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Aim: To investigate whether silibinin impacts diabetic periodontitis (DP) via mitochondrial regulation. Materials and Methods: In vivo, rats were divided into control, diabetes, DP and DP combined with silibinin groups. Diabetes and periodontitis were induced by streptozocin and silk ligation, respectively. Bone turnover was evaluated by microcomputed tomography, histology and immunohistochemistry. In vitro, human periodontal ligament cells (hPDLCs) were exposed to hydrogen peroxide (H2O2) with or without silibinin. Osteogenic function was analysed by Alizarin Red and alkaline phosphatase staining. Mitochondrial function and biogenesis were investigated by mitochondrial imaging assays and quantitative polymerase chain reaction. Activator and lentivirus-mediated knockdown of peroxisome proliferator-activated receptor gamma-coactivator 1-alpha (PGC-1α), a critical regulator of mitochondria biogenesis, was used to explore the mitochondrial mechanisms. Results: Silibinin attenuated periodontal destruction and mitochondrial dysfunction and enhanced mitochondrial biogenesis and PGC-1α expression in rats with DP. Meanwhile, silibinin promoted cell proliferation, osteogenesis and mitochondrial biogenesis and increased the PGC-1α level in hPDLCs exposed to H2O2. Silibinin also protected PGC-1α from proteolysis in hPDLCs. Furthermore, both silibinin and activator of PGC-1α ameliorated cellular injury and mitochondrial abnormalities in hPDLCs, while knockdown of PGC-1α abolished the beneficial effect of silibinin. Conclusions: Silibinin attenuated DP through the promotion of PGC-1α-dependent mitochondrial biogenesis.

Periodontitis is an oral microbiota-induced inflammatory disease, in which inflammation and oxidative stress play a critical role. Silibinin (SB), a Silybum marianum-derived compound, exhibits strong anti-inflammatory and antioxidative properties. We adopted a rat ligature-induced periodontitis model and a lipopolysaccharide- (LPS-) stimulated human periodontal ligament cells (hPDLCs) model to evaluate the protective effects of SB. In the in vivo model, SB reduced alveolar bone loss and apoptosis of PDLCs in the periodontal tissue. SB also maintained the expression of nuclear factor-E2-related factor 2 (Nrf2), a key regulator of cellular resistance to oxidative stress, and attenuated lipid, protein, and DNA oxidative damages in the periodontal lesion area. Meanwhile, in the in vitro model, SB administration reduced the production of intracellular reactive oxidative species (ROS). Furthermore, SB exerted a strong anti-inflammatory property in both in vivo and in vitro models by inhibiting the expression of inflammatory mediators including nuclear factor-κB (NF-κB) as well as nucleotide binding oligomerization domain- (NOD-) like receptor family pyrin domain-containing 3 (NLRP3) and downregulating the levels of proinflammatory cytokines. This study, for the first time, demonstrates that SB exhibits the anti-inflammatory and antioxidative properties against periodontitis by downregulating the expression of NF-κB and NLRP3 and upregulating Nrf2 expression, suggesting a promising potential clinical application of SB in periodontitis.

Teeth, long-lasting percutaneous organs, feature soft tissue attachment through adhesive structures, hemidesmosomes, in the junctional epithelium basement membrane adjacent to teeth. This soft tissue attachment prevents bacterial infection of the tooth despite the rich - and harsh - microbial composition of the oral cavity. Conversely, millions of percutaneous devices (catheters, dental, and orthopedic implants) fail from infection yearly. Standard of care antibiotic usage fuels antimicrobial resistance and is frequently ineffective. Infection prevention strategies, like for dental implants, have failed in generating durable soft tissue adhesion - like that seen with the tooth - to prevent bacterial colonization at the tissue-device interface. Here, inspired by the impervious natural attachment of the junctional epithelium to teeth, we synthesized four cell adhesion peptide (CAPs) nanocoatings, derived from basement membranes, to promote percutaneous device soft tissue attachment. The two leading nanocoatings upregulated integrin-mediated hemidesmosomes, selectively increased keratinocyte proliferation compared to fibroblasts, which cannot form hemidesmosomes, and expression of junctional epithelium adhesive markers. CAP nanocoatings displayed marked durability under simulated clinical conditions and the top performer CAP nanocoating was validated in a percutaneous implant murine model. Basement membrane CAP nanocoatings, inspired by the tooth and junctional epithelium, may provide an alternative anti-infective strategy for percutaneous devices to mitigate the worldwide threat of antimicrobial resistance. STATEMENT OF SIGNIFICANCE: Prevention and management of medical device infection is a significant healthcare challenge. Overzealous antibiotic use has motivated alternative material innovations to prevent infection. Here, we report implant cell adhesion peptide nanocoatings that mimic a long-lasting, natural "medical device," the tooth, through formation of cell adhesive structures called hemidesmosomes. Such nanocoatings sidestep the use of antimicrobial or antibiotic elements to form a soft-tissue seal around implants. The top performing nanocoatings prompted expression of hemidesmosomes and defensive factors to mimic the tooth and was validated in an animal model. Application of cell adhesion peptide nanocoatings may provide an alternative to preventing, rather that necessarily treating, medical device infection across a range of device indications, like dental implants.

