Xueqi Gan

Dual motion fretting wear behaviors of titanium and its alloy in artificial saliva

A dual motion combined by radial and tangential fretting was achieved on a modified hydraulic fretting wear test rig. The dual motion fretting tests of medical pure titanium (TA2) and Ti6Al7Nb alloy in artificial saliva were carried out under varied contact inclined angles (45° and 60°), and the maximum imposed load varied from 200 to 400 N at a constant loading speed of 6 mm/min. The effects of the cyclic vertical force and the inclined angle were investigated in detail. Dynamic analysis in combination with microscopic examinations shows that the wear scar and plastic deformation accumulation present a strong asymmetry. The Ti6Al7Nb has better wear resistance than TA2 in artificial saliva at the same test parameters, and with the increase of inclined angle and decrease of imposed load, the wear reduces accordingly. The wear mechanisms of pure titanium TA2 and Ti6Al7Nb alloy under the condition of dual motion fretting in artificial saliva are abrasive wear, oxidative wear and delamination.

Drp1-dependent mitochondrial fission mediates osteogenic dysfunction in inflammation through elevated production of reactive oxygen species

Although previous studies have implicated pro-inflammatory cytokines, such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6), to be detrimental for osteogenic activity, the related regulatory mechanisms are not yet fully validated. Since mitochondria host several essential metabolic processes and play a pivotal role in cellular functions, whether and how mitochondrial function contributes to inflammation-induced bone destruction needs further exploration. Our findings revealed that TNF-α impaired osteoblast function, including decreased mRNA levels of osteogenic markers, suppressed ALP expression and activity, and compromised cellular viability. Moreover, increased reactive oxygen species (ROS)-mediated oxidative stress in the TNF-α-treated group enhanced excessive mitochondrial fragmentation and disrupted mitochondrial function. However, treatment with antioxidant N-acetyl cysteine (NAC) or mitochondrial division inhibitor Mdivi-1 protected the cells from these adverse phenomena. These findings provide new insights into the role of the Drp1-dependent mitochondrial pathway in the osteogenic dysfunction during inflammation, indicating that this pathway may be a target for the development of new therapeutic approaches for the prevention and treatment of inflammation-induced bone destruction.

Blockade of cyclophilin D rescues dexamethasone-induced oxidative stress in gingival tissue

Glucocorticoids (GCs) are frequently used for the suppression of inflammation in chronic inflammatory diseases. Excessive GCs usage is greatly associated with several side effects, including gingival ulceration, the downward migration of the epithelium, attachment loss and disruption of transeptal fibers. The mechanisms underlying GCs-induced impairments in gingival tissue remains poorly understood. Mitochondrial dysfunction is associated with various oral diseases, such as chronic periodontitis, age-related alveolar bone loss and hydrogen peroxide-induced cell injury in gingival. Here, we reported an unexplored role of cyclophilin D (CypD), the major component of mitochondrial permeability transition pore (mPTP), in dexamethasone (Dex)-induced oxidative stress accumulation and cell dysfunctions in gingival tissue. We demonstrated that the expression level of CypD significantly increased under Dex treatment. Blockade of CypD by pharmaceutical inhibitor cyclosporine A (CsA) significantly protected against Dex-induced oxidative stress accumulation in gingival tissue. And the protective effects of blocking CypD in Dex-induced gingival fibroblasts dysfunction were evidenced by rescued mitochondrial function and suppressed production of reactive oxygen species (ROS). In addition, blockade of CypD by pharmaceutical inhibitor CsA or gene knockdown also restored Dex-induced cell toxicity in HGF-1 cells, as shown by suppressed mitochondrial ROS production, increased CcO activity and decreased apoptosis. We also suggested a role of oxidative stress-mediated p38 signal transduction in this event, and antioxidant N-acety-l-cysteine (NAC) could obviously blunted Dex-induced oxidative stress. These findings provide new insights into the role of CypD-dependent mitochondrial pathway in the Dex-induced gingival injury, indicating that CypD may be potential therapeutic strategy for preventing Dex-induced oxidative stress and cell injury in gingival tissue.

