Comparison between Sulphorhodamine-B dye staining and 51Cr-release method in cytotoxicity assay of endodontic sealers.

The aim of this study was to evaluate Sulphorhodamine-B (SRB) staining against 51Cr-release in cytotoxicity tests of six endodontic sealers, namely, MU sealer (Mahidol University) ROCANAL 2, ROCANAL 3, Apexit, Endomethasone, and AH-26. Monolayers (5 x 10(5) cells/ml) of the mouse cell line Mu-mu-1 were used as test cells. Following incubation at 37 degrees C in 5% CO2 for 24 h in the presence of each sealer, cells were stained with 0.4% SRB and the absorbance at 540 nm determined as measure of cell viability. For 51Cr-release assay, cells were labelled with 51Cr before testing with sealers, and radioactivity in the supernatant was measured in a liquid scintillation counter. Both techniques indicated that Apexit was the least toxic sealer. In view of the ease of conducting SRB staining for tests of cell viability, this may be the method of choice over 51Cr-release assay in the evaluation of endodontic sealer cytotoxicity.

Multilayer and monolayer cell cultures in a cytotoxicity assay of root canal sealers.

The aim of this study was to evaluate the response of a multilayer compared with a monolayer cell culture using six root canal sealers. Both monolayer and multilayer of MU-mu-1 (Mahidol University mouse cell line 1) were cultured in separate 96-well plates. Following incubation at 37 degrees C in 5% CO2 for 4 h in the presence of each sealer, cells were stained with 0.4% Sulphorhodamine-B, viable dye staining and the absorbance at 540 nm determined and calculated as cell viability. There was no statistical difference in the percentage viability for each sealer in both the multilayer and the monolayer cell culture (P > 0.01). Apexit and AH-26 were less toxic (P < 0.01) than MU (Mahidol University) sealer, ROCANAL 3, ROCANAL 2, and Endomethasone which demonstrated the same toxicity (P > 0.01).

Are laryngeal papilloma virus-infected cells viable in the plume derived from a continuous mode carbon dioxide laser, and are they infectious? A preliminary report on one laser mode.

The purpose of this study was to determine the potential risk of transmitting viable viral infected cells as well as viral infectivity of laryngeal papilloma in the plume derived from a continuous mode carbon dioxide laser. Each of 10 juvenile recurrent laryngeal papilloma specimens was divided into two equal parts, and one part was irradiated with a carbon dioxide laser employing a continuous mode at the power setting of 10 watts with 0.5 mm spot size and a power density of 1667 W/cm2. The resultant laser plume was trapped and was cultured simultaneously with the other part of the specimen which served as the control. All irradiated specimens tested yielded negative culture results while all the control counterparts revealed viable cell growth. To detect the viral infectivity, laser plume was cultured with two separate cell systems, one was the porcine PS clone D cell line and the other normal mucosal cells obtained from the same patient, and to control these systems both cell lines were also designed to be infected with polio virus. Both cell lines in the viral infectivity testing systems revealed no sign of viral infection. The results suggest that papilloma virus-infected cells cannot survive the continuous mode of carbon dioxide laser irradiation. We primarily conclude that, to avoid airborne transmission of plume containing laryngeal papilloma viral-infected cells and infectious viral particles, the carbon dioxide laser parameters should be in a continuous mode with the power density equal to, or more than, 1667 W/cm2.

Role of macrophages in Wesselsbron and Germiston virus infections of mice.

Mice develop age-dependent resistance to intraperitoneal infection with Wesselsbron virus, but not with Germiston virus. This resistance correlates with the capacity of peritoneal macrophages from older mice rapidly inacativated the infectivity of Wesselsbron virus, whereas Germiston virus replicated in these cells. Peritoneal macrophages from older mice protected cell cultures against Wesselsbron virus infection, but macrophages from newborn mice did not. Electron microscopic observations suggested that Wesselsbron virus was actively phagocytosed by macrophages, whereas Germiston virus entered the cells by other means and thus, presumably, circumvented the normal killing mechanisms of these cells. Germiston virus may also have directly impaired these killing functions, however, in that the ability of macrophages to kill phagocytosed Diplococcus pneumonaie was significantly less after macrophages were exposed to the virus.