Background:Cisplatin-based chemotherapy for oral squamous cell carcinoma (OSCC) is limited by intrinsic inefficacy and toxicity. Lycopene, a natural carotenoid, may enhance cisplatin's therapeutic potential. Objective:To explore lycopene's chemo-sensitizing effects on cisplatin and its mechanisms in OSCC. Methods:In vitro, CAL-27/SCC-9 cells were treated with lycopene and/or cisplatin; cell viability, colony formation, migration, invasion, and apoptosis were detected, and protein expression of MRP-1, PI3K/Akt/mTOR pathway components, and EMT markers was analyzed by Western blot. In vivo, a nude mouse xenograft model was used to verify the combination's effect on tumor growth. Results:Compared with cisplatin alone, the lycopene-cisplatin combination significantly inhibited OSCC cell proliferation, colony formation, migration, and invasion, while promoting apoptosis. Mechanistically, lycopene reversed cisplatin-induced upregulation of MRP-1 and activation of the PI3K/Akt/mTOR pathway, and restored cisplatin-suppressed E-cadherin while reducing N-cadherin and EpCAM. In vivo, the combination reduced tumor growth vs cisplatin alone without increasing toxicity. Conclusion:This is the first report that lycopene enhances cisplatin sensitivity in OSCC by coupling inhibition of MRP-1-mediated drug efflux with suppression of PI3K/Akt/mTOR and EMT/stemness-filling the gap of lycopene's synergistic mechanism with cisplatin, offering a strategy to improve therapeutic efficacy without exacerbating toxicity.

Functional tissue repair is often constrained by inflammation and fibrosis. Alternatively activated M2 macrophages have emerged as promising therapeutic targets for optimizing graft-to-host interactions; however, efficient induction methods are required. Presumably, the outcome of regenerative wound healing or scar formation/fibrosis might be dependent on the balance between M2a and M2c sub-phenotypes. This study utilized dual-functionalized graphene oxide (GO) as a DNA delivery agent to induce M2a and M2c macrophage polarization. Mechanistically, molecular characteristics were analyzed using RNA sequencing. We designed GO with polyethyleneimine (PEI) modification and subsequently conjugated it with polyethylene glycol (PEG)-folate (FA) to target human THP-1-derived macrophage activation. Specifically, the resulting GO-PEI-PEG-FA (GPPF) compound effectively activated CD206+CD209+M2a and CD163+MerTK+M2c phenotype polarization. The efficient delivery of IL4 or IL10 plasmid DNA using GPPF (GPPF/pIL4 or GPPF/pIL10) significantly enhanced macrophage cellular elongation and reduced MHC-II-associated antigen presentation. M2a(GPPF/pIL4) and M2c(GPPF/pIL10) were validated as negative regulators of the immune response and positive regulators of Th2 effectors. Up-regulated genes in M2a(GPPF/pIL4) even inhibited type I interferon production and restricted the innate immune response. Supplemental to the established data, M2a(GPPF/pIL4) behaved similar to IFN-responsive macrophages, restricting viral life cycles and promoting myogenesis and osteogenesis. Meanwhile, M2c(GPPF/pIL10) was characterized using IL10 signaling, anti-fibrosis, and neutrophil-mediated suppression of the LPS-bacterial response. Regarding the tissue remodeling process, the two subsets attenuated negative-regulated BMP signaling to facilitate osteoinduction and up-regulated NAMPT to establish a transient stem cell-activating niche for tissue regeneration. This study underscored the potential of functionalized GO-induced M2 sub-phenotypes as modulators in regenerative medicine.

