PDGF-BB accelerates TSCC via fibroblast lactates limiting miR-26a-5p and boosting mitophagy.

The tumor microenvironment and cancer-associated fibroblasts (CAFs) play crucial roles in tumor development, and their metabolic coupling remains unclear. Clinical data showed a positive correlation between PDGF-BB, CAFs, and glycolysis in the tumor microenvironment of oral tongue squamous cell carcinoma patients. In vitro, CAFs are derived from hOMF cells treated with PDGF-BB, which induces their formation and promotes aerobic glycolysis. Mitophagy increased the PDGF-BB-induced formation of CAF phenotypes and aerobic glycolysis, while autophagy inhibition blocked PDGF-BB-induced effects. Downregulation of miR-26a-5p was observed in CAFs; upregulation of miR-26a-5p inhibited the expression of mitophagy-related proteins ULKI, Parkin, PINK1, and LC3 and aerobic glycolysis in PDGF-BB-induced CAFs. PDGF-BB-induced CAFs promoted tumor cell proliferation, invasion, metastasis, NF-κB signaling pathway activation, and PDGF-BB secretion. Thus, PDGF-BB is associated with lactate-induced CAF formation and glucose metabolism reprogramming. These findings indicate potential therapeutic targets in oral tongue squamous cell carcinoma.

Design and application of modified CAD/CAM socket-shield preparation template in immediate implantation in the esthetic area.

OBJECTIVE: Designed and applicated a modified customized CAD-CAM socket-shield preparation guide template in immediate implant and followed up for 3 years. CLINICAL CONSIDERATIONS: Socket-shield technique could improve the esthetic effect of immediate implant restorations by preserving the labial fascicular bone-periodontal complex at the implant site. While the socket-shield technique is highly technique-sensitive. A modified customized CAD/CAM guided template was designed and fabricated by 3D printing. The movement of the carbide bur during preparing the socket-shield was limited by the socket-shield preparation template. In this case report, the socket-shield preparation template was used for preparing the socket-shield in the tooth root with irregular morphology and the case was followed up for 3 years. CONCLUSIONS: The modified CAD/CAM socket-shield preparation template effectively improved the accuracy and efficiency of preparing the socket-shield by limiting the movement of the high-speed carbide bur in both in both lip-to-palatal and crown-to-root orientation. The socket-shield with accurate morphology could effectively maintain the gingival marginal level and contour. CLINICAL SIGNIFICANCE: The modified CAD/CAM socket-shield preparation template with the depth-locking ring effectively reduced the technique sensitivity and time consumption of the socket-shield technique, especially for tooth roots with irregular morphology.

Inhibitory mechanism of phenolic compounds in rapeseed oil on α-amylase and α-glucosidase: Spectroscopy, molecular docking, and molecular dynamic simulation.

Developing naturally active components to control α-amylase/α-glucosidase activity is highly desired for preventing and managing type 2 diabetes. Rapeseed oil is rich in active phenolic compounds and seed oil is a major source of liposoluble inhibitors to these enzymes. However, it remains unclear about the interaction of phenolic compounds in rapeseed oil with α-amylase/α-glucosidase. This study found that the important phenolic compounds from rapeseed oil (Sinapic acid, SA; canolol, CAO; canolol dimer, CAO dimer) possessed effective inhibition performance against α-amylase and α-glucosidase. CAO showed the lowest and highest inhibitory effect, respectively. In the kinetics studies, the inhibition mechanism of SA/CAO/CAO dimer against α-glucosidase was non-competitive, exhibiting a different way from α-amylase. Fluorescence quenching spectra implied that the static processes were responsible for the spontaneous binding between the compounds and enzymes. Fourier-transform infrared spectroscopy (FT-IR) displayed these compounds-induced conformation alterations of α-amylase/α-glucosidase. Molecular docking revealed that SA/CAO/CAO dimer decreased the catalytic efficiency of α-amylase/α-glucosidase through hydrogen bonds, hydrophobic force, or π-π interaction. Molecular dynamics matched well with the experimental and docking results regarding the inhibitory behaviors and interactions toward α-amylase/α-glucosidase. These results demonstrated the potential benefits of phenolic compounds from rapeseed oil in antidiabetic-related activities.

