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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.

© 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.

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.

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.

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.

Background: Reactive oxygen species (ROS) overproduction promotes the alveolar bone loss during the development of periodontitis. Mitochondria are the principal source of ROS. Hydroxytyrosol (HT) 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. Methods: 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 MAPK signaling pathway were investigated. Meanwhile, the effect and related mechanisms of HT on bone loss in mice with periodontitis were also detected. Findings: 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. Interpretation: Our findings, for the first time, revealed a novel function of hydroxytyrosol in bone remodeling of periodontitis, and highlighted its therapeutical potential for the prevention/treatment of periodontitis. Funding: National Natural Science Foundation of China (81870757, 81870777), Zhejiang Provincial Outstanding Youth Science Foundation (LR21H140002) and Zhejiang Provincial Science and Technology Project for Public Welfare (GF21H140019). Ethical Approval: All animal-related experimental protocols were approved by the Animal Ethics Committee of Wenzhou Medical University (SYXK2019-0019).

Osteoblasts dysfunction, induced by oxidative stress (OS), is one of major pathological mechanisms for osteoporosis. Curcumin (Cur), a bioactive antioxidant compound, isolated from Curcumin longa L, was regarded as a strong reactive oxygen species (ROS) scavenger. However, it remains unveiled whether Cur can prevent osteoblasts from OS-induced dysfunction. To approach this question, we adopted a well-established OS model to investigate the preventive effect of Cur on osteoblasts dysfunction by measuring intracellular ROS production, cell viability, apoptosis rate and osteoblastogenesis markers. We showed that the pretreatment of Cur could significantly antagonize OS so as to suppress endogenous ROS production, maintain osteoblasts viability and promote osteoblastogenesis. Inhibiting Glycogen synthase kinase (GSK3β) and activating nuclear factor erythroid 2 related factor 2 (Nrf2) could significantly antagonize the destructive effects of OS, which indicated the critical role of GSK3β-Nrf2 signaling. Furthermore, Cur also abolished the suppressive effects of OS on GSK3β-Nrf2 signaling pathway. Our findings demonstrated that Cur could protect osteoblasts against OS-induced dysfunction via GSK3β-Nrf2 signaling and provide a promising way for osteoporosis treatment.

OBJECTIVEAdvancements in less invasive lateral retropleural/retroperitoneal approaches aim to address the limitation of posterolateral approaches and avoid complications associated with anterior open thoracotomy or thoracoabdominal approaches.METHODSConsecutive patients treated with a mini-open lateral approach for thoracic or thoracolumbar anterior column pathologies were analyzed in a retrospective case series including clinical and radiographic outcomes. Special attention is given to operative techniques and surgical nuances.RESULTSEleven patients underwent a mini-open lateral retropleural or combined retropleural/retroperitoneal approach for thoracic or thoracolumbar junction lesions. Surgical indications included chronic fracture/deformity (n = 5), acute fracture (n = 2), neoplasm (n = 2), and osteomyelitis (n = 2). The mean length of postoperative hospital stay was 7.2 days (range 2–19 days). All patients ultimately had successful decompression and reconstruction with a mean follow-up of 16.7 months (range 6–29 months). Axial back pain assessed by the visual analog scale improved from a mean score of 8.2 to 2.2. Complications included 1 patient with deep venous thrombosis and pulmonary embolism and 1 with pneumonia. One patient developed increased leg weakness, which subsequently improved. One patient undergoing corpectomy with only lateral plate fixation developed cage subsidence requiring posterior stabilization.CONCLUSIONSMini-open lateral retropleural and retroperitoneal corpectomies can safely achieve anterior column reconstruction and spinal deformity correction for various thoracic and thoracolumbar vertebral pathologies.

Background Supernumerary teeth (ST) is defined as an additional number of teeth compared to the normal dental formula. The prevalence rate of ST varies from 0.5 to 3.8% in the permanent dentition. When ST located distal to the third molar is acclaimed as distomolar. Moreover, kissing molar is an extremely scarce condition of distomolars, pointed in the opposite direction in a single follicular space. Meanwhile, macrodontia is also a rare shape anomaly characterized by a large crown and tapering root. Case presentation A 22-year-old Chinese man presented a combination of kissing molars, maxillary bilateral supernumerary teeth and macrodontia. Radiographically, two maxillary bilateral distomolars located at the buccal side of adjacent third molars. One mandibular distomolar with the adjacent third molar was contacted by occlusal surfaces while roots were pointed oppositely, which could be diagnosed as KM. Furthermore, the left mandibular third molar can be inferred to be a macrodontia, characterized by a large crown and tapering root. After a thorough investigation, we excluded the possibilities of systemic diseases and genetic inheritance. However, the etiology of this rare combination deserves to be further explored. Conclusion The combination of kissing molars, maxillary bilateral supernumerary teeth and macrodontia is very rare, especially presented in the patient with no syndromes. As there were no complications with these conditions, long-term observation has been recommended for the patient. In addition, the true etiology need a further exploration.