This study employed a modified digital technique to evaluate parameters of molar preparations for monolithic zirconia crown restoration, investigating whether clinical preparations with different tooth positions influence restorative outcomes. A total of 238 prepared posterior abutments were analyzed using an intraoral scanner, with parameters including total occlusal convergence (TOC) angle, margin perimeter, and mean abutment height assessed for statistical analysis. The results revealed that the average TOC angle of each posterior tooth exceeded 6°, with the maximum average observed in the mandibular left second molar (35.96 ± 20.21°) and the minimum in the maxillary right first premolar (10.97 ± 6.84°). Statistically significant differences were found in the TOC angle of homonymous second premolars (p < 0.05), where the mandibular left second molar was significantly larger than the other homonymous teeth. Additionally, significant differences existed between teeth in the same quadrant with different positions (p < 0.05), showing a linear increase in TOC angle as the tooth position moved backward. A positive correlation was observed between TOC angle and margin perimeter, while a negative correlation existed between TOC angle and mean abutment height. The findings indicate that clinical zirconia crown preparations often deviate from theoretical TOC recommendations, particularly requiring tailored criteria for mandibular teeth. The developed software integrates digital acquisition with clinical analysis, demonstrating its relevance in prosthodontic practice and education.

目的:探讨压膜保持器对后牙区种植单冠近中邻间隙的影响,并对患者接受度进行调查.方法:纳入后牙区种植单冠修复患者167例,牙冠平均戴用时间2.41年.以金属咬合纸和测力计评估邻间隙大小,对出现近中邻间隙及食物嵌塞的30例牙冠重新修复,嘱患者夜间戴用压膜保持器并每半年复查,随访到与第一次修复后相同的时间,比较未戴用与戴用压膜保持器时的种植单冠近中邻间隙大小,种植体周围指数与天然牙牙周指数,调查167例患者对压膜保持器的接受程度.结果:夜间戴用压膜保持器平均2.41年,30例种植单冠近中邻间隙明显小于未戴用压膜保持器时(P＜0.05),食物嵌塞情况有所缓解.佩戴压膜保持器时种植体周围指数(PD,mSBI)优于食物嵌塞时(P＜0.05),天然牙牙周指数(PD,BI)较佩戴前无明显变化.有夜磨牙或食物嵌塞的患者对压膜保持器接受度优于其他组别(P＜0.05).结论:夜间佩戴压膜保持器可能有助于减小种植单冠近中邻间隙,缓解食物嵌塞.对有夜磨牙或曾因邻间隙反复食物嵌塞的患者可有针对性地推荐使用.

OBJECTIVE:To develop dexamethasone plus minocycline-loaded liposomes (Dex/Mino liposomes) and apply them to improve bioinert polyetheretherketone (PEEK) surface, which could prevent post-operative bacterial contamination, enhance ossification for physiologic osseointegration, and finally reduce implant failure rates.METHODS:Dex/Mino liposomes were covalently grafted onto the PEEK surface using polydopamine (pDA) coating as a medium. Confocal laser scanning microscopy was used to confirm the binding of fluorescently labeled liposomes onto the PEEK substrate, and a microplate reader was used to semiquantitatively measure the average fluorescence intensity of fluorescently labeled liposome-decorated PEEK surfaces. Moreover, the mouse subcutaneous infection model and the beagle femur implantation model were respectively conducted to verify the bioactivity of Dex/Mino liposome-modified PEEK in vivo, by means of micro computed tomography (micro-CT) and hematoxylin and eosin (HE) staining analysis.RESULTS:The qualitative and quantitative results of fluorescently labeled liposomes showed that, the red fluorescence intensity of the PEEK-pDA-lipo group was stronger than that of the PEEK-NF-lipo group (P < 0.05); the liposomes were successfully and uniformly decorated on the PEEK surfaces due to the pDA coating. After mouse subcutaneous implantation of PEEKs for 24 hours, HE staining results showed that the number of inflammatory cells in the PEEK-Dex/Mino lipo group were lower than that in the inert PEEK group (P < 0.05), indicating a lower degree of infection in the test group. These results suggested that the Mino released from the liposome-functionalized surface provided an effective bacteriostasis in vivo. After beagle femoral implantation of PEEK for 8 weeks, micro-CT results showed that the PEEK-Dex/Mino lipo group newly formed more continuous bone when compared with the inert PEEK group; HE staining results showed that more new bones were formed in the PEEK-Dex/Mino lipo group than in the inert PEEK group, which were firmly bonded to the functionalized PEEK surface and extended along the PEEK interface. These results suggested that the Dex released from the liposome-functionalized surface induced effective bone regeneration in vivo.CONCLUSION:Dex/Mino liposome modification enhanced the bioactivity of inert PEEK, the functionalized PEEK with enhanced antibacterial and osseointegrative capacity has great potential as an orthopedic/dental implant material for clinical application.

