Objective To measure the anatomical parameters of the first maxillary molars in children of different age groups and evaluate the age-related changes in dental crowns.Methods A retrospective analysis was conduc-ted on cone beam computed tomography(CBCT)images of 4-8-year-old children.NNT software was used to ana-lyze multiple important indicators of maxillary first molar.Results A total of 308 first maxillary molars,including 154 pediatric patients,were evaluated in this study.The thickness of the pulp apex H1(left,P=0.01;right,P=0.02)and the thickness of the pulp chamber floor H3(left and right P＜0.01)were positively correlated with age,while the height of the pulp cavity H2(left and right P＜0.01)and the height of the palate tip D1(left P=0.003,right P=0.002)showed a negative correlation with age.There was no significant correlation between the height of the buccal tip and age(P＞0.05).There were significant differences in H1 and H3 between the 4-year-old and 5-year-old age groups between the 8-year-old age group(P＜0.05),as well as significant differences in H2 and D1 between the 4-year-old and 5-year-old between the 6-year-old,7-year-old and 8-year-old age groups(P＜0.05).Conclusion The age-related changes in the crowns of the first maxillary molars are important references for the clinical treatment,and can be accurately measured through CBCT data.

Objective To evaluate and compare the treatment efficacy between concentrated growth factor(CGF)and blood clots(BC)as scaffolds in regenerative endodontic procedures(REPs).Methods Twenty young permanent teeth from 18 healthy children with pulp necrosis or periapical periodontitis were randomly divided into CGF group and BC group.In the CGF group(n=10),after ap-ical bleeding,CGF was inserted into the root canal as a stent.In the BC group(n=10),by stimulating apical bleeding,blood entered the root canal and produced blood clots as scaffolds.Clinical examination and apical X-ray shooting were conducted for each follow-up visit.Cone beam computed tomographic(CBCT)images were acquired preoperatively and at the 24-month recall.The increase of root length,root wall thickness,and newly-formed calcified tissue were calculated.Results The root length increased by(1.68±0.90)mm in the CGF group and(2.36±1.34)mm in the BC group.Root wall thickness increased by(0.44±0.34)mm in the CGF group and(0.50±0.31)mm in the BC group.There was no statistically significant difference in root lengthening and root wall thickening between two groups(P＞0.05).The amount of newly formed calcified tissue in the CGF group((22.13±19.12)mm3)was significantly less than that in the BC group((42.97±22.69)mm3)(P＜0.05).According to the goals for success outlined by American Association of Endodontists(AAE),90%(9/10)of the CGF cases and100%(10/10)of the BC cases achieved the primary and secondary goals(P＞0.05).40%of the CGF cases(4/10)and 60%of the BC cases(6/10)achieved the tertiary goal(P＞0.05).Conclusion CGF is found to be use-ful as a scaffold for REPs,but the success rate is slightly lower than that of BC group and the difference is not statistically significant.

Objective: Investigate osteogenic differentiation of canine periodontal ligament stem cells ( cPDLSCs) via over-expression ephrinB2 in cPDLSCs． Methods : cPDLSCs were isolated from the premolars and molars of Beagle．After transfected with EfnB2-GFP-Bsd and GFP-Bsd empty Vector，cPDLSCs were induced to osteogenic differentiation．Western blot was used to invest the expression of ephrinB2 protein．The effect of osteogenic differentiation of EfnB2-cPDLSCs and Vector-cPDLSCs were analyzed by RT-PCR , CCK-8，Alizarin-red S staining and ALP. Results: There was no significant difference in cell proliferation between EfnB2-cPDLSCs and Vector-cPDLSCs．While EfnB2-cPDLSCs displayed an enhanced ALP activity and more prominent mineralized nodules compared with Vector-cPDLSCs．The odonto-/ osteogenic genes in EfnB2-cPDLSCs were also highly enhanced． Conclusion The results of our study indicated that ephrinB2 gene-transfected cPDLSCs showed enhanced osteogenic differentiation.

Objective: To investigate the effect of Ginsenoside Rg1 (GsRg1) on proliferation , migration and osteogenic differentiation of human gingival fibroblasts (HGFs) and its molecular mechanism. Methods: Human gingival fibroblasts (HGFs) were isolated and cultured by tissue block method , and identified by morphology and immunofluorescence. The effect of six concentrations of GsRg1 (0 , 6. 25 , 12. 5 , 25 , 50 , 100 mg/L) on the proliferation of HGFs was detected by CCK⁃8 method. Transwell assay was used to detect the effects of different concentrations of GsRg1 on the migration ability of HGFs. Alkaline phosphatase (ALP) staining was used to detect osteogenic ability. Alizarin red staining was used to observe and quantify calcium nodules. The expression of COL⁃ Ⅰ , OCN and OPN osteogenic genes was detected by qRT⁃PCR. Western blot was used to detect the protein expression of OCN ,OPN , COL⁃ Ⅰ and PI3K/AKT signaling pathway. Results: Compared with the control group , the proliferation ability of HGFs was significantly improved at the concentrations of 12. 5 ,25 ,50 and 100 mg/L GsRg1 (P < 0. 05) , and the proliferation promotion effect of 100 mg/L GsRg1 was the strongest. There was no significant difference between the 6. 25 mg/L GsRg1 group and the control group. After GsRg1 treatment , the migration ability of HGFs was enhanced and showed concentration dependence. Compared with the control group , the activity of ALP in 100 mg/L GsRg1 group significantly increased (P < 0. 01) . Alizarin red staining showed a significant increase in the number of calcium nodules(P < 0. 01) . The mRNA and egg white expression levels of osteogenic genes OCN , OPN and COL⁃ Ⅰ increased (P < 0. 05 ) . The expression levels of p ⁃PI3K and p ⁃Akt were significantly up⁃regulated with time ( P <0. 05) ,while the expression levels of PI3K and AKT had no significant changes. Conclusion GsRg1 can promote the proliferation and migration of HGFs , and 100 mg/L GsRg1 can promote the osteogenic differentiation of HGFs ,which may be related to the activation of PI3K/AKT signaling pathway.