Background To investigate the clinical efficacy of minimally invasive direct lateral approach debridement, interbody bone grafting, and interbody fusion in the treatment of the thoracic and lumbar spinal tuberculosis. Methods From January 2013 to January 2016, 35 cases with thoracic and lumbar spinal tuberculosis received direct lateral approach debridement, interbody bone grafting, and interbody fusion. Of the 35 cases, 16 patients were male and 19 were female and the median age was 55.2 (range 25–83). The affected segments were single interspace, and the involved vertebral bodies included: 15 cases of thoracic vertebrae (1 cases of T5/6, 2 cases of T6/7, 4 cases of T7/8, 3 cases of T8/9, 5 cases of T9/10) and 20 cases of lumbar spine (2 cases of L1/2, 6 cases of L2/3, 6 cases of L3/4, 6 cases of L4/5). After MIDLIF operation, all the patients received medication of four anti-tubercular drugs for 12 to18 months. Results The patients were followed up for 7 to 40 months with an average of 18.5 months. The visual analogue scale (VAS) at the last follow-up was 2.8 ± 0.5, which was significantly different from the preoperative VAS (8.2 ± 0.7). After MIDLIF, there was 5 cases occurred with transient numbness in one side of the thigh or inguinal region, and 10 cases suffered from flexion hip weakness. All the bone grafts were fused within 6~ 18 months (average of 11.5 months) after the operation. Conclusion Minimally invasive lateral approach interbody fusion technology have the advantage of less injury and quick recovery after surgery, which is the effective and safe treatment for thoracic and lumbar spinal tuberculosis.

Advanced glycation end products (AGEs) can stimulate osteoblast apoptosis and have a critical role in the pathophysiology of diabetic osteoporosis. Mitochondrial abnormalities are closely related to osteoblast dysfunction. However, it remains unclear whether mitochondrial abnormalities are involved in AGE-induced osteoblastic cell apoptosis. Silibinin, a major flavonolignan compound of silimarin, has strong antioxidant and mitochondria-protective properties. In the present study, we explored the possible mitochondrial mechanisms underlying AGE-induced apoptosis of osteoblastic cells and the effect of silibinin on osteoblastic cell apoptosis. We demonstrated that mitochondrial abnormalities largely contributed to AGE-induced apoptosis of osteoblastic cells, as evidenced by enhanced mitochondrial oxidative stress, conspicuous reduction in mitochondrial membrane potential and adenosine triphosphate production, abnormal mitochondrial morphology, and altered mitochondrial dynamics. These AGE-induced mitochondrial abnormalities were mainly mediated by the receptor of AGEs (RAGE). In addition, we found that silibinin directly downregulated the expression of RAGE and modulated RAGE-mediated mitochondrial pathways, thereby preventing AGE-induced apoptosis of osteoblastic cells. This study not only provides a new insight into the mitochondrial mechanisms underlying AGE-induced osteoblastic cell apoptosis, but also lays a foundation for the clinical use of silibinin for the prevention or treatment of diabetic osteoporosis.

The aim of this study was to evaluate the effect of maleic acid (MA) on both the bond strength of fibre post to root dentine and smear layer removal after post space preparation. Sixty, single-canal premolars were endodontically treated and randomly assigned to four groups: group 1 [0.9% saline solution (control]); group 2 [2.5% sodium hypochlorite (NaOCl)]; group 3 [17% ethylenediaminetetraacetic acid (EDTA) followed by 2.5% NaOCl]; and group 4 (7% MA followed by 2.5% NaOCl). Self-adhesive resin cement was used to test the adhesion of a glass-fibre post to the root dentine through a micropush-out test. Scanning electron microscopy was performed to examine and score the treated specimens for smear layer removal, and stereomicroscopy was applied to investigate the failure modes of fibre posts. Maleic acid exhibited the highest mean bond-strength values in the apical regions among all the groups. Most failure modes (31.9%) were adhesive-type failures between the dentine and luting materials. Maleic acid performed statistically significantly better than the other groups regarding smear layer removal, especially in the apical region. Maleic acid is an effective irrigant that can remove the smear layer, open dentinal tubules, and act as a high-efficiency final irrigant in activation protocols.

Background: Osteoblast apoptosis induced by oxidative stress plays a crucial role in the development and progression of osteoporosis. Curcumin, a natural antioxidant isolated from Curcuma longa, has highly protective effects against osteoporosis. However, the effects of curcumin on oxidative stress-induced osteoblast apoptosis remain unclear. This study aimed to explore the effect of curcumin on hydrogen peroxide (H2O2) induced osteoblast apoptosis and the underlying mechanisms. Methods: An osteoblastic cell line (Saos-2) was exposed to various concentrations of H2O2 with or without curcumin treatment. Cell viability was evaluated by MTT assays. The apoptosis rate was analyzed by flow cytometry and TUNEL assays. Mitochondrial ROS and membrane potential were determined using a fluorescence microscope. Mitochondrial respiratory enzyme activity was measured using a spectrophotometer. Protein levels were detected by western blotting. Results: Curcumin was cytoprotective because it greatly improved the viability of Saos-2 cells exposed to H2O2 and attenuated H2O2-induced apoptosis. Curcumin treatment also preserved the mitochondrial redox potential, decreased the mitochondrial oxidative status, and improved the mitochondrial membrane potential and functions. Furthermore, curcumin treatment markedly increased levels of phosphorylated protein kinase B (Akt) and phosphorylated glycogen synthase kinase-3β (GSK3β). Conclusion: Curcumin administration ameliorates oxidative stress-induced apoptosis in osteoblasts by preserving mitochondrial functions and activation of Akt-GSK3β signaling. These data provide experimental evidence supporting the clinical use of curcumin for prevention or treatment of osteoporosis.