Comprehensive Analysis of Prognostic Value and Immune Infiltration of MMP12 in Esophageal Squamous Cell Carcinoma.

Esophageal squamous cell carcinoma (ESCC) is a typical neoplastic disease and a frequent cause of death in China. The prognosis of most ESCC patients is still poor. Previous studies demonstrated that MMP12 is involved in tumor metastasis. However, its clinical significance and association with cancer immunity remained largely unclear. In this study, we first analyzed the expressing pattern of MMPs in ESCC from TCGA datasets and found that several MMPs expression was distinctly increased in ESCC. However, only MMP12 expression was associated with five-year survival of ESCC patients. Then, we focused on MMP12 and found its high expression was positively related to advanced clinical stages of ESCC specimens. KEGG assays revealed MMP12 may influence the activity of several tumor-related pathways, such as the Toll-like receptor signaling pathway, TNF signaling pathway, and IL-17 signaling pathway. Then, we sought to determine whether MMP12 expressions were related to immune cell infiltration in ESCC. We observed that increased MMP12 levels were positively associated with the infiltration levels of mast cells activated and macrophages M0. However, eosinophils, B cells naïve, and mast cells resting exhibited an opposite result. Finally, we showed that knockdown of MMP12 suppressed the proliferation of ESCC cells. Overall, our findings proved that high expression of MMP12 may be a novel and valuable prognostic factor in ESCC.

[Pilose antler polypeptide CNT14 promoted proliferation and migration of human oral mucosa fibroblast cells].

PURPOSE: To explore the effect of pilose antler polypeptides CNT14 on proliferation and migration of human oral mucosa fibroblast (hOMF) cells and the related molecular mechanism. METHODS: The biosafety of pilose antler polypeptides CNT14 on hOMF cells was verified by live-dead cell staining kit.CCK-8 assay was used to detect the effect of pilose antler polypeptides CNT14 on hOMF cell proliferation. The effect of pilose antler polypeptides CNT14 on hOMF cell migration was detected by scratch test. Western blot was used to detect the expression of α-SMA, TGF-ß1, Smad2 and p-Smad2 proteins in hOMF cells stimulated by pilose antler polypeptides CNT14. The effect of Smad2 inhibitors on fibroblast activation induced by pilose antler polypeptides CNT14 was evaluated.The model of keratinized gingival defect was established in New Zealand white rabbits, and the regenerated gingival tissue was stained with H-E. The expression levels of α-SMA, TGF-ß1, Smad2 and p-Smad2 proteins in the gingival tissues of regenerated New Zealand white rabbits were detected by immunohistochemistry, and the ability of pilose antler polypeptides CNT14 to promote regeneration of oral gingival tissues was verified. Statistical analysis was performed with SPSS 20.0 software package. RESULTS: The survival rate of hOMF cells was above 95% after treated with pilose antler polypeptides CNT14. After stimulation of hOMF cells with pilose antler polypeptides CNT14, the proliferation and migration rates of hOMF cells were increased compared with the control group (P＜0.05). The expression of α-SMA, TGF-ß1, Smad2 and p-Smad2 proteins in hOMF cells stimulated by pilose antler peptide CNT14 was increased, and the difference was statistically significant(P＜0.05). The expression of α-SMA in fibroblasts induced by Smad2 inhibitor was decreased. In animal experiments, H-E staining showed that the inflammatory response of oral mucosal wounds of New Zealand white rabbits treated with CNT14 was less than that of the control group. Immunohistochemical staining results showed that the expressions of α-SMA, TGF-ß1, Smad2 and p-Smad2 in the regenerated gingival tissues of New Zealand white rabbits treated with CNT14 were significantly increased compared with those in the control group on the 9th and 11th days within the gingival wounds(P＜0.05). CONCLUSIONS: Pilose antler polypeptides CNT14 has good biosafety and can promote the proliferation and migration of human oral mucosa fibroblast cells, and the expression levels of α-SMA, TGF-ß1, Smad2 and p-Smad2 were increased, promoting the regeneration of gingival tissues.