目的:比较高血压患者在笑气(N2 O)吸入条件下Er:YAG激光辅助牙周基础治疗与传统牙周基础治疗的临床效果.方法:28例高血压患者牙列的四个象限分次随机接受4种牙周基础治疗:(1)局麻下手工龈下刮治根面平整(scalingandroot-planing,SRP);(2)N2 O吸入下SRP;(3)局麻下,Er:YAG激光+手工SRP;(4)N2 O吸入下,Er:YAG激光+手工SRP.治疗中记录血压、疼痛VAS评分与牙周临床指标.使用SPSS 22.0进行统计学分析.结果:激光辅助牙周治疗的两组牙周临床指标改善值显著高于局麻+SRP组(P<0.05).N2 O吸入2组VAS评分均显著低于局麻下治疗的2组,其中N2 O+激光+SRP组VAS评分最低(P<0.05).麻醉时N2O吸入2组的血压值低于局麻2组的血压值(P<0.05).结论:N2O吸入联合Er:YAG激光治疗较传统牙周基础治疗临床效果好、更舒适,并可能有助于维持血压的稳定.

Commonly recognized mechanisms of the xenogeneic-extracellular matrix-based regenerative medicine include timely degradation, release of bioactive molecules, induced differentiation of stem cells, and well-controlled inflammation. This process is most feasible for stromal tissue reconstruction, yet unsuitable for non-degradable scaffold and prefabricated-shaped tissue regeneration, like odontogenesis. Treated dentin matrix (TDM) has been identified as a bioactive scaffold for dentin regeneration. This study explored xenogeneic porcine TDM (pTDM) for induced odontogenesis. The biological characteristics of pTDM were compared with human TDM (hTDM). To investigate its bioinductive capacities on allogeneic dental follicle cells (DFCs) in the inflammation microenvironment, pTDM populated with human DFCs were co-cultured with human peripheral blood mononuclear cells (hPBMCs), and pTDM populated with rat DFCs were transplanted into rat subcutaneous model. The results showed pTDM possessed similar mineral phases and bioactive molecules with hTDM. hDFCs, under the induction of pTDM and hTDM, expressed similar col-I, osteopontin and alkaline phosphatase (ALP) (all expressed by odontoblasts). Whereas, the expression of col-I, dentin matrix protein-1 (DMP-1) and bone sialoprotein (BSP) were down-regulated when cocultured with hPBMCs. The xenogeneic implants inevitably initiated Th1 inflammation (up-regulated CD8, TNF-α, IL-1β, etc) in vivo. However, the biomineralization of pre-dentin and cementum were still processed, and collagen fibrils, odontoblast-like cells, fibroblasts contributed to odontogenesis. Although partially absorbed at 3 weeks, the implants were positively expressed odontogenesis-related-proteins like col-I and DMP-1. Taken together, xenogeneic TDM conserved ultrastructure and molecules for introducing allogeneic DFCs to odontogenic differentiation, and promoting odontogenesis and biomineralization in vivo. Yet effective immunomodulation methods warrant further explorations.

目的:比较高血压患者一氧化二氮吸入和传统牙周基础治疗时的疼痛评分及血压状况差异.方法:本研究为随机对照临床试验.纳入药物性牙龈增生患者40例,其中36例完成了临床检查和治疗.36名患者在牙周探诊时分为2组(n =18),A组在一氧化二氮吸入下进行,B组在无麻醉下进行;4周后2组交换麻醉方式,比较2组临床指标、VAS评分、血压差异.龈下刮治根面平整阶段将患者分为2组(n =18),第一次治疗C组在一氧化二氮吸入下进行,D组在局部浸润下进行;第二次治疗阶段2组交换麻醉方式,比较2组临床指标、VAS评分、血压差异.结果:一氧化二氮吸入牙周探诊VAS疼痛评分均显著低于常规探诊组(P＜0.05);A、B组内一氧化二氮吸入牙周探诊检查中的血压低于治疗前(P＜0.05).C、D两组组内一氧化二氮吸入组VAS疼痛评分显著低于局麻组(P＜0.05).结论:与传统的牙周基础治疗比较,高血压患者在一氧化二氮吸入条件下牙周治疗疼痛较轻,血压更稳定.