Large bone defect repair requires biomaterials that promote angiogenesis and osteogenesis. In present work, a nanoclay (Laponite, XLS)-functionalized 3D bioglass (BG) scaffold with hypoxia mimicking property was prepared by foam replication coupled with UV photopolymerization methods. Our data revealed that the incorporation of XLS can significantly promote the mechanical property of the scaffold and the osteogenic differentiation of human adipose mesenchymal stem cells (ADSCs) compared to the properties of the neat BG scaffold. Desferoxamine, a hypoxia mimicking agent, encourages bone regeneration via activating hypoxia-inducible factor-1 alpha (HIF-1α)-mediated angiogenesis. GelMA-DFO immobilization onto BG-XLS scaffold achieved sustained DFO release and inhibited DFO degradation. Furthermore, in vitro data demonstrated increased HIF-1α and vascular endothelial growth factor (VEGF) expressions on human adipose mesenchymal stem cells (ADSCs). Moreover, BG-XLS/GelMA-DFO scaffolds also significantly promoted the osteogenic differentiation of ADSCs. Most importantly, our in vivo data indicated BG-XLS/GelMA-DFO scaffolds strongly increased bone healing in a critical-sized mouse cranial bone defect model. Therefore, we developed a novel BG-XLS/GelMA-DFO scaffold which can not only induce the expression of VEGF, but also promote osteogenic differentiation of ADSCs to promote endogenous bone regeneration., Graphical abstract Image 1, Highlights ● A nanoclay-functionalized 3D bioglass scaffolds with hypoxia mimicking ability were developed. ● These scaffolds had the ability to sustain release of DFO and induce VEGF expression in ADSCs. ● Nanoclay together with bioglass promoted the osteogenic differentiation of ADSCs in vitro and cranial bone formation in vivo. ● The scaffolds could act as favorable synthetic ECM for large bone defect repair.

Titanium (Ti) ion can stimulate osteoblast apoptosis and therefore have a high potential to play a negative role in the aseptic loosening of implants. Mitochondrial abnormalities are closely related to osteoblast dysfunction. However, the mitochondrial molecular mechanism of Ti ion induced osteoblastic cell apoptosis is still unclear. This study investigated in vitro mitochondrial oxidative stress (mtROS) mediated mitochondrial dysfunction involved in Ti ion-induced apoptosis of murine MC3T3-E1 osteoblastic cells. In addition to reducing mitochondrial membrane potential (MMP) and decreasing adenosine triglyceride production, exposure to Ti ions increased mitochondrial oxidative stress. Moreover, mitochondrial abnormalities significantly contributed to Ti ion induction of osteoblastic cellular apoptosis. A mitochondria-specific antioxidant, mitoquinone (MitoQ), alleviated Ti ion-induced mitochondrial dysfunction and apoptosis in osteoblastic cells, indicating that Ti ion mainly induces mitochondrial oxidative stress to produce a cytotoxic effect on osteoblasts. Here we show that the primary regulator of mitochondrial permeability transition pore (mPTP), cyclophilin D (CypD), is involved in mitochondrial dysfunction and osteoblast cell apoptosis induced by Ti ion. Overexpression of CypD exacerbates osteoblast apoptosis and impairs osteogenic function. Moreover, detrimental effects of CypD were rescued by cyclosporin A (CsA), an inhibitor of CypD, which shows its protective effect on mitochondrial and osteogenic osteoblast functions. Based on new insights into the mitochondrial mechanisms underlying Ti ion-induced apoptosis of osteoblastic cells, the findings of this study lay the foundation for the clinical use of CypD inhibitors to prevent or treat implant failure.

