Tooth movement is a biological process of bone remodeling induced by mechanical force. Sclerostin secreted by osteocytes is mechanosensory and important in bone remodeling. However, little is known regarding the role of sclerostin in tooth movement. In this study, models of experimental tooth movement were established in rats and mice. Sclerostin expression was investigated with immunohistochemistry staining, and osteoclastic activity was analyzed with tartrate-resistant acid phosphatase (TRAP) staining. MLO-Y4 osteocyte-like cells underwent uniaxial compression and tension stress or were cultured in hypoxia conditions. Expression of sclerostin was assessed by RT-qPCR and ELISA. MLO-Y4 cells were cultured with recombinant human sclerostin (rhSCL) interference and then co-cultured with RAW264.7 osteoclast precursor cells. Expressions of RANKL and OPG were analyzed by RT-qPCR, and osteoclastic activity was assessed by TRAP staining. During tooth movement, sclerostin was expressed differently in compression and tension sites. In SOST knock-out mice, there were significantly fewer TRAP-positive cells than in WT mice during tooth movement in compression sites. In-vitro studies showed that the expression of sclerostin in MLO-Y4 osteocyte-like cells was not different under a uniaxial compression and tension force, whereas hypoxia conditions significantly increased sclerostin expression in MLO-Y4 cells. rhSCL interference increased the expression of RANKL and the RANKL/OPG ratio in MLO-Y4 cells and the osteoclastic induction ability of MLO-Y4 cells in experimental osteocyte-osteoclast co-culture. These data suggest that sclerostin plays an important role in the bone remodeling of tooth movement.

Based on current clinical evidence obtained from RCTs, SLBs do not show clinical superiority compared to CBs in expanding transversal dimensions, space closure, or orthodontic efficiency. Further high-level studies involving randomized, controlled, clinical trials are warranted to confirm these results.

Introduction: A protocol was introduced to achieve accurate bracket placement in vivo, which consisted of operative procedures for precise control, and a computer-aided design and computer-aided manufacturing-guided bonding device. To evaluate the accuracy of this protocol, a 3-dimensional assessment was performed. Methods: Ten consecutive patients were enrolled. Strictly following the protocol, from December 2017 to March 2018, brackets were placed on the teeth of each patient using the device. To evaluate the accuracy, deviations of positions and orientations for bracket placement were measured. Each patient was followed up after 3 months regarding bracket failures. Results: The guided bonding device was used in all cases, and a total of 205 brackets were successfully bonded and evaluated. Except for 15.12% brackets with torque deviation over 2 , the deviations in mesiodistal, buccolingual, vertical, rotation, and angulation were below the clinical acceptable range (0.5 mm in translation or 2 in orientation) for all brackets. In the 3-month follow-up, there was no bracket failure in any patient. Conclusion: This protocol transferred the planned bracket position from the digital setup to patient's dentition with generally high positional accuracy. (Am J Orthod Dentofacial Orthop 2020;157:269-77)

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In full‐arch implant‐supported rehabilitation of patients with severe periodontitis, prediction of lateral facial profile with modified dental position remains a challenge, especially for patients with protruded anterior teeth. This clinical report describes a digital workflow to predict lateral profiles and then guide the implant placement and restoration fabrication.

Treatment outcomes of Angle Class II subdivision malocclusions may be compromised because of the uncertainty of the aetiology. Previous studies have reported controversial ideas about the origins, but the existence of a primary contributor still remains unknown. Functional factors have been mentioned as a probable cause, but until now, there have been no supporting data. This study was a cross-sectional investigation of the characteristics of Angle Class II subdivision malocclusion, including dental, skeletal and functional factors, by comparison of the subdivision group and the normal occlusion group. The evaluations of dental and skeletal asymmetries of both groups were carried out by cone-beam computed tomography (CBCT) and analysis of dental casts. The functional deviations were evaluated by cast mounting and measuring. In the subdivision group, the asymmetric position of the glenoid fossa was found to be the most significant skeletal asymmetry. No dentoalveolar asymmetry was found in this group. The most important finding was that, in subdivision malocclusions, functional deviation resulting in pseudoasymmetry occurred in 32.86% of the study participants. This deviation is probably related to the disharmonious arch width between maxillary and mandibular dental arches in the premolar section. The origin of Angle Class II subdivision malocclusion is multifactorial, with dental, skeletal and functional factors included. Functional deviation occurs, probably due to dental arch width disharmony. Asymmetric position of the glenoid fossa may account for most of the skeletal asymmetry.

During orthodontic tooth movement (OTM), periodontal ligament cells (PDLCs) receive the mechanical stimuli and transform it into myofibroblasts (Mfbs). Indeed, previous studies have demonstrated that mechanical stimuli can promote the expression of Mfb marker α-smooth muscle actin (α-SMA) in PDLCs. Transforming growth factor β1 (TGF-β1), as the target gene of yes-associated protein (YAP), has been proven to be involved in this process. Here, we sought to assess the role of YAP in Mfbs differentiation from PDLCs. The time-course expression of YAP and α-SMA was manifested in OTM model in vivo as well as under tensional stimuli in vitro. Inhibition of RhoA/Rho-associated kinase (ROCK) pathway using Y27632 significantly reduced tension-induced Mfb differentiation and YAP expression. Moreover, overexpression of YAP with lentiviral transfection in PDLCs rescued the repression effect of Mfb differentiation induced by Y27632. These data together suggest a crucial role of YAP in regulating tension-induced Mfb differentiation from PDLC interacted with RhoA/ROCK pathway.

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