Ultrathin 2D NbWO6 Perovskite Semiconductor Based Gas Sensors with Ultrahigh Selectivity under Low Working Temperature.

Hydrogen sulfide (H2 S) detection with high selectivity and low working temperature is of great significance due to its strong toxicity both to the environment and to humans and also as an endogenous signaling molecule existing in various physiological processes. 2D perovskites with high carrier mobility are promising candidates for gas sensing; however, the development of stable and nontoxic 2D perovskites nanosheets still remains a challenge. Herein, 2D all-inorganic NbWO6 perovskite nanosheets with thicknesses down to 1.5 nm are synthesized by liquid exfoliation, and the gas-sensing performance based on these ultrathin nanosheets is investigated. A few-layer NbWO6 -based sensor exhibits fast H2 S sensing speed (<6 s) with high selectivity and sensitivity (S = 12.5 vs 50 ppm) at low temperature (150 °C). A small variation of H2 S concentration (<0.5 ppm) can be detected with a fully reversible resistance signal. This work sheds light on the development of high-performance gas sensors working in ambient conditions based on low-dimensional, nontoxic, and wide-bandgap perovskite semiconductors. The high carrier mobility, ultrathin structure, and soft nature make this type of 2D perovskite semiconductor an ideal material candidate for the fabrication of flexible, transparent, and wearable sensing devices in the future.

Salvia miltiorrhiza (SM) Injection Ameliorates Iron Overload-Associated Cardiac Dysfunction by Regulating the Expression of DMT1, TfR1, and FP1 in Rats.

Previous studies have found that Salvia miltiorrhiza (SM) injection have a protective effect on the iron overloaded (IO) heart. However, the mechanisms are not completely known. In the present study, we investigated the underlying mechanisms based on the iron transport-related proteins. The rats were randomly divided into five groups: control, IO group, low-dose SM group, high-dose SM group, and deferoxamine control group. Iron dextran was injected to establish the IO model. After 14 days of treatment, cardiac histological changes were observed by hematoxylin and eosin (H&E) staining. Iron uptake-related proteins divalent metal transporter-1 (DMT-1), transferrin receptor-1 (TfR-1), and iron export-related proteins ferroportin1 (FP1) in the heart were detected by Western blotting. The results showed that SM injection decreased cardiac iron deposition, ameliorated cardiac function, and inhibited cardiac oxidation. Most important of all, SM injection downregulated the expression of DMT-1 and TfR-1 and upregulated FP1 protein levels compared with the IO group. Our results indicated that reducing cardiac iron uptake and increasing iron excretion may be one of the important mechanisms of SM injection reducing cardiac iron deposition and improving cardiac function under the conditions of IO.

Removing and recycling mercury from scrubbing solution produced in wet nonferrous metal smelting flue gas purification process.