Oxidative stress (OS) induces osteoblast apoptosis, which plays a crucial role in the initiation and progression of osteoporosis. Although OS is closely associated with mitochondrial dysfunction, detailed mitochondrial mechanisms underlying OS-induced osteoblast apoptosis have not been thoroughly elucidated to date. In the present study, we found that mitochondrial abnormalities largely contributed to OS-induced osteoblast apoptosis, as evidenced by enhanced production of mitochondrial reactive oxygen species; considerable reduction in mitochondrial respiratory chain complex activity, mitochondrial membrane potential, and adenosine triphosphate production; abnormality in mitochondrial morphology; and alteration of mitochondrial dynamics. These mitochondrial abnormalities were primarily mediated by an imbalance in mitochondrial fusion and fission through a protein kinase B- (AKT-) glycogen synthase kinase 3β-(GSK3β-) optic atrophy 1- (OPA1-) dependent mechanism. Hydroxytyrosol (3,4-dihydroxyphenylethanol (HT)), an important compound in virgin olive oil, significantly prevented OS-induced osteoblast apoptosis. Specifically, HT inhibited OS-induced mitochondrial dysfunction by decreasing OPA1 cleavage and by increasing AKT and GSK3βphosphorylation. Together, our results indicate that the AKT-GSK3βsignaling pathway regulates mitochondrial dysfunction-associated OPA1 cleavage, which may contribute to OS-induced osteoblast apoptosis. Moreover, our results suggest that HT could be an effective nutrient for preventing osteoporosis development.

Mitochondrial dependent oxidative stress (OS) and subsequent cell death are considered as the major cytotoxicity caused by Triethylene glycol dimethacrylate (TEGDMA), a commonly monomer of many resin-based dental composites. Under OS microenvironment, autophagy serves as a cell homeostatic mechanism and maintains redox balance through degradation or turnover of cellular components in order to promote cell survival. However, whether autophagy is involved in the mitochondrial oxidative damage and apoptosis induced by TEGDMA, and the cellular signaling pathways underlying this process remain unclear. In the present study, we demonstrated that TEGDMA induced mouse preodontoblast cell line (mDPC6T) dysfunctional mitochondrial oxidative response. In further exploring the underlying mechanisms, we found that TEGDMA impaired autophagic flux, as evidenced by increased LC3-II expression and hindered p62 degradation, thereby causing both mitochondrial oxidative damage and cell apoptosis. These results were further verified by treatment with chloroquine (autophagy inhibitor) and rapamycin (autophagy promotor). More importantly, we found that the JNK/MAPK pathway was the key upstream regulator of above injury process. Collectively, our finding firstly demonstrated that TEGDMA induced JNK-dependent autophagy, thereby promoting mitochondrial dysfunction-associated oxidative damage and apoptosis in preodontoblast.

Incomplete polymerization or biodegradation of dental resin materials results in the release of resin monomers such as triethylene glycol dimethacrylate (TEGDMA), causing severe injury of dental pulp cells. To date, there has been no efficient treatment option for this complication, in part due to the lack of understanding of the mechanism underlying these phenomena. Here, for the first time, we found that notoginsenoside R1 (NR1), a bioactive ingredient extracted from Panax notoginseng, exerted an obvious protective effect on TEGDMA-induced mitochondrial apoptosis in the preodontoblast mDPC6T cell line. In terms of the mechanism of action, NR1 enhanced the level of phosphorylated Akt (protein kinase B), resulting in the activation of a transcriptional factor, nuclear factor erythroid 2-related factor 2 (Nrf2), and eventually upregulating cellular ability to resist TEGDMA-related toxicity. Inhibiting the Akt/Nrf2 pathway by pharmaceutical inhibitors significantly decreased NR1-mediated cellular antioxidant properties and aggravated mitochondrial oxidative damage in TEGDMA-treated cells. Interestingly, NR1 also promoted mitophagy, which was identified as the potential downstream of the Akt/Nrf2 pathway. Blocking the Akt/Nrf2 pathway inhibited mitophagy and abolished the protection of NR1 on cells exposed to TEGDMA. In conclusion, these findings reveal that the activation of Akt/Nrf2 pathway-mediated mitophagy by NR1 might be a promising approach for preventing resin monomer-induced dental pulp injury.