Excessive generation of reactive oxygen species (ROS) have great impacts on the development of periodontitis. Dynamin-related protein 1 (Drp1) mediated mitochondrial fission is the main reason and the result of excessive ROS generation. However, whether Drp1 and crosstalk between ROS and Drp1 contribute to the process of periodontitis remains elusive. We herein investigated the role and functional significance of crosstalk between ROS and Drp1 in periodontitis. Firstly, human periodontal ligament cells (hPDLCs) were treated with hydrogen peroxide (H2O2) and ROS inhibitor N-acetyl-cysteine (NAC) or Drp1 inhibitor mitochondrial division inhibitor 1 (Mdivi-1). Cell viability, apoptosis, osteogenic differentiation, expression of Drp1, and mitochondrial function were investigated. Secondly, mice with periodontitis were treated with NAC or Mdivi-1. Finally, gingival tissues were collected from periodontitis patients and healthy individuals to evaluate ROS and Drp1 levels. H2O2 induced cellular injury and inflammation, excessive ROS production, mitochondrial abnormalities, and increased expression of p-Drp1 and Drp1 in hPDLCs, which could be reversed by NAC and Mdivi-1. Moreover, both NAC and Mdivi-1 ameliorated tissue damage and inflammation, and decreased expression of p-Drp1 and Drp1 in mice with periodontitis. More importantly, patients with periodontitis presented significantly higher levels of ROS-induced oxidative damage and p-Drp1 than that in healthy individuals and correlated with clinical parameters. In summary, ROS-Drp1 crosstalk greatly promotes the development of periodontitis. Pharmacological blockade of this crosstalk might be a novel therapeutic strategy for periodontitis.

Highlights • Few pregnant women had COVID-19 related close contacts, nor considered a high risk of being infected in Shenzhen during the epidemic of COVID-19. • A notable proportion of the pregnant women exhibited mild anxiety and depression symptoms, which strongly linked with poor sleep conditions during the epidemic of COVID-19 in Shenzhen. • Targeted interventions in improving sleep conditions might help alleviate gestational anxious and depressive symptoms when encountering public health emergencies., Background Pregnant women often encounter psychiatric symptoms and declined sleep quality as pregnancy proceeds. The associations between sleep conditions and anxious and depressive symptoms among pregnant women remained to be investigated, particularly during the epidemic of COVID-19. Methods An online cross-sectional survey on pregnant women was conducted at the time period of fast increasing cases of COVID-19 in Shenzhen. The Self-Rating Anxiety Scale (SAS) and the Patient Health Questionnaire (PHQ-9) were applied to detect anxious and depressive symptoms. Multivariable logistic regressions models were established to explore the associations of sleep conditions with psychological symptoms. Results In total, 751 pregnant women were enrolled, with a mean age of 30.51 years (Standard deviation: 4.28). Overall, 82.7% of the respondents considered low risk of being infected by COVID-19. The prevalence of anxiety and depression symptoms during the epidemic of COVID-19 among pregnant women were 13.4% and 35.4%, respectively, but most of which were mild. Variables referred to poor sleep conditions were strongly associated with anxious and depressive symptoms, including random or late time of going to bed, difficulty in falling sleep, short sleep duration, and ordinary or poor subjective sleep quality. Limitations Non-random sample restricted generalization of our findings to the whole population of pregnant women. Conclusions Our research revealed a notable proportion of the pregnant women who exhibited mild anxiety and depression symptoms during the epidemic of COVID-19 in Shenzhen. Targeted interventions in improving sleep conditions might help alleviate gestational anxious and depressive symptoms.

A 19‐year‐old female affected by dentinogenesis imperfecta type II (DI‐II), a genetic disease that affects the structural integrity of the dentin, presented with a chief complaint of discolored teeth. For this patient, digital techniques, including digital smile design (DSD), the ARCUSdigma axiograph and computer‐aided design/computer‐aided manufacturing (CAD/CAM), were extensively used in all phases of the rehabilitation process. Compared to traditional analog methods, these digital techniques could reduce the constant confirmation of occlusion, promote communication between clinicians and dental technicians, achieve accurate occlusion with relatively high efficiency, and improve the efficacy of esthetic rehabilitation in the treatment of this patient with DI‐II.

Zinc (Zn)-based metals and alloys are emerging as promising biodegradable implant materials due to their inherent biodegradability and good biocompatibility. However, this class of materials exhibits low mechanical strength and a slow degradation rate, which hinders their clinical application. Here we report the development of a new biodegradable Fe/Zn-3Cu composite fabricated by infiltration casting of a Zn-3Cu alloy into an Fe foam followed by hot-rolling. Our results indicate that the hot-rolled (HR) Fe/Zn-3Cu composite exhibited an α-Zn matrix phase, a secondary CuZn