Wet purification technology for nonferrous metal smelting flue gas is important for mercury removal; however, this technology produces a large amounts of spent scrubbing solution that contain mercury. The mercury in these scrubbing solutions pose a great threat to the environment. Therefore, this research provides a novel strategy for removing and recycling mercury from the scrubbing solution, which is significant for decreasing mercury pollution while also allowing for the safe disposal of wastewater and a stable supply of mercury resources. Some critical parameters for the electrochemical reduction of mercury were studied in detail. Additionally, the electrodeposition dynamics and electroreduction mechanism for mercury were evaluated. Results suggested that over 92.4% of mercury could be removed from the scrubbing solution in the form of a Hg-Cu alloy under optimal conditions within 150 min and with a current efficiency of approximately 75%. Additionally, mercury electrodeposition was a quasi-reversible process, and the controlled step was the mass transport of the reactant. A pre-conversion step from Hg(Tu)42+ to Hg(Tu)32+ before mercury electroreduction was necessary. Then, the formed Hg(Tu)32+ on the cathode surface gained electrons step by step. After electrodeposition, the mercury in the spent cathode could be recycled by thermal desorption. The results of the electrochemical reduction of mercury and subsequent recycling provides a practical and easy-to-adopt alternative for recycling mercury resources and decreasing mercury contamination.

[Corrigendum] Epithelial mesenchymal transition induced by the CXCL9/CXCR3 axis through AKT activation promotes invasion and metastasis in tongue squamous cell carcinoma.

Subsequently to the publication of this paper, an interested reader drew to the authors' attention that two pairs of data panels containing strikingly similar data were featured in Fig. 4A and B. The authors have re­examined their data and realized that Fig. 4 was assembled incorrectly. The revised version of Fig. 4, containing the correct data for Fig. 4A and B, is shown on the next page. The authors regret the errors that were made in the preparation of the published figure, and confirm that these errors did not seriously affect the conclusions reported in the paper. The authors are grateful to the editor of Oncology Reports for allowing them the opportunity to publish a Corrigendum, and all the authors agree to this Corrigendum. Furthermore, they apologise to the readership for any inconvenience caused. [the original article was published in Oncology Reports 39: 1356-1368, 2018; DOI: 10.3892/or.2017.6169].

Mechanisms underlying the protective effect of tannic acid against arsenic trioxide­induced cardiotoxicity in rats: Potential involvement of mitochondrial apoptosis.

Arsenic trioxide (ATO) is a frontline chemotherapy drug used in the therapy of acute promyelocytic leukemia. However, the clinical use of ATO is hindered by its cardiotoxicity. The present study aimed to observe the potential effects and underlying mechanisms of tannic acid (TA) against ATO­induced cardiotoxicity. Male rats were intraperitoneally injected with ATO (5 mg/kg/day) to induce cardiotoxicity. TA (20 and 40 mg/kg/day) was administered to evaluate its cardioprotective efficacy against ATO­induced heart injury in rats. Administration of ATO resulted in pathological damage in the heart and increased oxidative stress as well as levels of serum cardiac biomarkers creatine kinase and lactate dehydrogenase and the inflammatory marker NF­κB (p65). Conversely, TA markedly reversed this phenomenon. Additionally, TA treatment caused a notable decrease in the expression levels of cleaved caspase­3/caspase­3, Bax, p53 and Bad, while increasing Bcl­2 expression levels. Notably, the application of TA decreased the expression levels of cytochrome c, second mitochondria­derived activator of caspases and high­temperature requirement A2, which are apoptosis mitochondrial­associated proteins. The present findings indicated that TA protected against ATO­induced cardiotoxicity, which may be associated with oxidative stress, inflammation and mitochondrial apoptosis.

Crocin protects against cardiotoxicity induced by doxorubicin through TLR-2/NF-κB signal pathway in vivo and vitro.