To evaluate the effect of maleic acid (MA) on the cleaning efficacy and mechanical properties of root canal dentine with respect to different time exposure.One hundred and eighty single-canal premolars were instrumented with rotary-files and then randomly assigned to test groups receiving 7% MA for 30 s, 45 s, 1 min, or 3 min or to control groups treated with 0.9% saline or 17% ethylenediaminetetraacetic acid for 45 s. The micro-hardness, nano-hardness and elastic modules were measured before and after treatment, while the amount of smear and erosion in the coronal, middle and apical thirds in root canal were evaluated by scanning electron microscopy, finally, the fracture strength was assessed by vertical root fracture testing.The efficacy of smear layer removal increased with increasing MA application time. The largest effect was observed at 45 s, even in the apical third, whereas the treatment for 1 min resulted in irreversible erosion of the dentine surface. The micro-hardness and nano-indentation testing confirmed that the micro- and nano-scale mechanical properties were significantly decreased after MA application for 1 min. Furthermore, the specimens treated with MA for 3 min presented the lowest fracture resistance among all groups. In contrast, the 45 s treatment appeared to increase the fracture resistance of the tooth.The cleaning efficacy and mechanical properties of root canal dentine varied with MA exposure time. The application of MA for 45 s was found to be the most promising for clinical use.

The objective of this study was to evaluate the effect of gamma irradiation on the wear behavior of human tooth dentin in terms of possible alterations in crystallinity, grain size, and composition. Human premolars (n = 19) were collected to obtain the perpendicular or parallel to the direction of the dentin tubule specimens. Each specimen was subjected to 60 Gy of gamma irradiation, in daily increments of 2 Gy. The nanoscratch tests were conducted. The scratch traces were observed via scanning electron microscope (SEM) and surface profilometer. X-ray diffraction (XRD) and Fourier transform infrared spectroscopy (FTIR) were used to investigate the alteration of crystallography and chemical composition of dentin after irradiation. The change of surface microhardness (SMH) was also evaluated. The nanoscratch results showed that the friction coefficient of dentin after irradiation became higher, and the depths and widths of scratch were greater than that of dentin before irradiation. Additionally, irradiation decreased the crystallinity of dentin and induced the formation of bigger crystals. The carbonate/mineral ratio was increased. Furthermore, a significant reduction in microhardness after irradiation was observed. The main damage mechanisms consisted of the formation of delamination and crack in both the specimens cut perpendicular and parallel to tubule dentin after irradiation. Irradiation affected directly the wear behavior of tooth dentin, accompanied by the alterations in crystallography, chemical composition, and surface microhardness of dentin. This would help extend understanding the influence of irradiation on dentin and provide suggestions for selecting more suitable materials for irradiated tooth.

Numerous studies suggested that oxidative stress (OS) played a central role in the onset and development of postmenopausal osteoporosis (PO); however, conflicting results were obtained as to the association of OS-related biomarkers and PO. This meta-analysis aimed to identify the association between these markers and PO, and explore factors that may explain the inconsistencies in these results. A systematic literature search was conducted in relevant database. Search terms and selection criteria were priorly determined to identify and include all studies that detected markers of OS in PO patients. We pooled data with a random effects meta-analysis with standardized mean differences and 95% confidence interval. Total 17 studies including 12 OS markers were adopted. The results showed that superoxide dismutase (SOD) in erythrocytes, catalase (CAT), total antioxidant status (TAS), hydroperoxides (HY), advanced oxidation protein products (AOPP), malondialdehyde (MDA), and vitamin B12 (VB12) in plasma/serum were not statistically different between the PO and control group, whereas significantly increased level of homocysteine (Hcy) and nitric oxide (NO), along with decreased SOD, glutathione peroxidase (GPx), folate, and total antioxidant power (TAP) in plasma/serum were obtained in the PO group. In summary, OS might serve as potential biomarkers in the etiopathophysiology and clinical course of PO.

Oxidative stress (OS)-induced apoptosis of periodontal ligament cells (PDLCs) has been suggested to be an important pathogenic factor of periodontitis. Mitochondrial abnormalities are closely linked to OS and act as the main players in apoptosis. Our aim was to investigate the potential mitochondrial abnormalities in PDLCs apoptosis induced by OS. In this study, significant reduction in viability and increased apoptosis were observed in H2O2-treated hPDLCs. H2O2 also induced mitochondrial dysfunction, judging by increased mitochondrial reactive oxygen species amounts, and decreased mitochondrial membrane potential as well as ATP levels. Furthermore, H2O2 significantly enhanced mitochondrial fission by decreasing the expression of Mfn1 and Mfn2, along with increasing the expression of Drp1, Fis1 and the cleavage of OPA1. Notably, NAC stabilized the balance of the mitochondrial dynamics, attenuated mitochondrial dysfunction, and inhibited apoptosis of hPDLCs in the presence of H2O2. In conclusion, the OS-induced apoptosis of hPDLCs may be mediated by mitochondria-dependent pathway.