Vibration loading promotes osteogenic differentiation of bone marrow-derived mesenchymal stem cells via p38 MAPK signaling pathway

Low magnitude high frequency vibration (LMHFV) exhibits effectively anabolic effects on the bone tissue, and can promote osteogenic differentiation of mesenchymal stem cells (MSCs) in vitro. The role of p38 MAPK signaling in LMHFV-induced osteogenesis remains unclear. In this current study, LMHFV loading was applied to BMSCs in vitro, and cell proliferation, alkaline phosphatase (ALP), matrix mineralization, as well as osteogenic genes expression were assayed. The mechanism of mechanical signal transduction was analysed using PCR array, qRT-PCR and Western blot. LMHFV increased cell proliferation in the growth medium, while inhibited proliferation in the osteogenic medium. ALP activity, matrix mineralization and osteogenic genes expression of Runx2, Col-I, ALP, OPN and OC were increased by LMHFV. p38 and MKK6 genes expression, and p38 phosphorylation were promoted in LMHFV-induced osteogenesis. Inhibition of p38 MAPK with SB203580 and targeted p38 siRNA blunted the increased ALP activity and osteogenic genes expression by LMHFV. These findings suggest that LMHFV promotes osteogenic differentiation of BMSCs, and p38 MAPK signaling shows an important function in LMHFV-induced osteogenesis.

Low magnitude high frequency vibration promotes adipogenic differentiation of bone marrow stem cells via P38 MAPK signal

Low magnitude high frequency vibration (LMHFV) has been mainly reported for its influence on the musculoskeletal system, particularly the bone tissue. In the bone structure, osteogenic activity is the main focus of study with regards to LMHFV. However, adipogenesis, another important mode of differentiation in the bone marrow cavity that might be affected by LMHFV, is much less researched. Furthermore, the molecular mechanism of how LMHFV influences adipogenesis still needs to be understood. Here, we tested the effect of LMHFV (0.3g, 40 Hz, amplitude: 50μm), 15min/d, on multipotent stem cells (MSCs), which are the common progenitors of osteogenic, chondrogenic, adipogenic and myogenic cells. It is previously shown that LMHFV promotes osteogenesis of MSCs. In this study, we further revealed its effect on adipo-differentiation of bone marrow stem cells (BMSCs) and studied the underlying signaling pathway. We found that when treated with LMHFV, the cells showed a higher expression of PPARγ, C/EBPα, adiponectin and showed more oil droplets. After vibration, the protein expression of PPARγ increased, and the phosphorylation of p38 MAPK was enhanced. After treating cells with SB203580, a specific p38 inhibitor, both the protein level of PPARγ illustrated by immunofluorescent staining and the oil droplets number, were decreased. Altogether, this indicates that p38 MAPK is activated during adipogenesis of BMSCs, and this is promoted by LMHFV. Our results demonstrating that specific parameters of LMHFV promotes adipogenesis of MSCs and enhances osteogenesis, highlights an unbeneficial side effect of vibration therapy used for preventing obesity and osteoporosis.

Fracture toughness comparison of five indirect resin composites under the effect of thermal cycling

ABSTRACT This study investigated the microhardness and fracture toughness values of five dental indirect resin composites under the effect of thermal cycling by single-edge notched beam method. Highest microhardness and fracture toughness were reached in AP-X and Filtek P60 groups (microhybrid resin composite) (P < 0.05). After thermal cycling, significant changes of fracture toughness were found for the tested composites except AP-X. Microdifferences between scanning electron microscope images with and without thermal cycling were observed. It is concluded that irregular-shaped fillers and higher filler content contribute to higher mechanical properties, microhardness, and fracture toughness and result in superior fracture toughness under the effect of thermal cycling.

Aging Effect of pH on the Mechanical and Tribological Properties of Dental Composite Resins

ABSTRACT This study evaluated the microhardness and wear behavior alterations of dental resins exposed to strong acid and alkaline degradation regimens. Fifty specimens of AP-X, Z350, P60, VITA ZETA and VITA LC resins were distributed into 10 groups. The control group was not subjected to aging treatment, while the other nine groups were assigned to the following pH solutions: 1, 7 or 13 for 1, 13 or 20 d, respectively. Vickers microhardness and wear behavior of materials without aging served as the reference. Repeated measurements were conducted for other specimens. Scanning electron microscopy was used to observe the morphology. Data were analyzed by repeated-measures one-way ANOVA, followed by the least significant difference (LSD) t-test (P ≤ 0.05) for multiple comparisons. The aging process was aggravated over time. Alkaline medium significantly decreased the microhardness and wear resistance of resins, and led to serious surface damage. AP-X, P60 and Z350 immersed in different media showed a lower degradation than the nanoresin. The mechanical degradation of resin composites was aggravated with increased aging time. Strong alkaline media induced the largest reduction in mechanical and tribological properties. Hybrid resin composites with high filler loading exhibited better mechanical performance than nanoresins with low filler loading under different pH conditions.

