A variety of shapes has been reported for the roots and root canals of maxillary first premolars. The purposes of the present study were to determine branching and shapes of the roots of maxillary first premolars, as well as age-related changes using slice images obtained with cone-beam computed tomography (CBCT) for dental use. CBCT-reconstructed images of 125 cases that included maxillary first premolars were used as subjects. Slice images at the cervical one-third, center, and apical one-third positions of the root were prepared. Root branching and number of root canals was determined at each measurement position in the images. The subjects were divided into three groups: younger than 30 years, 30 to 50 years, and over 50 years. The root canal morphology was compared among these age groups. Single-rooted premolars were the most frequent. As for number of root canals, a single-canal premolar was observed at the position of the cervical one-third in 33.6%, at the center in 35.2%, and at the apical one-third in 56.0%. Thereafter the subjects were divided into groups by age, namely, younger than 30 years, 30 to 50 years, and over 50 years old, and it was revealed that the ratio of the two-canal type increased with age. In regard to tooth morphology, it was confirmed that the two-canal type shows more frequent occurrence with aging in maxillary first premolar. Based on our findings, we consider that CBCT can be useful for determining the root canal morphology with complicated shapes.

We have examined whether propofol activates complement. In the first study, blood was mixed with saline, propofol or the lipid solvent for propofol, and the activated complement 3 (C3a) and 4 (C4a) concentrations in the supernatant were assayed. In the second study, blood and propofol were mixed with various levels of nafamostat mesilate (anti-complement agent) up to 0.3 mmol/l and the C3a was assayed. In the third study, the time course of plasma C3a concentration in patients during propofol anaesthesia was examined. The results showed that the lipid solvent activated complement and produced similar levels of C3a to propofol, probably via both the classical and alternative pathways. This activation was not inhibited by any of the nafamostat concentrations used. There was no significant change in plasma C3a concentration during propofol anaesthesia. These results suggest that C3a is generated by the lipid solvent, but its accumulation during propofol anaesthesia is minimal.