在牙齿的发育期间,由于压力使两个牙胚发生完全或者不完全融合,形成融合牙.融合牙在乳牙和恒牙均可发生,同时也可以发生在正常牙与多生牙之间.本文报道左上颌恒中切牙与近中多生牙融合并发生慢性根尖囊肿1例,就其口腔检查、治疗过程、愈合及讨论进行阐述,使临床医生对本病有进一步的认识.

目的:探讨牙源性间充质干细胞对成骨前体细胞成骨分化的影响.方法:将小鼠成骨前体细胞MC3T3-El分为两组,观察组为牙源性间充质干细胞与MC3T3-E1细胞共培养,对照组为单一MC3T3-E1细胞培养.采用CCK-8法检测细胞增殖水平,采用酶联免疫法检测碱性磷酸酶(Alkaline phosphatase,ALP)活性并进行茜素红染色,采用qRT-PCR、Western blot检测ALP与骨桥素(osteopontin,OPN)mRNA与蛋白表达水平.结果:细胞共培养1d与3d后,观察组的细胞增殖指数、ALP活性显著高于对照组(P＜0.05).与对照组相比,观察组的矿化结节显著增加,经茜素红染色呈红褐色.细胞共培养1d与3d后,观察组的ALP、OPN mRNA与蛋白相对表达水平显著高于对照组(P＜0.05).结论:牙源性间充质干细胞能促进成骨前体细胞的ALP、OPN表达,提高ALP活性,增加细胞增殖能力,诱发矿化,从而促进成骨分化.

Background Autophagy degraded and recycled cytoplasmic components to maintain cellular homeostasis under stress conditions, which was recognized as double-edged sword in oncogenesis and novel target in cancer treatment. However, comprehensive analysis of the relationship between autophagy regulation and immunity has not been reported yet. Methods Unsupervised consensus clustering algorithm was used to identify autophagy regulation patterns. LASSO cox regression algorithm was used to build a scoring system (ATGscore) to represent the individual autophagy regulation pattern. Then integrated analysis of autophagy regulation patterns and ATGscore was performed. Results We have successful depicted five autophagy regulation patterns and established a scoring system (ATGscore) to represent it, which was shown to be significantly correlated with TIME infiltration, immune phenotypes, molecular subtypes, and genetic variation, etc. in 1165 head and neck squamous cell carcinoma (HNSCC) patients. Moreover, ATGscore was an independent prognostic factor and potent predictor for clinical response to immune-checkpoint inhibitors (ICIs) targeting immunotherapy. Conclusion Understanding the molecular characteristics of autophagy regulation patterns in HNSCC could help us to depict the underlying mechanism of tumour immunity and lay a solid foundation on combination of autophagy targeting therapies and immunotherapies for clinical application in HNSCC.