Diabetes mellitus is a well-recognized risk factor for periodontitis. The goal of the present study was to elucidate whether oxidative stress and nuclear factor erythroid 2-related factor 2 (Nrf2) participate in the aggravation of periodontitis by diabetes. For this purpose, we assigned Wistar rats to control, periodontitis, diabetes, and diabetic periodontitis groups. Two weeks after induction of diabetes by streptozotocin, periodontitis was induced by ligation. Two weeks later, periodontal tissues and blood were harvested and analyzed by stereomicroscopy, immunohistochemistry, and real-time polymerase chain reaction. We found that ligation induced more severe bone loss and periodontal cell apoptosis in diabetic rats than in normal rats (p<0.05). Compared with the control group, periodontitis significantly enhanced local oxidative damage (elevated expression of 3-nitrotyrosine, 4-hydroxy-2-nonenal, and 8-hydroxy-deoxyguanosine), whereas diabetes significantly increased systemic oxidative damage and suppressed antioxidant capacity (increased malondialdehyde expression and decreased superoxide dismutase activity) (p<0.05). Simultaneous periodontitis and diabetes synergistically aggravated both local and systemic oxidative damage (p<0.05); this finding was strongly correlated with the more severe periodontal destruction in diabetic periodontitis. Furthermore, gene and protein expression of Nrf2 was significantly downregulated in diabetic periodontitis (p<0.05). Multiple regression analysis indicated that the reduced Nrf2 expression was strongly correlated with the aggravated periodontal destruction and oxidative damage in diabetic periodontitis. We conclude that enhanced local and systemic oxidative damage and Nrf2 downregulation contribute to the development and progression of diabetic periodontitis.

Oxidative stress (OS) plays crucial roles in triethylene glycol dimethacrylate (TEGDMA, a major component in dental resin)-induced apoptosis of dental pulp cells. Mitochondria are important target organelles for regulating the balance of OS, meanwhile, imbalance of the mitochondrial dynamic associated with mitochondrial dysfunction is one major molecular mechanism for oxidative damages. However, whether these mitochondrial dependent pathways were involved in the apoptosis of dental pulp cells induced by TDGDMA remains unclarified. We demonstrated that TEGDMA decreased viability and induced apoptosis of mouse preodontoblasts (mDPC6T cell line) in a time- and dose-dependent manner. Furthermore, TEGDMA elevated the mitochondrial OS status and induced mitochondrial dysfunction, as reflected by the significant decrease of mitochondrial membrane potential, ATP production, the activity of Complex III and citrate synthase. In this process, we detected a dramatically impaired mitochondrial dynamic that was reflected by significantly enhanced mitochondrial fragmentation. Consistently, we also found a significant enhancement of the key upstream regulators for mitochondrial fission, such as short form of optic atrophy 1, dynamic related protein 1 oligomer and Fission 1. The respective inhibition of mitochondrial OS or mitochondrial fission could mutually attenuate each other, thereby significantly preventing both mitochondrial dysfunction and cell apoptosis. In conclusion, TEGDMA-induced preodontoblasts apoptosis was mediated by the vicious circle between mitochondrial OS and dynamic abnormality, which represented a new target to prevent TEGDMA-induced dental pulp cells apoptosis.

Aim Oxidative stress (OS) biomarkers have been detected in saliva and gingival crevicular fluid (GCF) during chronic periodontitis (CP) progression; however, the relationship between OS biomarkers and CP progression remains elusive. The purpose of this meta-analysis is to investigate the relationship between local OS biomarkers and CP. Methods This review was conducted through a systematic search from three databases. Studies on CP participants were included as an experimental group, and studies on periodontally healthy (PH) participants were included as a control. Mean effects were expressed as standardized mean difference with their associated 95% confidence intervals. Results From a total of 2,972 articles, 32 articles fulfilled the inclusion criteria. We found a significant decrease of total antioxidant capacity and a significant increase of malondialdehyde (MDA), nitric oxide, total oxidant status (TOS), and 8-hydroxy-deoxyguanosine levels in the saliva of CP patients. Moreover, we also found an elevation of MDA level in GCF of CP group when compared with the PH group. There were no significant differences of salivary and GCF superoxide dismutase levels, salivary glutathione peroxidase level, and GCF TOS level between two groups. However, a high heterogeneity was observed among evaluated studies. Conclusions Despite the limitations of this study, the result of our meta-analysis supported the rationale that there was a direct link between CP and OS-related biomarkers' levels in the local site, indicating the important role of OS in the onset and development of CP.