Doxorubicin (DOX) is widely used to treat multiple of tumors, but its clinical trials are allied with some serious adverse events mainly cardiac functional abnormalities. So the objective of our investigation is to identify the cardioprotective action of crocin (CRO), a natural compound derived from saffron, against DOX-induced cardiotoxicity. CRO was injected intraperitoneally (i.p.) to rats for sixconsecutive days and DOX (i.p.) was administered on the fourth day. H9c2 cells were treated with DOX for 24 h after being pre-treated by CRO for 2 h. CROreduced tachycardiaand J-point elevation,decreased the levelsof serum creatine kinase, lactate dehydrogenase,glutamic-oxalacetic transaminase and glutamic-pyruvic transaminase.CRO exerted positive effect on DOX-induced ROS productionand changes of oxidative stress biomarkers. CRO significantlydecreased intracellular Ca2+ concentration andincreased mitochondria membrane potentialin H9c2 cells. CRO also resisted the DOX-induced high expressionof tumor necrosis factor-αand interleukin-6, inhibitedapoptosisand improved the abnormal expression levels of Bcl-2, Bax and Caspase-3 proteins.CRO obviously restrained DOX-mediatedhigh expression of toll-like receptor-2 (TLR-2) and nuclear factor kappa-B (NF-κB) in ventricular tissue. Inbrief,CRO distinctly restrained DOX-mediated cardiotoxicity by inhibiting oxidative stress, inflammation, apoptoticandredressingcardiomyocyte calcium dyshomeostasis and mitochondria damage.These cardioprotective effects may berelated closely with the TLR2/NF-κB pathway.

Tannic acid ameliorates arsenic trioxide-induced nephrotoxicity, contribution of NF-κB and Nrf2 pathways.

BACKGROUND AND PURPOSE: Tannic acid (TA), a group of polyphenolic compounds, has multiple anticancer, antimutagenic, antioxidant and anti-inflammatory activities. However, the effects of TA on arsenic trioxide (ATO)-induced nephrotoxicity are still relatively unknown. This study investigated the protective effects and potential mechanisms of TA on ATO-induced nephrotoxicity in rats. METHODS: Rats were intragastrically administered TA with concurrent ATO infused intraperitoneally over 10 days. Renal morphology changes were observed through light microscopy. The levels of antioxidants and pro-inflammatory factors were measured in the serum and renal tissue, respectively. Further, expression of B-cell lymphoma-2, B-cell lymphoma-extra large, p53, and Bcl-2-associated X protein were measured using an immunohistochemical method. The protein expression of nuclear factor kappa B (NF-κB), nuclear factor-erythroid-2-related factor 2 (Nrf2), and kelch-like ECH-associated protein 1 (Keap1) were measured by Western blot. RESULTS: The data showed that ATO exposure significantly increased the serum nephritic, oxidative stress, apoptosis and inflammatory markers in the renal tissue of rats. Conversely, pretreatment with TA reversed these changes. Furthermore, TA treatment caused a significant decrease in NF-κB expression (P < 0.05), while increasing Nrf2 and Keap1 expressions (P < 0.05). CONCLUSION: TA ameliorates ATO-induced nephrotoxicity, which is related to the inhibition of oxidative stress, inflammation and apoptosis, potentially through the NF-κB/Nrf2 pathway.

Crocin attenuates isoprenaline-induced myocardial fibrosis by targeting TLR4/NF-κB signaling: connecting oxidative stress, inflammation, and apoptosis.

Crocin is isolated from saffron and has multiple activities. There are many reports on its beneficial effects for cardiovascular disease, but crocin's effects on anti-myocardial fibrosis have not yet been reported. This study investigated crocin's effects and potential mechanisms on isoproterenol (ISO)-induced myocardial fibrosis (MF) in mice. Mice were infused intraperitoneally with crocin with concurrent ISO subcutaneous injections over 2 weeks. Electrocardiography, cardiac weight index (CWI), hydroxyproline content, and heart morphology changes were observed. Administration of crocin markedly decreased heart rate, J-point elevation, QRS interval, CWI, and hydroxyproline content in the myocardial tissues, and improved heart pathologic morphology. Versus the control group, the ISO group showed an increase in lactate dehydrogenase and creatine kinase activities and malondialdehyde content. Meanwhile, superoxide dismutase, catalase, and glutathione contents decreased in the ISO group; crocin caused a significant reduction in oxidative stress levels in ISO-induced MF. ISO led to a significant increase in interleukin-1 and -6 and tumor necrosis factor-α in addition to nuclear factor kappa B (NF-κB) (p65) and toll-like receptor (TLR) 4 expressions. Crocin treatment suppressed these inflammatory cytokine expressions. Moreover, crocin treatment caused a significant decrease in connective tissue growth factor and transforming growth factor-ß1 mRNA levels in addition to a decrease in B cell lymphoma-2, Bcl-2-associated X protein, caspase-3, and cleaved caspase-3 expressions. Crocin has a protective effect on ISO-induced MF, which may be associated with the TLR4/NF-κB (p65) signal transduction pathway.

