Objective : To investigate the effect of incremental saliva contamination mixed directly into the orthodontic primer on the shear bond strength (SBS) of stainless-steel brackets and to analyze the associated failure modes. Methods : A total of 150 freshly extracted bovine mandibular incisors were randomly allocated into five groups (n = 30 per group) based on the volume ratio of artificial saliva to Transbond XT™ Primer (Primer:Saliva, v/v): G0 (100:0, control), G5 (95:5), G10 (90:10), G20 (80:20), and (50:50). Brackets were bonded following standard protocols, including acid etching, primer application, and light curing. After 24 hours water storage and 500 thermocycles (5–55℃), SBS was tested using a universal testing machine. Adhesive Remnant Index (ARI) scores were evaluated under a stereomicroscope. Data were analyzed using one-way ANOVA with Tukey’s HSD post-hoc test and the Kruskal-Wallis H test with Dunn-Bonferroni correction. Results : The Shapiro-Wilk test confirmed normal distribution across all groups, and Levene’s test indicated homogeneity of variances ( P > 0.05). One-way ANOVA revealed significant intergroup differences in SBS ( F = 145.67, P < 0.001). No significant difference was observed between G0 (16.76 ± 1.87 MPa) and G5 (15.53 ± 2.16 MPa) ( P = 0.053). However, SBS decreased significantly in groups with ≥ 10% contamination (G10: 10.24 ± 1.59 MPa, G20: 7.07 ± 1.34 MPa, G50: 4.26 ± 1.42 MPa, all P < 0.001). ARI scores shifted significantly toward lower values with increasing contamination ( H = 63.82, P < 0.0001), indicating a transition from cohesive/adhesive failure to interfacial failure at the enamel-resin junction. Conclusions : Inadvertent mixing of saliva into orthodontic primer significantly compromises bracket bond strength in a dose-dependent manner. While minimal contamination (≤ 5% v/v) may be clinically tolerable, contamination levels of 10% or higher result in a statistically and potentially clinically significant reduction in bond integrity. Clinicians should strictly avoid cross-contamination between the primer brush and saliva, as this form of contamination creates an irreversible weak interface.

This case report illustrates the treatment of a 17-year-old male patient characterized by an anterior open bite, skeletal Class III malocclusion, mandibular deviation, and severe temporomandibular joint symptoms. Given the complexity of the patient's condition, a strategic treatment approach was employed. Stabilization splint was used initially for a duration of 9 months to alleviate TMJ symptoms and repositioning the condyle. Through model analysis on the articulator pretreatment, we found a worsening of his V-shape open bite due to occlusal interference in molars. The patient refused the surgery, so the multiloop edgewise archwire treatment was provided to upright the molars and eliminate occlusal interference. After 26 months of treatment, a functional and aesthetic occlusion, and a relatively well-balanced facial profile were established. After a 6 years post-treatment follow-up, the results of this case have demonstrated long-term stability.

This systematic review aimed to investigate the factors that may contribute to the development of OSA after orthognathic surgery in patients with skeletal class III. Electronic searches of PubMed, Embase, Web of Science, and Cochrane databases were conducted up to December 10, 2022. In total, 277 studies were retrieved and screened according to the inclusion and exclusion criteria, and 14 were finally selected. All studies were of medium quality (moderate risk of bias). The occurrence of OSA after orthognathic surgery in patients with class III skeletal relationships depends on surgical factors and patient self-factors. Surgical factors include surgery type, amount of maxillary and mandibular movement, and the patient's postoperative swelling. Patient self-factors include weight, age, gender, and hypertrophy of the soft palate, tonsils, and tongue. According to information in the 14 selected articles, the incidences of OSA after Le Fort I impaction and BSSO setback, BSSO setback, and Le Fort I advancement and BSSO setback were 19.2%, 8.57%, and 0.7%, respectively, mostly accompanied with greater amounts of mandibular recession. However, no clear evidence exists to confirm that orthognathic surgery is a causative factor for postoperative sleep breathing disorders in patients with mandibular prognathism. The wider upper airway in patients with class III skeletal might be the reason for the rare occurrence of OSA after surgery. In addition, obesity and advanced age may lead to sleep apnea after orthognathic surgery. Obese patients should be advised to lose weight preoperatively.