© 2021 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.Oxidative stress (OS)-induced mitochondrial damage and the subsequent osteoblast dysfunction contributes to the initiation and progression of osteoporosis. Notoginsenoside R1 (NGR1), isolated from Panax notoginseng, has potent antioxidant effects and has been widely used in traditional Chinese medicine. This study aimed to investigate the protective property and mechanism of NGR1 on oxidative-damaged osteoblast. Osteoblastic MC3T3-E1 cells were pretreated with NGR1 24 h before hydrogen peroxide administration simulating OS attack. Cell viability, apoptosis rate, osteogenic activity and markers of mitochondrial function were examined. The role of C-Jun N-terminal kinase (JNK) signalling pathway on oxidative injured osteoblast and mitochondrial function was also detected. Our data indicate that NGR1 (25 μM) could reduce apoptosis as well as restore osteoblast viability and osteogenic differentiation. NGR1 also reduced OS-induced mitochondrial ROS and restored mitochondrial membrane potential, adenosine triphosphate production and mitochondrial DNA copy number. NGR1 could block JNK pathway and antagonize the destructive effects of OS. JNK inhibitor (SP600125) mimicked the protective effects of NGR1while JNK agonist (Anisomycin) abolished it. These data indicated that NGR1 could significantly attenuate OS-induced mitochondrial damage and restore osteogenic differentiation of osteoblast via suppressing JNK signalling pathway activation, thus becoming a promising agent in treating osteoporosis.

Zinc (Zn) and its alloys are currently regarded as one of the promising families of biodegradable metals for implant applications owing to their suitable biodegradability and biofunctionality. However, the inadequate mechanical properties of as-cast (AC) pure Zn restricted the practical clinical bone-implant applications due to its coarse grain size and hexagon close-packed crystal structure. Here, the impact of gadolinium (Gd) on the mechanical properties, corrosion resistance, hemolysis percentage, anticoagulant activity, and cytotoxicity of AC and hot-rolled (HR) Zn-1Mg-xGd (x = 0.1, 0.2, and 0.3) (wt.%) alloys were investigated for biodegradable bone-implant applications. Tensile testing showed that the HR Zn-1Mg-0.3Gd alloy exhibited the highest tensile strength of 288.1 MPa, tensile yield strength of 250.9 MPa, and elongation of 13.2%. Electrochemical corrosion and immersion tests revealed that the corrosion rates of both AC and HR specimens increased with increasing Gd content in Hanks' solution, and the HR Zn-1Mg-xGd specimens exhibited higher corrosion rates compared to their AC counterparts. The HR Zn-1Mg-xGd specimens showed an increasing hemolysis percentages and decreasing activated partial thromboplastin time (APTT) values with increasing Gd addition. The alloy extracts of HR samples at ≤ 25% concentration exhibited no cytotoxicity toward MG-63 cells, and the HR Zn-1Mg-0.3Gd alloy displayed the highest cell viability among all three alloy extracts at 12.5% concentration. Overall, the HR Zn-1Mg-0.3Gd can be considered a promising biodegradable implant material for bone-implant materials owing to its high mechanical strength and ductility, suitable degradation rate, and satisfying biocompatibility. STATEMENT OF SIGNIFICANCE: In this work, Zn-1Mg-xGd (x = 0.1, 0.2, and 0.3 wt.%) alloys were developed by alloying with gadolinium (Gd) and hot-rolling, and their mechanical properties, corrosion behavior, hemolysis percentage, anticoagulant activity, and cytotoxicity were investigated for biodegradable implant application. Our findings demonstrated that the hot-rolled Zn-1Mg-0.3Gd alloy exhibit the highest ultimate tensile strength of 288.1 MPa, yield strength of 250.9 MPa, and elongation of 13.2%. Hot-rolled Zn-1Mg-xGd alloys show slowly increasing hemolysis percentages and decreasing activated partial thromboplastin time (APTT) values with increasing Gd addition. Extracts of hot-rolled Zn-1Mg-xGd alloys at a concentration of ≤ 25% show no cytotoxicity towards MG-63 cells, and Zn-1Mg-0.3Gd exhibit good cytocompatibility among all three alloys at a concentration of 12.5%.

BACKGROUND: Accurate preoperative puncture and localization is a key step in percutaneous endoscopic lumbar discectomy (PELD). This study investigated the benefit of puncture and localization for PELD by C-arm navigation over conventional methods. METHODS: Sixteen adult cadavers were randomly divided into two groups (group A defined as the C-arm navigation method, and group B defined as the conventional localization method). Two junior orthopedic surgeons who specialized in spinal surgeries were randomly allocated to each group. Conventional localization using C-arm fluoroscopy and localization using C-arm navigation were performed during the procedure. The intervertebral foramen on both sides at L3-L4, L4-L5, and L5-S1 levels were punctured using the two methods. Technical parameters, such as fluoroscopy time, puncture time, overall time taken for puncture and localization, as well as the number of fluoroscopies, number of puncture attempts, and success rate of the first puncture were compared between the two methods. The learning curves were plotted for the two methods, and correlations between all technical parameters were analyzed. RESULTS: Puncture and localization for PELD assisted by C-arm navigation had a flatter learning curve compared with the conventional localization method. The fluoroscopy, puncture, and total puncture-localization time for group A were 5.61 (±1.37), 2.29 (±1.22), and 9.78 (±2.66) minutes compared with 15.72 (±3.59), 4.87 (±1.70), and 20.59 (±4.79) minutes for group B, respectively (P