CypD-mPTP axis regulates mitochondrial functions contributing to osteogenic dysfunction of MC3T3-E1 cells in inflammation

Bone is a dynamic organ, the bone-forming osteoblasts and bone-resorbing osteoclasts form the physiological basis of bone remodeling process. During pathological process of numerous inflammatory diseases, these two aspects are uncoupled and the balance is usually tipped in favor of bone destruction. Evidence suggests that the inflammatory destruction of bone is mainly attributed to oxidative stress and is closely related to mitochondrial dysfunction. The mechanisms underlying osteogenic dysfunction in inflammation still need further investigation. Reactive oxygen species (ROS) is associated with mitochondrial dysfunction and cellular damage. Here, we reported an unexplored role of cyclophilin D (CypD), the major modulator of mitochondrial permeability transition pore (mPTP), and the CypD-mPTP axis in inflammation-induced mitochondrial dysfunction and bone damage. And the protective effects of knocking down CypD by siRNA interference or the addition of cyclosporin A (CsA), an inhibitor of CypD, were evidenced by rescued mitochondrial function and osteogenic function of osteoblast under tumor necrosis factor-α (TNF-α) treatment. These findings provide new insights into the role of CypD-mPTP-dependent mitochondrial pathway in the inflammatory bone injury. The protective effect of CsA or other moleculars affecting the mPTP formation may hold promise as a potential novel therapeutic strategy for inflammation-induced bone damage via mitochondrial pathways.

Quality improvement in randomized controlled trial abstracts in prosthodontics since the publication of CONSORT guideline for abstracts: A systematic review

OBJECTIVES This study aimed to compare the reporting quality of randomized controlled trial (RCT) abstracts in prosthodontics before and after the publication of Consolidated Standards of Reporting Trials (CONSORT) guideline for abstracts and identify the characteristics associated with better reporting quality. SOURCES PubMed was searched for RCT abstracts published from 2001 to 2007 (pre-CONSORT period) and from 2010 to 2016 (post-CONSORT period) in six leading prosthodontic journals. STUDY SELECTION After applying the inclusion/exclusion criteria, 131 RCT abstracts were selected. The t test was performed to compare the overall quality between the two periods. Univariable and multivariable linear regressions were used to identify any factors relating to the reporting quality. The level of significance was set at P < 0.05. DATA The investigators extracted data and scored the abstracts independently based on CONSORT. The mean overall CONSORT score was 5.20 and 6.11 in the pre- and post-CONSORT samples, respectively. Significant changes were observed in reporting for only three items: title, conclusions, and trial registration. Most abstracts adequately reported interventions, objectives, and conclusions (>90%), but failed to report recruitment and outcome in the results section (<3%). Funding was not reported in both periods. The reporting quality was related to a higher impact factor, structured format, and published after CONSORT. CONCLUSIONS The quality of RCT abstracts in prosthodontics improved over time, but adherence to the CONSORT guideline for abstracts was still suboptimal.

CoCl2 induces apoptosis via a ROS-dependent pathway and Drp1-mediated mitochondria fission in periodontal ligament stem cells

Oxygen deficiency is associated with various oral diseases, including chronic periodontitis, age-related alveolar bone loss, and mechanical stress-linked cell injury from orthodontic appliances. Nevertheless, our understanding of the impact of hypoxia on periodontal tissues and its biochemical mechanism is still rudimentary. The purpose of this research was to elucidate the effects of hypoxia on the apoptosis of human periodontal ligament stem cells (PDLSCs) in vitro and the underlying mechanism. Herein, we showed that cobalt chloride (CoCl2) triggered cell dysfunction in human PDLSCs in a concentration-dependent manner and resulted in cell apoptosis and oxidative stress overproduction and accumulation in PDLSCs. In addition, CoCl2 promoted mitochondrial fission in PDLSCs. Importantly, CoCl2 increased the expression of dynamin-related protein 1 (Drp1), the major regulator in mitochondrial fission, in PDLSCs. Mitochondrial division inhibitor-1, pharmacological inhibition of Drp1, not only inhibited mitochondrial fission but also protected against CoCl2-induced PDLSC dysfunction, as shown by increased mitochondrial membrane potential, increased ATP level, reduced reactive oxygen species (ROS) level, and decreased apoptosis. Furthermore, N-acety-l-cysteine, a pharmacological inhibitor of ROS, also abolished CoCl2-induced expression of Drp1 and protected against CoCl2-induced PDLSC dysfunction, as shown by restored mitochondrial membrane potential, ATP level, inhibited mitochondrial fission, and decreased apoptosis. Collectively, our data provide new insights into the role of the ROS-Drp1-dependent mitochondrial pathway in CoCl2-induced apoptosis in PDLSCs, indicating that ROS and Drp1 are promising therapeutic targets for the treatment of CoCl2-induced PDLSC dysfunction.