The current review aims to explore the evidence regarding the effectiveness of mandibular advancement orthodontic appliances with maxillary expansion device in treating pediatric Obstructive Sleep Apnea (OSA). A systematic literature search was conducted across PubMed, Cochrane Central, Web of Science, Embase, Scopus databases, Chinese Biomedical Database, Chinese National Knowledge Infrastructure, and Wanfang. The research involved children and adolescents (under 16 years old) who received mandibular advancement and maxillary expansion functional orthopedic appliances for OSA treatment. We performed narrative reviews and subsequently amalgamated the findings from the studies. Six articles were included for review. Although a small number of studies were included, the research suggested the potential advantages of mandibular advancement for children with OSA. Following treatment, there was a decrease in AHI/RDI, an improvement in sleep quality, and the increase in oxygen saturation. The limited quantity and quality of existing studies necessitate caution when drawing conclusions about the effectiveness of mandibular advancement and maxillary expansion for OSA. In the future, larger and well-designed randomized controlled trials (RCTs) are needed to provide more robust evidence. Patients should be carefully selected, and their orthodontic indications should be thoroughly evaluated before inclusion in such trials.We encourage researchers to design studies that monitor patients over several years to provide a comprehensive understanding of the long-term effectiveness. This study was registered in PROSPERO(CRD42023480407) on November 20, 2023.

Background: Root resorption, an unwanted side effect often seen in orthodontics, depends largely on osteoclasts. Osteoclastic protein tyrosine phosphatase (PTP-oc) plays a major role in controlling osteoclast activity. This study aimed to investigate the effects of Ursolic acid (UA), a novel PTP-oc inhibitor, on osteoclastogenesis and root resorption. Methods: UA was pinpointed using a PTP inhibition assay. Its inhibitory characteristics, inhibitor constant (Ki) against triangle PTP-oc, and selectivity were through an Inhibition Kinetics assay. The effects of UA on osteoclastogenesis were examined by treating human U937 histiocytic lymphoma cells with or without UA and then assessing osteoclastogenesis mediated by phorbol 12-myristate 13-acetate /1 alpha, 25 di-hydroxy vitamin D-3 (1,25(OH)(2)D-3). The cell counting kit-8 (CCK-8) evaluated how a UA affects U937 cell proliferation in vitro. Osteoclast-like cell development was examined using tartrate-resistant acid phosphatase (TRAP) Staining, while Real-time-polymerase chain reaction (qPCR) was used to assess the expression of tartrate-resistant acid phosphatase (TRAP), receptor activator of nuclear factor-kappa B (RANK), matrix metalloproteinase-9 (MMP-9), cathepsin K (CK), and calcitonin receptor (CTR). Tyrosine kinase c-Src (c-Src) protein was measured using Western Blot. A rat model was used to study the levels of root resorption and tyrosine phosphorylation of c-Src (PY-527) by histology and immunohistochemistry. Results: UA displayed a strong and reversible inhibitory effect on PTP-oc in a competitive manner, showing selective in vitro (p < 0.001). The compound did not impact the viability of U937 cells at concentrations between 1-5 mu M UA. UA's inhibition of osteoclastogenesis depends on its concentration, and the compound effectively suppresses the expression of osteoclast marker genes, TRAP, RANK, MMP-9, CK, and CTR. Additionally, the area of TRAP-positive cells was reduced. This effect is facilitated by inhibiting enzymatically active PTP-oc, which elevates the levels of c-Src tyrosine phosphorylation, thereby decreasing the activity of c-Src Protein Tyrosine Kinases (PTK). In animal studies, as UA concentration increased, there was a noticeable delay and weakening in root resorption. Finally, IHC staining results revealed that compared to the 0 mu M UA (control) group, c-Src PY-527 in the model groups increased alongside the rise in UA concentration (p < 0.05). Conclusions: This study demonstrates that UA application effectively suppresses osteoclastogenesis and root resorption by inhibiting the enzymatic activity of PTP-oc. This effect is dose-dependent and may be mediated by the regulation of c-Src signaling pathway.