Background: Resin monomer induced dental pulp injury presents a mitochondrial dysfunction related pathology. Melatonin has been regarded as a strong mitochondrial protective bioactive compound from pineal gland. However, it remains unknown whether melatonin can prevent dental pulp from resin monomer induced injury. The aim of the study is to investigate the effects of melatonin on TEGDMA, a major component in dental resin, induced mouse pre-odontoblast cell lines (mDPC6T) mitochondrial apoptosis and to verify whether JNK/MAPK signaling pathway mediate the protective effect of melatonin. Methods: We adopted a well-established TEGDMA-induced mDPC6T apoptosis model to investigate the preventive effect of melatonin by detecting cell viability, apoptosis rate, expression of apoptosis related protein, mitochondrial ROS (mtROS) production, mitochondrial membrane potential (MMP) and adenosine triphosphate (ATP) level. Inhibitors of MAPKs signaling were used to explore which pathway was participated in TEGDMA induced apoptosis. Finally, we verified the role of JNK/MAPK pathway during the protective effects of melatonin above by the agonist and antagonists of JNK.Results: Melatonin attenuated TEGDMA induced mDPC6T apoptosis via reducing mtROS production, rescuing MMP and ATP level. Meanwhile, the mitochondrial dysfunction and apoptosis was alleviated by the JNK/MAPK inhibitor SP600125 but not the other MAPKs signaling inhibitors. Furthermore, melatonin down-regulated the expression of phosphorylated-JNK, and eliminated the active effects of Anisomycin on JNK/MAPK pathway, which mimicked the effects of the SP600125.Conclusion: Our findings demonstrated that melatonin protected mDPC6T against TEGDMA induced apoptosis via JNK/MAPK signaling and maintenance of mitochondrial function, which presented a novel therapeutic strategy for prevention against resin monomer-induced dental pulp injury.

Reactive oxygen species (ROS) overproduction promotes the alveolar bone loss during the development of periodontitis. Mitochondria are the principal source of ROS. Hydroxytyrosol (HT), a natural phenolic compound present in olive oil, is well known for its antioxidant and mitochondrial-protective prosperities. Nonetheless, the impact of HT on periodontitis and its related mechanisms underlying bone cell behavior remains unknown. Osteoclasts differentiated from RAW264.7 model and oxidative stress (OS) induced pre-osteoblast MC3T3-E1 cell injury model were treated with and without HT. Cell viability, apoptosis, differentiation, mitochondrial function along with mitogen-activated protein kinase (MAPK) signaling pathway were investigated. Meanwhile, the effect and related mechanisms of HT on bone loss in mice with periodontitis were also detected. HT inhibited osteoclast differentiation and prevented OS induced pre-osteoblast cells injury via regulating mitochondrial function as well as ERK and JNK signaling pathways. Moreover, HT attenuated the alveolar bone loss, increased bone forming activity, inhibited the osteoclasts differentiation and decreased the level of OS in mice with periodontitis. Our findings, for the first time, revealed a novel function of HT in bone remodeling of periodontitis, and highlighted its therapeutical potential for the prevention/treatment of periodontitis.

The present study aimed at investigating the influence of norspermidine on the formation of dual-species biofilms composed of Streptococcus mutans (S. mutans) and Streptococcus sanguinis (S. sanguinis). Crystal violet assay was conducted to assess the formation of single-species biofilms of S. mutans and S. sanguinis, and the growth curve was carefully observed to monitor the growth of these two species of bacteria. Fluorescence in situ hybridization (FISH) and MTT array were used to analyze the composition and metabolic activity of the dual-species biofilms, respectively. Extracellular polysaccharides (EPS)/bacteria staining, anthrone method, and scanning electron microscopy (SEM) imaging were conducted to study the synthesis of EPS by dual-species biofilms. Lactic acid assay and pH were measured to detect dual-species biofilm acid production. We found that norspermidine had different effects on S. mutans and S. sanguinis including their growth and biofilm formation. Norspermidine regulated the composition of the dual-species biofilms, decreased the ratio of S. mutans in dual-species biofilms, and reduced the metabolic activity, EPS synthesis, and acid production of dual-species biofilms. Norspermidine regulated dual-species biofilms in an ecological way, suggesting that it may be a potent reagent for controlling dental biofilms and managing dental caries.