Development of Recyclable Iron Sulfide/Selenide Microparticles with High Performance for Elemental Mercury Capture from Smelting Flue Gas over a Wide Temperature Range.

Fast and effective removal of elemental mercury in a wide temperature range is critical for the smelting industry. In this work, a recyclable magnetic iron sulfide/selenide sorbent is developed to capture and recover Hg0 from smelting flue gas. Benefiting from Se doping, the Hg0 capture performance of prepared FeSxSey is significantly enhanced compared with traditional iron sulfide, especially at high temperatures. Considering the recyclability and working temperature, FeS1.32Se0.11 exhibits the best Hg0 capture performance. The average capture rate of FeS1.32Se0.11 is 3.661 µg/g/min at 80 °C and its saturation adsorption capacity is 20.216 mg/g. The flue gas compositions have almost no effect on Hg0 capture. X-ray photoelectron spectroscopy and mercury thermal programmed desorption suggest that the stable active Se-Sn2- adsorption site can combine with Hg0 to form HgSe, consequently improving Hg0 capture performance at high temperatures. After Hg0 capture, the spent FeSxSey can be collected by magnetic separation and regenerated through selective extraction, which facilitates harmless treatment and resource reuse of mercury. With the advantages of excellent Hg0 capture performance, wide operating temperature range, and remarkable recycling property, FeSxSey microparticles may be a promising sorbent for Hg0 capture in industrial applications, while opening a new avenue to realize the resource utilization toward toxic elements.

Epithelial mesenchymal transition induced by the CXCL9/CXCR3 axis through AKT activation promotes invasion and metastasis in tongue squamous cell carcinoma.

The present study aimed to assess the induction of epithelial-mesenchymal transition (EMT), invasion, and metastasis by the chemokine CXCL9/receptor CXCR3 axis in tongue squamous cell carcinoma (TSCC), unveiling the underlying mechanisms and providing new insights into the prevention and treatment of oral cancer metastasis. The expression levels of CXCL9 and CXCR3 in TSCC tissue specimens were determined by immunohistochemistry, assessing differences between samples with cervical lymph node metastasis and those without. Moreover, protein expression or activity in the TSCC Cal-27 cell line was controlled by neutralizing antibodies, gene transfection, or knock-out. Then, alterations of cell proliferation, migration, invasion, and the cytoskeleton were analyzed by CCK-8, cell scratch, Transwell, and cyto-skeleton staining assays, respectively. Alterations of EMT markers (E-cadherin and vimentin) in Cal-27 cells were detected by immunofluorescence and western blotting. In addition, western blotting was utilized to detect protein expression levels of Akt2, p-Akt2, eIF4E and p-eIF4E, and to explore the regulatory roles and mechanisms of the CXCL9/CXCR3 axis in invasion and metastasis. Significantly increased expression levels of CXCL9 and CXCR3 were detected in tissue specimens with lymph node metastasis compared with those without (P<0.01). Overexpression of CXCL9/CXCR3 in Cal-27 cells resulted in cytoskeleton alterations, decreased E-cadherin expression, increased vimentin levels, enhanced migration and invasion (P<0.05), and increased phosphorylated Akt2 and eIF4E levels (P<0.05). These results revealed that in TSCC, the CXCL9/CXCR3 axis could activate the Akt signaling pathway, with EMT and cytoskeleton rearrangement, promoting invasion and metastasis.