Aim: To elucidate whether mitochondrial dysfunction contributes to aggravated periodontitis in diabetes. Materials and Methods: Sixty-four wistar rats were randomly assigned into four groups: control, periodontitis, diabetes, and diabetic periodontitis. Two weeks after induction of diabetes, periodontitis was induced by silk ligation for 2 weeks and thereafter evaluated by assessing alveolar bone loss and apoptosis of periodontium cells. Mitochondrial oxidative stress was detected by MitoSOX staining. Mitochondrial function was determined by measuring ATP production, and by assessing mitochondrial DNA copy number, activities of electron transport chain complexes, and biogenesis with real-time PCR.Results: Significantly severer bone loss, enhanced periodontium cell apoptosis, and mitochondrial oxidative stress were found in the rats with diabetic periodontitis than the others. Furthermore, diabetic rats with periodontitis presented severer mitochondrial dysfunction than lean rats with periodontitis, as reflected by compromised ATP production, decreased mitochondrial DNA copy number, reduced gene expression of electron transport chain complex I subunits, and impaired mitochondrial biogenesis (p Conclusions: Mitochondrial dysfunction was positive correlated to aggravated periodontitis in diabetes and might represent a therapeutic target for diabetic periodontitis.

Diabetes has adverse effects on the brain, especially the hippocampus, which is particularly susceptible to synaptic injury and cognitive dysfunction. The underlying mechanisms and strategies to rescue such injury and dysfunction are not well understood. Using a mouse model of type 2 diabetes (db/db mice) and a human neuronal cell line treated with high concentration of glucose, we demonstrate aberrant mitochondrial morphology, reduced ATP production, and impaired activity of complex I. These mitochondrial abnormalities are induced by imbalanced mitochondrial fusion and fission via a glycogen synthase kinase 3β (GSK3β)/dynamin-related protein-1 (Drp1)-dependent mechanism. Modulation of the Drp1 pathway or inhibition of GSK3β activity restores hippocampal long-term potentiation that is impaired in db/db mice. Our results point to a novel role for mitochondria in diabetes-induced synaptic impairment. Exploration of the mechanisms behind diabetes-induced synaptic deficit may provide a novel treatment for mitochondrial and synaptic injury in patients with diabetes.

Mild cognitive impairment (MCI) occurs during the predementia stage of Alzheimer disease (AD) and is characterized by a decline in cognitive abilities that frequently represents a transition between normal cognition and AD dementia. Its pathogenesis is not well understood. Here, we demonstrate the direct consequences and potential mechanisms of oxidative stress and mitochondrial dynamic and functional defects in MCI-derived mitochondria. Using a cytoplasmic hybrid (cybrid) cell model in which mitochondria from MCI or age-matched non-MCI subjects were incorporated into a human neuronal cell line depleted of endogenous mitochondrial DNA, we evaluated the mitochondrial dynamics and functions, as well as the role of oxidative stress in the resultant cybrid lines. We demonstrated that increased expression levels of mitofusin 2 (Mfn2) are markedly induced by oxidative stress in MCI-derived mitochondria along with aberrant mitochondrial functions. Inhibition of oxidative stress rescues MCI-impaired mitochondrial fusion/fission balance as shown by the suppression of Mfn2 expression, attenuation of abnormal mitochondrial morphology and distribution, and improvement in mitochondrial function. Furthermore, blockade of MCI-related stress-mediated activation of extracellular signal-regulated kinase (ERK) signaling not only attenuates aberrant mitochondrial morphology and function but also restores mitochondrial fission and fusion balance, in particular inhibition of overexpressed Mfn2. Our results provide new insights into the role of the oxidative stress-ERK-Mfn2 signal axis in MCI-related mitochondrial abnormalities, indicating that the MCI phase may be targetable for the development of new therapeutic approaches that improve mitochondrial function in age-related neurodegeneration.

The present study evaluated the wear behavior of human root canal dentin and the lubricating effect of EDTA pastes using nano-scratch tests in vitro. The human root canal wall specimens were tested under a constant load of 80 mN and the lubricating effect of different concentrations of EDTA pastes were analyzed. EDTA lubrication strengthened wear effect on the root canal dentin. The application of EDTA paste decreased the microhardness and wear resistance of root canal wall. The wear mechanism of root canal dentin changed from plastic deformation to a combination of deformation, delamination, and microcrack propagation because of the strengthening effect of EDTA pastes.

Background To our best knowledge, there was little research to assess the changes of quality of life and satisfaction after orthognathic in one trial. The aim of this study was to evaluate the changes of oral health related quality of life and satisfaction between surgery-first and orthodontic-first orthognathic surgery. Methods Fifty Chinese orthognathic adluts patients completed two questionnaires: the Dental Impact on Daily Living questionnaire for assessment of his/her satisfaction and 14-item Oral Health Impact Profile for assessment of patient’s quality of life. The subjects completed six sets of interviews and clinical evaluations at before treatment; 1 month after surgery (surgery-first); 6 months after treatment; 12 months after treatment ; and 18 month after treatment ; the finished treatment. The pre and post surgical orthodontic period was also recorded. Chi square tests and repeated-measures analysis of variance (ANOVA) were used to compare categorical variables and measure results. All analyses were carried out used Stata software. Results The quality of life was significant improved when finished treatment and the amounts of change did not show any significant difference in each domain and at 1, 6, 12 month after orthognathic surgery between two groups. However, in orthodontic-first group, the quality of life was deteriorated before orthognathic surgery. In surgery-first group, the quality of life was immediately improved which lead to better satisfaction. Conclusions Although the quality of life scores was no significant difference between two groups, surgery-first treatment could significant reduce treatment during and no deterioration stage of quality of life score which lead to better satisfactory compare to orthodontic-first group. However, some of limitations we need take caution. In future we still need conduct more study to assess the influence of surgery-first method on quality of life.