A 20-year-old woman presented with an unesthetic appearance and severe wear of the anterior teeth. Definitive expected treatment was designed by multidisciplinary combination therapy. Meanwhile, gene sequencing was used diagnostically, and digital smile design (DSD) was used to design the esthetics of the anterior teeth. The 3-month follow-up showed an acceptable outcome. The whole-exon sequencing and direct sequencing of polymerized chain reaction products of dentin sialophosphoprotein were performed, but further sequencing was needed in the repeat region of dentin sialophosphoprotein exon 5 (the data were not shown). DSD assisted and improved the esthetic design of the definitive restoration, communication with the patient, and predictability of the treatment. This treatment demonstrates that the diagnosis and differential diagnosis of patients with dentinogenesis imperfecta (DGI)-II are essential and effective for implementing the definitive treatment plan. Gene screening can be used as an auxiliary method of diagnosing DGI-II. In terms of esthetic design, DSD played an important role in ensuring a satisfactory result. Moreover, a multidisciplinary treatment protocol focusing on prosthodontics, which is different from the traditional treatment of DGI-II and consists solely of prosthodontic rehabilitation, proved highly effective in the esthetic restoration of a patient with DGI-II.

This study evaluated radiation exposure and operation time of percutaneous endoscopic lumbar discectomy (PELD) by using a fluoroscopy-based navigation system for access and localization.Eighty-six PELDs performed by a single surgeon were retrospectively analyzed. Patients were separated into 2 groups: group A (using a three-dimensional [3D]-printed navigation instrument and fluoroscopy-based navigation system) and group B (with conventional fluoroscopy and standard instrumentation). The operation, fluoroscopy, and total access time were collected, as well as fluoroscopy and access times.The operative time for group A was 59 minutes (standard deviation [SD], 6 minutes) and 106 minutes (SD, 15 minutes) in group B (P0.001). In group A, fluoroscopy was used an average of 5 times (SD, 0.7) and 29 times (SD, 8) in group B (P0.001). The fluoroscopy time was 9 minutes (SD, 2 minutes) in group A and 40 minutes (SD, 8 minutes) in group B (P0.001). The number of access attempts was 1.3 (SD, 0.5) in group A and 8 (SD, 2 times) in group B (P 0.001). The total access time was 11 minutes (SD, 2 minutes) in group A and 28 minutes (SD, 5 minutes) in group B (P0.001).PELD using the fluoroscopy-based navigation system showed lower operative, fluoroscopy, and access time compared with conventional techniques. In addition, fewer fluoroscopy images and access attempts were made in the navigation group. These data suggest that this novel technique reduces fluoroscopy and operation time and may reduce risks of repeated surgical access attempts.

Pathological stimuli, such as bacterial activity, dental bleaching, and nonpolymerized resin monomers, can cause death of dental pulp cells (DPCs) through oxidative stress- (OS-) induced mitochondrial dysfunction. However, the crucial molecular mechanisms that mediate such a phenomenon remain largely unknown. OS is characterized by the overproduction of reactive oxygen species (ROS), e.g., H2O2, O2−, and ⋅OH. Mitochondria are a major source of ROS and the principal attack target of ROS. Cyclophilin D (CypD), as the only crucial protein for mitochondrial permeability transition pore (mPTP) induction, facilitates the opening of mPTP and causes mitochondrial dysfunction, leading to cell death. In the present study, we hypothesized that CypD-mediated mitochondrial molecular pathways were closely involved in the process of OS-induced death of human DPCs (HDPCs). We tested the phenotypic and molecular changes of HDPCs in a well-established OS model—H2O2 treatment. We showed that H2O2 dramatically reduced the viability and increased the death of HDPCs in a time- and dose-dependent manner by performing MTT, flow cytometry, and TUNEL assays and quantifying the expression changes of Bax and Bcl-2 proteins. H2O2 also induced mitochondrial dysfunction, as reflected by the increased mitochondrial ROS, reduced ATP production, and activation of mPTP (decreased mitochondrial membrane potential and enhanced intracellular Ca2+ level). An antioxidant (N-acetyl-L-cysteine) effectively preserved mitochondrial function and significantly attenuated H2O2-induced cytotoxicity and death. Moreover, H2O2 treatment markedly upregulated the CypD protein level in HDPCs. Notably, genetic or pharmacological blockade of CypD significantly attenuated H2O2-induced mitochondrial dysfunction and cell death. These findings provided novel insights into the role of a CypD-dependent mitochondrial pathway in the H2O2-induced death in HDPCs, indicating that CypD may be a potential therapeutic target to prevent OS-mediated injury in dental pulp.

