Purpose To investigate the prevalence of isthmi and middle mesial (MM) canals in the mesial roots of mandibular first molars (MFM) in a Mongoloid subpopulation and to evaluate their association with demographic and anatomic characteristics. Methods Cone-beam computed tomography (CBCT) images of 496 patients with 823 MFMs were selected and analyzed. The following data were collected: patient age and gender, side, presence and distribution of MM canal and isthmus, distance between mesiobuccal (MB) and mesiolingual (ML) orifices, and MB–ML root canal system (RCS) morphology. Logistic regression was used to determine the association between demographic and anatomic characteristics and the presence of isthmi in the apical third. Results The overall prevalence of isthmus and an MM canal in MFM was 64.6% and 10.8%, respectively. The highest prevalence of isthmi and MM canals was found in patients of ≤ 20 and of 41–60 years, respectively ( p < 0.05). The prevalence of isthmi declines with age. A total of 41.3% of the MFMs had isthmi in the apical third of the mesial roots. Younger age, shorter MB–ML orifice distance, and Weine type II RCS increased the probability of the presence of an isthmus in the apical third ( p < 0.05). Conclusion The prevalence of isthmus in MFM is high in the subject population, but the prevalence of MM canals is not as high as previously reported. Demographic and anatomic characteristics could aid clinicians to better predict the presence of MM canal and an isthmus.

Objective To evaluate the shaping ability of three thermally-treated rotary nickel-titanium (NiTi) systems including ProTaper Next (PTN), HyFlex™ CM (HFCM) and HyFlex™ EDM (HFEDM) during root canal preparation in simulated root canals. Methods A total of 45 simulated root canals were divided into three groups ( n = 15) and prepared with PTN, HFCM or HFEDM files up to size 25. Microcomputed tomography (microCT) was used to scan the specimens before and after instrumentation. Volume and diameter changes, transportations and centring ratios at 11 levels of the simulated root canals were measured and compared. Results HFEDM caused significantly greater volume increases than HFCM and PTN in the entire root canal and in the apical and middle thirds. HFCM removed the least amount of resin in the coronal third compared with HFEDM and PTN. Overall, HFCM caused significantly less transportation in the apical 2 mm and was better centred than PTN in the apical 3 mm. Conclusion Under the conditions of this study, all systems prepared curved canals without significant shaping errors and instrument fracture. PTN and HFCM cut less resin than HFEDM. HFCM stayed centred apically and cut the least material coronally.

Background: Receptor tyrosine kinase-like orphan receptor 2 (Ror2) plays a key role in bone formation, but its signaling pathway is not completely understood. Signal transducer and activator of transcription 3 (Stat3) takes part in maintaining bone homeostasis. The aim of this study is to reveal the role and mechanism of Ror2 in the osteogenic differentiation from mouse bone marrow mesenchymal stem cells (mBMSCs) and to explore the effect of Stat3 on Ror2-mediated osteogenesis. Methods: Ror2 CKO mice were generated via the Cre-loxp recombination system using Prrx1-Cre transgenic mice. Quantitative real-time PCR and western blot were performed to assess the expression of Stat3 and osteogenic markers in Ror2-knockdown mBMSCs (mBMSC-sh-Ror2). After being incubated in osteogenic induction medium for 3 weeks, Alizarin Red staining and western blot were used to examine the calcium deposit and osteogenic markers in Stat3 overexpression in mBMSC-sh-Ror2. Results: Loss of Ror2 in mesenchymal or osteoblast progenitor cells led to a dwarfism phenotype in vivo. The mRNA expression of osteogenic markers (osteocalcin, osteopontin (OPN), and collagen I) in the ulna proximal epiphysis of Ror2 CKO mice was significantly decreased (P < 0.05). The mRNA and protein expression of Stat3 and osteogenic markers (Runx2, osterix, and OPN) decreased in mBMSC-sh-Ror2 cells (P < 0.05). The overexpression of Stat3 in mBMSC-sh-Ror2 cells rescued the calcium deposit and expression of Runx2, osterix, and OPN to a level comparable to normal mBMSCs. Conclusions: Ror2 was essential for skeleton development by regulating mBMSCs' osteogenesis and osteoblast differentiation. Loss of Ror2 may impair the osteogenesis of mBMSCs by inhibiting Stat3.