The benefits of navigation-assisted technologies are not entirely understood. Therefore, this study aimed to examine the outcomes of patients with lumbar tuberculosis who received computer navigation-assisted minimally invasive direct lateral interbody fusion (DLIF). This was a retrospective study of 33 patients with lumbar tuberculosis who underwent minimally invasive DLIF at the Department of Spine and Orthopedics of Guigang People's Hospital (Guangxi, China) between January 2015 and December 2016. The patients were pathologically diagnosed as lumbar tuberculosis and grouped into the navigation-assisted fluoroscopy (NAV; n = 18) and non-navigation-assisted fluoroscopy (non-NAV; n = 15) groups. X-ray exposure and operation times were assessed in all patients. All surgical procedures were successfully completed. No case was converted into open surgery. The NAV group had longer surgical preparation time but shorter operation time compared with the non-NAV group (both P .05). Computer navigation-assisted minimally invasive DLIF could significantly reduce intraoperative radiation exposure, with no increase in total operation time.

Objectives The aim of the present study was to investigate the combined effects of nano-hydroxyapatite and Galla chinensis on remineralisation of initial enamel lesion. Methods Bovine enamel blocks with in vitro produced initial lesion were used. The lesions were subjected to a pH-cycling regime for 12 days. Each daily cycle includes 4 × 3 min application with one of five treatments: NaF (positive control), deionised water (negative control), crude aqueous extract of G. chinensis (GCE), nano-hydroxyapatite (nano-HA) and GCE with nano-HA. The samples were subsequently evaluated using a microhardness tester, polarised light microscopy (PLM), X-ray diffraction (XRD) and scanning electron microscopy (SEM). Results Surface hardness measurements and integrated mineral recovery value obtained from cross-sectional microhardness test (CSMH) revealed that all the treatment groups had significantly greater effect on enhancing remineralisation than that of the negative control group. Detailed investigation of both CSMH and PLM indicated that nano-HA would only help mineral deposition predominate in the outer layer of lesion and had limited capacity to reduce the lesion depth significantly. In GCE–nano-HA combined treatment group, more mineral deposition occurred in the lesion body and lesion depth was reduced significantly. Meanwhile, significantly greater mineral deposition in the outer portion of the lesion was also observed in comparison with GCE group. The results of XRD and SEM also showed that GCE could influence the deposition and adsorption of nano-HA. Conclusion There was a significant synergistic effect of combined GCE and nano-HA treatment on promoting the remineralisation of initial enamel lesion.

Osteoblast dysfunction, induced by oxidative stress, plays a critical role in the pathophysiology of osteoporosis. However, the underlying mechanisms remain unclarified. Imbalance of mitochondrial dynamics has been closely linked to oxidative stress. Here, we reveal an unexplored role of dynamic related protein 1(Drp1), the major regulator in mitochondrial fission, in the oxidative stress-induced osteoblast injury model. We demonstrate that levels of phosphorylation and expression of Drp1 significantly increased under oxidative stress. Blockade of Drp1, through pharmaceutical inhibitor or gene knockdown, significantly protected against H2O2-induced osteoblast dysfunction, as shown by increased cell viability, improved cellular alkaline phosphatase (ALP) activity and mineralization and restored mitochondrial function. The protective effects of blocking Drp1 in H2O2-induced osteoblast dysfunction were evidenced by increased mitochondrial function and suppressed production of reactive oxygen species (ROS). These findings provide new insights into the role of the Drp1-dependent mitochondrial pathway in the pathology of osteoporosis, indicating that the Drp1 pathway may be targetable for the development of new therapeutic approaches in the prevention and the treatment of osteoporosis.

Radiotherapy is a frequently used treatment for oral cancer. Extensive research has been conducted to detect the mechanical properties of dental hard tissues after irradiation at the macroscale. However, little is known about the influence of irradiation on the tribological properties of enamel at the micro- or nanoscale. Therefore, this study aimed to investigate the effect of gamma irradiation on the wear behaviour of human tooth enamel in relation to prism orientation. Nanoscratch tests, surface profilometer and scanning electron microscope (SEM) analysis were used to evaluate the friction behaviour of enamel slabs before and after treatment with identical irradiation procedures. X-ray diffraction (XRD) and Fourier transform infrared spectroscopy (FTIR) were performed to analyse the changes in crystallography and chemical composition induced by irradiation. Surface microhardness (SMH) alteration was also evaluated. The results showed that irradiation resulted in different scratch morphologies, friction coefficients and remnant depth and width at different loads. An inferior nanoscratch resistance was observed independent of prism orientation. Moreover, the variation of wear behaviours was closely related to changes in the crystallography, chemical composition and SMH of the enamel. Together, these measures indicated that irradiation had a direct deleterious effect on the wear behaviour of human tooth enamel.