目的 研究下调长链非编码RNA(lncRNA)人类白细胞抗原复合体18(HCG18)靶向调控miR-34a影响口腔鳞癌细胞增殖、侵袭以及迁移的分子机制.方法 Realtime PCR方法测定HCG18在口腔鳞癌CAL27、SCC4、HB96细胞和正常口腔黏膜NOK细胞中的表达变化.在口腔鳞癌SCC4细胞中转染HCG18 shRNA,Realtime PCR方法测定下调效果,MTT测定各细胞增殖变化,Transwell小室测定各细胞侵袭和迁移能力变化,Western blot测定各细胞中N-cadherin、E-cadherin蛋白表达变化.生物信息学软件发现HCG18与miR-34a可能互为靶向关系,利用荧光素酶系统鉴定二者靶向关系.将miR-34a inhibitor、inhibitor control和HCG18 shRNA分别共转染到口腔鳞癌SCC4细胞中,利用上述方法测定各细胞增殖、迁移和侵袭能力变化.结果 HCG18在口腔鳞癌CAL27、SCC4、HB96细胞中的表达水平高于正常口腔黏膜NOK细胞,并且口腔鳞癌SCC4细胞中HCG18表达水平最高,差异有统计学意义(P<0.05).转染HCG18 shRNA可以下调口腔鳞癌SCC4细胞中HCG18表达水平,降低细胞增殖、迁移和侵袭能力,促进细胞中E-cadherin蛋白表达,抑制细胞中N-cadherin蛋白表达.HCG18靶向负调控miR-34a的表达.与共转染inhibitor control和HCG18 shRNA后的细胞相比,共转染miR-34a inhibitor和HCG18 shRNA后的细胞增殖、迁移和侵袭能力升高,差异有统计学意义(P<0.05).结论 下调HCG18靶向调控miR-34a抑制口腔鳞癌SCC4细胞增殖、侵袭以及迁移.

Background: Cisplatin (DDP) is the first-line chemotherapy agent for the treatment of oral squamous cell carcinoma (OSCC). The emergence of DDP resistance leads to diminished drug efficacy and survival benefit. lncRNA MALAT1 has been considered as one of the most important factors in OSCC. It has also been reported to enhance chemo-resistance in other kinds of carcinomas. However, little is known about the role of lncRNA MALAT1 in DDP resistance of OSCC. Materials and Methods: Two kinds of human DDP-resistant cell lines (CAL-27R and SCC-9R) were developed from cisplatin-naive cell lines (CAL-27 and SCC-9, respectively) as in vitro cell models. Cell transfection was performed to overexpress or knockdown MALAT1 in these cells. Mouse xenograft models were also established. The following measurements were performed: cell proliferation, colony formation, wound healing, trans-well, and TUNEL assays, as well as Western blot and immunofluorescence staining. Results: DDP-resistant cells showed higher expression level of MALAT1 compared to cisplatin-naive cells. The overexpression of MALAT1 in cisplatin-naive cells enhanced DDP resistance and suppressed apoptosis in OSCC cells. However, the knockdown of MALAT1 in DDP-resistance cells induced apoptotic cell death and restored the sensitivity to DDP. Further analyses suggested that MALAT1 might promote DDP resistance via regulating P-glycoprotein expression, epithelial-mesenchymal transition process, and the activation of PI3K/AKT/m-TOR signaling pathway. Conclusion: MALAT1 might be a potential therapeutic target for the treatment of DDP-resistant OSCC.

BACKGROUND:Oral cancer (OC) is one of the most common cancers around the world. Despite the progress in treatment, the prognosis of OC remains poor, especially for patients with advanced diseases. It urges the development of novel therapeutic options against OC. Lycopene (LYC) is an antioxidant with chemoprotective properties against cancer. However, little is known about the mechanisms underlying the protective role of LYC in OC tumorigenesis.METHODS:In this study, we investigated the anti-cancer effect of LYC on the progression of OC in vitro and in vivo and explored the underlying mechanisms involved in this process.RESULTS:LYC inhibited OC cell proliferation, migration, invasion, apoptosis, and xenograft tumor growth in a dose-dependent manner. Furthermore, we found that LYC might inhibit epithelial-mesenchymal transition and induce apoptosis in OC cells by deactivating the PI3K/AKT/m-TOR signaling through increasing the levels of E-cadherin and Bax and downregulating N-cadherin, p-PI3K, p-AKT, p-m-TOR, and bcl-2.CONCLUSION:We reported for the first time that LYC exhibited anti-cancer effects on OC development both in vitro and in vivo via regulating EMT process and apoptosis. These findings provide support for the potential clinical use of LYC in OC treatment.