After bonding brackets to the first deciduous molar in a 2 × 4 technique, a three-dimensional finite element analysis (3D FEA) is used to demonstrate the biomechanical changes in an orthodontic system. This study aims to opt for the appropriate type of orthodontic technology by analyzing and comparing the mechanical systems produced by two types of 2 × 4 techniques employing rocking-chair archwires. Herein, the maxilla and maxillary dentition are modeled by cone beam computed tomography (CBCT) and 3D FEA. Common clinically used 0.016-inch round archwires (material: titanium-molybdenum alloy and stainless-steel) and 0.018-inch round archwires (material: titanium-molybdenum alloy and stainless-steel) are bent into the shape of a rocking chair with a depth of 3 mm. The forces and moments applied to the brackets are transferred to the dentition to evaluate the biomechanical effects of the 2 × 4 technique after the bracket is bonded to the first deciduous molar. For the central incisor, the teeth-moving distance in all three directions increases with bracket bonding to the first deciduous molar applying the 0.016-inch rocking-chair archwire. For the lateral incisor, the tooth root moves toward the gingival side when using 0.016-inch and 0.018-inch archwires. Moreover, for the same archwire size, the lateral incisors move toward the gingival side by bonding the bracket to the first deciduous molar. After bonding a bracket to the first deciduous molar, using rocking-chair archwires of 0.016 inch or 0.018 inch, the buccal movement distance of the first molar crown increases in the X-axis direction. In the Y-axis and Z-axis directions, the modified 2 × 4 technique significantly increases the effect of backward-tipping compared with the traditional 2 × 4 technique. In clinical practice, the modified 2 × 4 technique can be used to increase the movement distance of anterior teeth to a certain extent and accelerate the orthodontic teeth movement. Moreover, the modified 2 × 4 technique is better in anchorage conservation of the first molar than the traditional technique. Although the traditional 2 × 4 technique is widely used in early orthodontic treatment, we found mucosal damage and abnormal archwire deformation might affect orthodontic treatment time and effect. The modified 2 × 4 technique is a novel approach that avoids these drawbacks and improves orthodontic treatment efficiency.

Bone metabolism consists of bone formation and resorption and maintains a dynamic balance in vivo. When bone homeostasis is broken, it can manifest as osteoarthritis (OA), rheumatoid arthritis (RA), osteosarcoma (OS), etc. MiR-671, an important class of non-coding nucleotide sequences in vivo, is regulated by lncRNA and regulates bone metabolism balance by regulating downstream target proteins and activating various signaling pathways. Based on the structure and primary function of miR-671, this paper summarizes the effect and mechanism of miR-671 in bone-related inflammation and cancer diseases, and prospects the application possibility of miR-671, providing reference information for targeted therapy of bone-related disorders.

骨代谢是指骨的转化过程,包括骨形成和骨吸收,临床上骨代谢异常疾病的治疗包括手术治疗和药物治疗等.雷奈酸锶(SrR)是同时具有抗骨吸收和促骨形成双重作用的常用药,主要依靠其中的锶(Sr)元素调节骨代谢.目前,国内外学者对SrR在骨代谢异常中的临床应用研究较多,但对其在调节骨吸收和骨形成作用中的机制研究报道较少,尤其各类信号通路在骨代谢中的调控作用及相关分子表达变化报道较少.现通过各类信号通路及蛋白靶点,主要从SrR对骨代谢影响、作用机制和不良反应等方面进行综述,为SrR的临床应用提供理论依据.

Periodontitis (PD) may affect temporomandibular joint disorders (TMD) and TMD may influence PD in previous observational studies. Nevertheless, these studies were prone to confounders and reverse causation, leading to incorrect conclusions about causality and direction of association. This research investigates the associations between PD and TMD employing bidirectional two-sample Mendelian randomization (MR) analysis. Single-nucleotide polymorphisms (SNPs) related to PD (p < 5 × 10−6) were selected from a genome-wide association study (GWAS) from the Gene-Lifestyle Interaction in the Dental Endpoints (GLIDE) consortium, and related these to SNPs from FinnGen and UK Biobank (UKB) consortia, and vice versa. We implemented the standard inverse variance weighted (IVW), weighted median (WM), MR-Egger regression, and MR-PRESSO methods to estimate the potential causality between PD and TMD. Sensitive tests were conducted using robust MR methods. Results from FinnGen and UKB were combined using the fixed model. PD did not appear to causally affect TMD. Additionally, the reverse MR analysis did not reveal a significant causal effect of TMD on PD. The results of other MR methods were similar to those of the IVW method. Sensitivity analyses addressed no potential pleiotropy in MR estimations. Results from the meta-analysis were consistent with the above-mentioned consequences. This research does not support a causal relationship between PD and TMD. PD does not appear to worsen TMD directly, and vice versa.

Skeletal Class Ⅲ malocclusion is a commonly encountered clinical malocclusion. It can be into three types based on its pathogenesis: maxillary deficiency, mandibular overdevelopment, or a combination of both. Among these, patients with skeletal Class Ⅲ malocclusion due to maxillary deficiency can benefit from rapid maxillary expansion and maxillary protraction. In recent years, alternate rapid maxillary expansion and constriction has gained widespread acceptance in clinical practice due to its ability to yield more satisfactory correction outcomes. This paper primarily introduces the application, biological basis, and clinical relevance of alternate rapid maxillary expansion.