Apoptotic death of osteocytes was recognized over 15 years ago, but its significance for bone homeostasis has remained elusive. A new paradigm has emerged that invokes osteocyte apoptosis as a critical event in the recruitment of osteoclasts to a specific site in response to skeletal unloading, fatigue damage, estrogen deficiency and perhaps in other states where bone must be removed. This is accomplished by yet to be defined signals emanating from dying osteocytes, which stimulate neighboring viable osteocytes to produce osteoclastogenic cytokines. The osteocyte apoptosis caused by chronic glucocorticoid administration does not increase osteoclasts; however, it does negatively impact maintenance of bone hydration, vascularity, and strength.

The application of nano-hydroxyapatite (HA) in the repair of early caries lesion has received considerable attention. Neither the effects of the size of HA nor the effects of the effective pH range of nano-HA on remineralization have been investigated comprehensively, and the protective mechanism is still open for debate. To address these factors, the remineralization effect of nano-HA on demineralized bovine enamel is investigated under pH cycling conditions through surface and cross-sectional microhardness (CSMH) tests and polarized light microscopy (PLM). The percentage of surface microhardness recovery and integrated mineral loss obtained from CSMH tests demonstrated that nano-HA provides better remineralization than micro-HA. However, detailed investigation using CSMH tests and PLM indicated that nano-HA helped mineral deposition predominantly in the outer layer of the lesion and only had a limited capacity to reduce lesion depth. Nevertheless, the remineralization effect of nano-HA increased significantly when the pH was less than 7.0. Clearly, nano-HA has potential as an effective repair material and anticaries agent. Our findings also suggest that both the particle- and ion-mediated remineralization pathways in nano-HA may contribute to the repair of demineralized enamel.

An in vitro pH cycling model was used to evaluate the effect of nano-hydroxyapatite on the remineralization of artificial root caries. Sound human teeth fragments obtained from the cervical portion of the root were immersed in a demineralization solution for 96 h at 37°C to induce artificial root caries lesions. The demineralized samples were pH-cycled through treatment solutions, acidic buffer and neutral buffer for 8 days at 6 cycles per day. The samples were subsequently evaluated using a microhardness tester and scanning electron microscope (SEM). Nano-hydroxyapatite (nano-HA) and fluoride significantly increased the microhardness of the lesions (p ≪ 0.05) when compared to a control group. SEM revealed nano-HA adhered to the dentin surface densely and some of them even covered the openings of dentin tubules. We concluded that nano-HA positively affects the demineralization and/or remineralization processes of artificial root caries lesions and may be a promising agent for non-invasive root caries therapy.

The purpose of the research was to determine the effect of nano-hydroxyapatite concentrations on initial enamel lesions under dynamic pH-cycling conditions. Initial enamel lesions were prepared in bovine enamel with an acidic buffer. NaF (positive control), deionized water (negative control) and four different concentrations of nano-hydroxyapatite (1%, 5%, 10% and 15% wt%) were selected as the treatment agents. Surface microhardness (SMH) measurements were performed before/after demineralization and after 3, 6, 9 and 12 days of application, and the percentage surface microhardness recovery (%SMHR) was calculated. The specimens were then examined by a scanning electron microscope. The %SMHR in nano-hydroxyapatite groups was significantly greater than that of negative control. When the concentration of nano-HA was under 10%, SMH and %SMHR increased with increasing nano-hydroxyapatite concentrations. There were no significant differences between the 10% and 15% groups at different time periods in the pH-cycling. The SEM analysis showed that nano-hydroxyapatite particles were regularly deposited on the cellular structure of the demineralized enamel surface, which appeared to form new surface layers. It was concluded that nano-hydroxyapatite had the potential to remineralize initial enamel lesions. A concentration of 10% nano-hydroxyapatite may be optimal for remineralization of early enamel caries.

The purpose of this research was to investigate the wear behavior of early carious enamel remineralized with gallic acid. Forty natural human premolar specimens with early caries lesions were prepared. A remineralization pH-cycling treatment agent of 4000 ppm gallic acid was used for 12 days to treat the early lesions. The changes in microhardness were monitored. Nanoscratch tests were used to evaluate wear resistance. The experimental data were analyzed by using a t-test. The widths of traces were measured by an AMBIOS XP-2 stylus profilometer. After remineralization, all samples re-hardened significantly. The coefficients of friction became higher, and the widths of scratches were larger than they were before remineralization. Gallic acid significantly improved the early carious enamel's hardness. The wear damage of the samples treated with gallic acid was more severe than that of the control group. There were more obvious cracks and delaminations on the traces of the treated group. Compared with the control group, the enamel remineralized with gallic acid had inferior wear resistance. After remineralization, the dominant damage mechanisms of early carious enamel had changed from plastic deformation and adhesive wear to a combination of brittle cracks and delamination of enamel.