Objective The present study aimed to investigate the molecular events in alisol B 23-acetate (ABA) cytotoxic activity against a liver cancer cell line. Methods First, we employed a quantitative proteomics approach based on stable isotope labeling by amino acids in cell culture (SILAC) to identify the different proteins expressed in HepG2 liver cancer cells upon exposure to ABA. Next, bioinformatics analyses through DAVID and STRING on-line tools were used to predict the pathways involved. Finally, we applied functional validation including cell cycle analysis and Western blotting for apoptosis and mTOR pathway-related proteins to confirm the bioinformatics predictions. Results We identified 330 different proteins with the SILAC-based quantitative proteomics approach. The bioinformatics analysis and the functional validation revealed that the mTOR pathway, ribosome biogenesis, cell cycle, and apoptosis pathways were differentially regulated by ABA. G1 cell cycle arrest, apoptosis and mTOR inhibition were confirmed. Conclusions ABA, a potential mTOR inhibitor, induces the disruption of ribosomal biogenesis. It also affects the mTOR-MRP axis to cause G1 cell cycle arrest and finally leads to cancer cell apoptosis.

This study evaluated the influence of polydopamine treatment on the surface properties and bond strength of yttria-stabilised tetragonal zirconia polycrystal (Y-TZP). Sixty-three zirconia blocks (10 × 10 × 2 mm) were randomly divided into three groups defined by surface treatment: (i) control group (C), (ii) grit-blasted with 110 μm alumina particles (GB), and (iii) polydopamine (PDA) coating. The surfaces of specimens subjected to different treatments were investigated by X-ray photoelectron spectroscopy (XPS), scanning electron microscopy (SEM), and water contact angle measurements. After the surface treatments, the specimens were cemented to resin composite cylinders. After bonding, the shear bond strength of the ceramic to the resin was measured, and the failure mode of each specimen was analysed using a stereomicroscope. The results indicated that the shear bond strength is highest for the GB treatment and lowest for the controls. However, the difference between groups GB and PDA was not statistically significant. In the control group, adhesive failure was predominant, whereas in the treatment groups, mixed mode failure was predominant. The pre-treatment of Y-TZP ceramic with the polydopamine coating might improve the bond strength of the resin cement to the zirconia ceramic.

β-type titanium (Ti) alloys have been extensively investigated as orthopedic implant materials due to their unique combination of low elastic modulus, high specific strength, corrosion resistance, and biocompatibility. In this study the mechanical properties, corrosion behavior, friction and wear performance, and cytotoxicity of β-type Ti–24Nb–38Zr–2Mo (TNZM) and Ti–24Nb–38Zr–2Mo–0.1Sc (TNZMS) have been comparatively investigated for orthopedic applications. Cold-rolling (CR) and cold-rolling plus solution-treatment (CR+ST) were performed on the as-cast (AC) alloys and their microstructures and material properties were characterized. The impact of Sc addition on the mechanical and corrosion properties, friction and wear behavior, and in vitro cytocompatibility of the TNZMS alloy was assessed. The CR+ST TNZMS alloy exhibited the best combination of properties among all the alloy samples, with a yield strength of 780 MPa, ultimate strength of 809 MPa, elongation of 19%, Young's modulus of 65.4 GPa, and hardness of 265 HV. Electrochemical testing in Hanks’ Solution indicated that the CR+ST TNZMS sample also showed the highest corrosion resistance with a corrosion potential of -0.234 V, corrosion current density of 0.07 µA/cm2, and corrosion rate of 1.2 µm/y. Friction and wear testing revealed that the TNZMS alloy showed higher wear resistance compared to the TNZM alloy and the wear resistance of the different samples was ranked CR > CR+ST > AC. Finally, both the CR+ST TNZM and TNZMS showed no-cytotoxicity towards MG-63 cells and the TNZMS exhibited slightly higher cytocompatibility than the TNZM alloy. Statement of significance This work reports the β-type Ti–24Nb–38Zr–2Mo (TNZM) and Ti–24Nb–38Zr–2Mo–0.1Sc (TNZMS) alloys fabricated by as-cast (AC), cold-rolling (CR), and cold-rolling plus solution-treatment (CR+ST) for potential orthopedic applications. The experimental results showed that the TNZMS alloy exhibited significantly enhanced mechanical, wear, and corrosion properties than those of TNZM alloy; and the CR+ST TNZMS possess a unique combination of the best mechanical and corrosion properties including a yield strength of 780 MPa, ultimate strength of 809 MPa, elongation of 19%, Young's modulus of 65.4 GPa, and corrosion rate of 1.2 µm/y in Hanks’ Solution. Both the CR+ST TNZM and TNZMS alloys exhibited non-cytotoxicity towards MG-63 cells and TNZMS showed a higher cytocompatibility than that of TNZM.

