF alone and GF plus UDCA) in comparison with the control group. Pathologic findings in the group treated with GF alone include focal liver cell necrosis(esp, zone 3), Mallory bodies in hepatocytes(esp, zone 1), Kupffer cell activation, and brown protoporphyrin pigments in the hepatocytes, bile canaliculi and interlobular bile ducts with a marked inflammatory cell infiltration in the portal tracts. Under the polarizing light microscope, bile ductular and canalicular thrombi showed a "Maltese cross" birefringence in mice treated with GF alone. There is no definite finding of fatty change in hepatocyte. Under the microscope, the liver appeared normal with an intact lobular architecture in the GF plus UDCA treated group. Electron microscopically, GF-induced changes include swelling of mitochondria, globular protoporphyrin crystals in the hepatocyte cytoplasm, markedly dilated bile cannaliculi and bile ducts and the formation of a Mallory hyaline bodies in the hepatocytes. There were no noticeable structural changes in the GF plus UDCA-treated group. Therefore the results suggest that GF causes hepatic injury, namely porphyria and cholestasis, and the treatment of UDCA may have cytoprotective and choleretic effects on GF-induced hepatic injuries.