Objective: To evaluate the effect of 3D-printed oval root canal preparation by using small field-of-view cone beam CT (CBCT) combined with computer-aided technologies. Methods: An extracted tooth with a suitable single oval canal was selected by small field-of-view CBCT scanning. Three-dimensional (3D)-printed resin teeth were obtained based on the CBCT data after data conversion and processing. 50 general dentists were selected to prepare the oval root canal of the resin teeth with X-Gold rotary Ni-Ti instruments. Small field-of-view CBCT was applied to scan the oval root canals before and after preparation. Then, computer-aided technologies were used to calculate and compare these CBCT data, analyzing the effects of oval root canal cleaning as well as the root canal deviation by 3D reconstruction and rendering of the images. Results : Among the 50 cases, the mean unprepared area of the oval root canal wall was（56.20 ± 11.91）% and the mean maximum deviation distance of the root canal was（0.140 ± 0.041）mm. There was no correlation between root canal cleanliness and deviation (r=0.18, P=0.212). Conclusion Combined with small field-of-view CBCT and computer-aided technology, we can effectively quantitatively evaluate the root canal preparation effect.

Aristolochic acids (AAs) have long been considered as a potent carcinogen due to its nephrotoxicity. Aristolochic acid I (AAI) reacts with DNA to form covalent aristolactam (AL)-DNA adducts, leading to subsequent A to T transversion mutation, commonly referred as AA mutational signature. Previous research inferred that AAs were widely implicated in liver cancer throughout Asia. In this study, we explored whether AAs exposure was the main cause of liver cancer in the context of HBV infection in mainland China. Totally 1256 liver cancer samples were randomly retrieved from 3 medical centers and a refined bioanalytical method was used to detect AAI-DNA adducts. 5.10% of these samples could be identified as AAI positive exposure. Whole genome sequencing suggested 8.41% of 107 liver cancer patients exhibited the dominant AA mutational signature, indicating a relatively low overall AAI exposure rate. In animal models, long-term administration of AAI barely increased liver tumorigenesis in adult mice, opposite from its tumor-inducing role when subjected to infant mice. Furthermore, AAI induced dose-dependent accumulation of AA-DNA adduct in target organs in adult mice, with the most detected in kidney instead of liver. Taken together, our data indicate that AA exposure was not the major threat of liver cancer in adulthood.