对于深覆（牙合）深覆盖患者如何更有效地打开咬合,从而实现咬合功能的提升以及面型的改善一直是正畸医生关注的问题[1].而低角患者因牙槽骨致密[2]其咬合打开也更为困难,同时也增加关闭拔牙间隙的难度.本病例报道一例低角型深覆（牙合）深覆盖成人矫治病例,通过平面导板、细丝轻力、摇椅弓等多种矫治方法实现咬合打开以及面型美观的提升.

前牙区是口腔美学治疗的关键,前牙形态和位置的调整是系统性美学治疗的重要部分.临床诊疗中,口腔期望恢复天然牙形态使之与面型协调;关闭前牙间隙、调整中线位置使弓形美观、对称;通过垂直向和水平向控制使牙列与龈、颊组织关系协调,展现美丽微笑.完善的前牙美学治疗需要多学科联合、多种治疗方法介入,同时应考虑患者的文化背景和审美习惯,以实现最佳治疗效果.数字化诊疗技术为治疗前美学分析预测、治疗后美学评估提供了保障.该文结合国内外最新研究成果,从前牙位置、形态以及牙列与龈、颊等软组织关系等方面对口腔治疗中前牙美学考量因素作一综述,为美学区口腔治疗规划提供参考.

上颌牙弓狭窄是正畸临床常见的错畸形,在乳、替牙列的发病率为8％～23％,恒牙列约为10％[1,2].牙弓狭窄往往是造成许多错殆畸形的重要原因,甚至导致矢状向或垂直向的不调[3].现报道1例应用上颌骨性扩弓器(maxillary skeletal expansion,MSE)治疗上颌牙弓狭窄的骨性Ⅱ类高角病例,通过上颌骨性扩弓匹配牙弓宽度以改善患者面型,掩饰性治疗Ⅱ类高角错畸形.

在正畸固定矫治中,通过改变颌面部硬组织形态、结构和空间位置使软组织产生适应性变化是获得协调和美观面部形貌的主要方式.软、硬组织的改变密切相关,前牙的内收和外展使唇部的凸度、长度、紧张度及颏部的形态发生改变;后牙的近中、远中、伸长和压低移动使下颌骨旋转,从而改变包括鼻、唇部和颏部在内的面下1/3的软组织形态.但颌面软、硬组织的改变并非单一的对应关系,各要素之间相互作用,软组织效应既受其本身长度、厚度和紧张度等特性影响,也受前牙空间位置、牙槽骨及骨面型等个体牙性和骨性特征的影响.此外,矫治过程中个体生长发育对软、硬组织形态产生持续性改变,这将增加治疗结束后患者软组织形貌预测的不确定性.三维面部扫描技术的应用和统计学分析方法的改进使客观、精准的预测成为可能.现结合国内外相关最新研究成果,从牙弓前、后段牙齿的空间位置改变和个体生长发育等角度,对口腔正畸固定矫治过程中硬组织因素对软组织形态的影响进行综述,为临床诊疗制定矫治方案及预测矫治效果提供参考.

本文介绍一例伴有局部牙槽骨缺损和下切牙缺失的严重深覆、低角安氏Ⅱ类2分类患者的多学科联合治疗.固定矫治器排齐牙列,整平牙弓,第一前磨牙区利用颌间交互牵引解除锁.在关闭上颌散在间隙的同时,逐步调整上前牙转矩.待转矩得到适当的恢复后,行上颌中切牙牙根间植骨和上颌前牙区的牙周辅助加速成骨正畸治疗技术保证牙周安全.矫治结束后,马里兰桥修复缺失的下切牙,附有斜面导板的Hawley保持器进行保持.完成矫治后,患者的侧貌协调,上下前牙覆覆盖正常,中线一致,尖磨牙达到中性关系.功能和美观都得到了改善,患者对矫治效果满意.

With the continuous progress of materials science and biology, the significance of biomaterials with dual characteristics of materials science and biology is keeping on increasing. Nowadays, more and more biomaterials are being used in tissue engineering, pharmaceutical engineering and regenerative medicine. In repairing bone defects caused by trauma, tumor invasion, congenital malformation and other factors, a variety of biomaterials have emerged with different characteristics, such as surface charge, surface wettability, surface composition, immune regulation and so on, leading to significant differences in repair effects. This paper mainly discusses the influence of surface charge of biomaterials on bone formation and the methods of introducing surface charge, aiming to promote bone formation by changing the charge distribution on the surface of the biomaterials to serve the clinical treatment better.