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This study was an in vivo comparison of the bacterial leakage associated with three endodontic temporary restorative materials: Cavit, Intermediate Restorative Material (IRM), and TERM. The access openings of 51 endodontically treated teeth were randomly sealed with a 4-mm thickness of one of the three materials. Three wk after placement of each temporary restoration, bacterial leakage was evaluated by sampling from beneath the temporary restoration and then culturing the samples both aerobically and anaerobically. Positive growth occurred in 4 of 14 TERM samples and in 1 of 18 IRM samples. Cavit did not demonstrate leakage in any of the teeth in which it was used. Cavit provided a significantly better seal than TERM over the study period.

Previous studies from several laboratories have demonstrated that glucose-starved Chinese hamster ovary (CHO) cells and other cells in culture switch from synthesis of the normal Glc3Man9GlcNAc2-P-P-Dol to Man5-GlcNAc2-P-P-Dol. In this study we have investigated this phenomenon in CHO cells in vitro and in vivo in order to determine the possible site of this block. Our results demonstrate that enzymatic activities responsible for Man9GlcNA2 synthesis in vitro are normal in glucose-starved cells. In vivo, however, the pool of GDP-[3H]Man is severely depleted, while [3H]mannose incorporation into lipid-linked and protein-bound Man5GlcNAc2 is increased. This result suggests that the available GDP-Man in starved cells is utilized to synthesize Man5GlcNAc2 preferentially, resulting in a reduction of Dol-P-Man and Man6-Man9 GlcNAc2 synthesis in vivo in glucose-starved cells. Conditions which prevent the depletion of GDP-[3H]Man in glucose-starved cells, such as puromycin or cycloheximide treatment, result in normal synthesis of Man9GlcNAc2 by glucose-starved cells. An unexpected finding in the course of this study is that puromycin or cycloheximide treatment of cells, which is known to inhibit lipid-linked oligosaccharide synthesis in glucose-fed cells, has no such inhibitory effect on glucose-starved cells.