Isoalantolactone induces apoptosis in human breast cancer cells via ROS-mediated mitochondrial pathway and downregulation of SIRT1.

Isoalantolactone possessed various biological activities. However, whether it could treat breast cancer and its underlying mechanism remained largely unknown. This study was designed to evaluate the anticancer effects of isoalantolactone on breast cancer and explored the molecular mechanism. Two human breast cancer cell lines (MDA-MB-231 and MCF-7) and one normal breast cell line (MCF-10A) were applied. Our data suggested that isoalantolactone decreased breast cancer cell viability in a dose-dependent manner, but showed almost no toxicity to MCF-10A cells. The anticancer effects of isoalantolactone were related to the overexpression of reactive oxygen species. Isoalantolactone significantly induced breast cancer cell apoptosis by activating caspase cascade, cleaving poly (ADP-ribose) polymerase. Increase of Bax/Bcl-2 ratio, depolarization of mitochondrial membrane potential, release of cytochrome c from mitochondria to cytoplasm and cell cycle arrest at G2/M phase were associated to the apoptosis induction. Additionally, isoalantolactone increased the protein expression of p38 MAPK and JNK. The apoptosis-induction of isoalantolactone could be abrogated by co-treatment with SB203580 (inhibitor of p38 MAPK) or SP600125 (inhibitor of JNK). Furthermore, isoalantolactone induced breast cancer cells apoptosis in a caspase-independent pathway, which was downregulation of SIRT1. Therefore, isoalantolactone may serve as a chemotherapeutic agent for the treatment of human breast cancer.

[Applications of minimally invasive bone splitting technique in cases with missing maxillary anterior teeth and obvious labial alveolar bone depression for dental implantation].

PURPOSE: The purpose of this study was to introduce a minimally invasive bone splitting technique which is suitable for cases with missing anterior teeth and obvious depression of alveolar bone in labial side, and to evaluate its clinical results. METHODS: Minimally invasive bone splitting technique was used in 8 healthy adults with bone defects in the aesthetic zone. The labial alveolar bone incisions were confined around the bone defects which were smaller than traditional incisions. The other procedures were the same as conventional bone splitting technique. Cone-beam CT (CBCT) for missing anterior teeth was taken before surgery, after the surgery and 6 months after surgery and alveolar bone height and width were recorded with landmark identification designed by ourselves in this study. The data were analyzed with SPSS 21.0 software package for paired t test. RESULTS: Paired t test indicated that after surgery and six months after surgery, the labial bone defect was significant improved (P<0.05), but the height of the alveolar ridge bone didn't increase significantly (P>0.05) while the width of the alveolar ridge bone significant improved (P>0.05). CONCLUSIONS: This minimally invasive technique can achieve good clinical results for not only intact labial alveolar ridge bones but also good bone grafts, which is beneficial to implantation and prosthetic aesthetics. The long-term outcome needs to be observed.

[Clinical observation of assisted occlusion therapy for repositioning temporomandibular joint discs].

PURPOSE: To investigate the occurrence of postoperative malocclusion of patients with temporomandibular joint disc repositioning and the necessity of postoperative orthodontic treatment. METHODS: One hundred and eight patients who received temporomandibular joint disc repositioning from 2010.10 to 2015.10 were selected in this study. The patients' occlusion was recorded preoperatively and postoperatively. All patients received functional appliance or orthodontic treatment after surgery. The occlusion and the relative position of the articular disc and condyle were evaluated at regular follow-up. RESULTS: Postoperative malocclusion occurred in all patients. The use of functional appliance for 3-6 months may decrease the proportion of malocclusion. After orthodontic treatment, all patients had a complete recovery of malocclusion and remained good articular disc and condyle relationship during long term follow-up. CONCLUSIONS: Postoperatively malocclusion may occur after temporomandibular joint disc repositioning, and the use of functional appliance and orthodontic treatment are strongly recommended to retain good articular disc and condyle relationship.