Objectives The aim of this study was to investigate the wear behavior of Dentinogenesis imperfecta type II (DGI-II) dentin and elucidate the correlation between its tribological properties and components. Methods The mid-coronal dentin of normal and DGI-II teeth were divided into two groups: perpendicular and parallel to the dentin tubules. The microstructure of dentin was detected using atomic force microscopy (AFM). The wear behavior of dentin was evaluated by nanoscratch tests and scanning electron microscopy (SEM). Meanwhile, changes in molecular groups and chemical composition were analyzed by Raman and Energy-Dispersive X-ray (EDX) tests, respectively. Nanohardness was also evaluated. Results AFM images of DGI-II dentin illustrated a decrease in the number of tubules and the tubule diameter. Nanoscratch test showed a higher friction coefficient and a greater depth-of-scratch in DGI-II dentin. The wear resistance of DGI-II dentin was reduced independent of tubule orientation. EDX results indicated that DGI-II dentin mineral content decreased and Raman spectra results showed DGI-II dentin had a decreased collagen matrix structure stability coupled with hypomineralization. Furthermore, a significant reduction in nanohardness and elastic modulus of DGI-II dentin was observed. Regression analysis revealed a close correlation between dentin components and inferior wear resistance. Conclusions All results indicated the wear behavior of DGI-II dentin was significantly deteriorated, presumably caused by the disorder in microstructures and the reduction of chemical composition.

Background Pregnant women are emotionally vulnerable and have suffered great psychological impacts. Following the coronavirus disease 2019 (COVID-19) outbreak, a study was undertaken of the prevalence of, and factors contributing to, symptoms of anxiety and depression among pregnant women in Shenzhen, China. Methods A cross-sectional study on pregnant women was conducted from September to December 2020 in Shenzhen, using a random-recruit method. The General Anxiety Disorder (GAD-7) and Patient Health Questionnaire (PHQ-9) surveys were used to evaluate symptoms of anxiety and depression. A multivariate logistic regression model was developed to explore factors potentially associated with symptoms of anxiety and depression during pregnancy. Results A total of 3,434 pregnant women aged 15 to 59 years were enrolled. Symptoms of anxiety and depression were present in 9.8% and 6.9%, respectively. Logistic regression analysis using a stepwise procedure revealed that an increased risk of symptoms of anxiety and depression was associated with unmarried/divorced/widowed, unemployed, received professional psychological counseling, family dysfunction, the first trimester of pregnancy, pregnancy complications and vaginal bleeding, unplanned pregnancy, decline in household income and disputes between partners caused by the COVID-19 pandemic, consumption of alcoholic drinks by women and their partners, smoking, lack of exercise and sedentary lifestyle. Women with education from junior high school through college were less likely to experience symptoms of prenatal depression. Conclusions Our study revealed factors associated with psychological symptoms among pregnant women in the post-COVID-19-pandemic era. These results should help to update guidance for psychological interventions for pregnant women during the period of COVID-19.

To investigate the effects of ficin on biofilm formation of conditionally cariogenic Streptococcus mutans (S. mutans). Biomass and metabolic activity of biofilm were assessed using crystal violet assay, colony-forming unit (CFU) counting, and MTT assay. Extracellular polysaccharide (EPS) synthesis was displayed by SEM imaging, bacteria/EPS staining, and anthrone method while acid production was revealed by lactic acid assay. Growth curve and live/dead bacterial staining were conducted to monitor bacterial growth state in both planktonic and biofilm form. Total protein and extracellular proteins of S. mutans biofilm were analyzed by protein/bacterial staining and sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE), severally. qRT-PCR was conducted to detect acid production, acid tolerance, and biofilm formation associated genes. Crystal violet assay, CFU counting, and MTT assay showed that the suppression effect of ficin on S. mutans biofilm formation was concentration dependent. 4 mg/mL ficin had significant inhibitory effect on S. mutans biofilm formation including biomass, metabolic activity, EPS synthesis, and lactic acid production ( p < 0.05 ). The growth curves from 0 mg/mL to 4 mg/mL ficin were aligned with each other. There was no significant difference among different ficin groups in terms of live/dead bacterial staining result ( p > 0.05 ). Protein/bacterial staining outcome indicated that ficin inhibit both total protein and biofilm formation during the biofilm development. There were more relatively small molecular weight protein bands in extracellular proteins of 4 mg/mL ficin group when compared with the control. Generally, ficin could inhibit biofilm formation and reduce cariogenic virulence of S. mutans effectively in vitro; thus, it could be a potential anticaries agent.