*These authors contributed equally to this work Background: Cisplatin (DDP) is the first-line chemotherapy agent for the treatment of oral squamous cell carcinoma (OSCC). The emergence of DDP resistance leads to diminished drug efficacy and survival benefit. lncRNA MALAT1 has been considered as one of the most important factors in OSCC. It has also been reported to enhance chemo-resistance in other kinds of carcinomas. However, little is known about the role of lncRNA MALAT1 in DDP resistance of OSCC. Materials and Methods: Two kinds of human DDP-resistant cell lines (CAL-27R and SCC-9R) were developed from cisplatin-naïve cell lines (CAL-27 and SCC-9, respectively) as in vitro cell models. Cell transfection was performed to overexpress or knockdown MALAT1 in these cells. Mouse xenograft models were also established. The following measurements were performed: cell proliferation, colony formation, wound healing, transwell, and TUNEL assays, as well as Western blot and immunofluorescence staining. Results: DDP-resistant cells showed higher expression level of MALAT1 compared to cisplatin-naïve cells. The overexpression of MALAT1 in cisplatin-naïve cells enhanced DDP resistance and suppressed apoptosis in OSCC cells. However, the knockdown of MALAT1 in DDP-resistance cells induced apoptotic cell death and restored the sensitivity to DDP. Further analyses suggested that MALAT1 might promote DDP resistance via regulating P-glycoprotein expression, epithelial–mesenchymal transition process, and the activation of PI3K/AKT/m-TOR signaling pathway. Conclusion: MALAT1 might be a potential therapeutic target for the treatment of DDPresistant OSCC.

*These authors contributed equally to this work Background: Oral cancer (OC) is one of the most common cancers around the world. Despite the progress in treatment, the prognosis of OC remains poor, especially for patients with advanced diseases. It urges the development of novel therapeutic options against OC. Lycopene (LYC) is an antioxidant with chemoprotective properties against cancer. However, little is known about themechanisms underlying the protective role of LYC in OC tumorigenesis. Methods: In this study, we investigated the anti-cancer effect of LYC on the progression of OC in vitro and in vivo and explored the underlying mechanisms involved in this process. Results: LYC inhibited OC cell proliferation, migration, invasion, apoptosis, and xenograft tumor growth in a dose-dependent manner. Furthermore, we found that LYC might inhibit epithelial–mesenchymal transition and induce apoptosis in OC cells by deactivating the PI3K/AKT/m-TOR signaling through increasing the levels of E-cadherin and Bax and downregulating N-cadherin, p-PI3K, p-AKT, p-m-TOR, and bcl-2. Conclusion: We reported for the first time that LYC exhibited anti-cancer effects on OC development both in vitro and in vivo via regulating EMT process and apoptosis. These findings provide support for the potential clinical use of LYC in OC treatment.

OBJECTIVE:To investigate the effect of recombinant human tumor necrosis factor alpha (rhTNF-α) on the osteogenesis potential of the osteo-induced human adipose-derived stromal cells (hASCs) in vitro.METHODS:hASCs at passage 4 were divided into four groups according to culturing conditions: basal medium [BM, DMEM + 10% FBS + antibiotics], BM with 10 μg/L rhTNF-α, osteogenic medium (OM, BM + dexamethasone + L-ascorbate + β-glycerophosphate) and OM with 10 μg/L rhTNF-α. On days 3, 7, 14 and 21, alkaline phosphatase (ALP) activities were examined. On days 14 and 21, the staining and quantitation of calcium deposition were performed. For the cells under osteogenic induction, osteoblast-related genes, such as core-binding factor α1 (Cbfa1), Osterix (Osx) and osteocalcin (OC) were analyzed with reverse transcription PCR on days 3, 7, 14, and 21, and real time PCR was performed to confirm the effect of rhTNF-α on genes expression on day 3 .RESULTS:rhTNF-α promoted ALP activities of induced hASCs on day 14 (3.527 ± 0.415 vs. 2.345 ± 0.354,P<0.01) and on day 21 (3.106 ± 0.105 vs. 2.442 ± 0.163,P<0.01) and promoted calcium deposition of induced hASCs on day 14 (2.896 ± 0.173 vs. 0.679 ± 0.173,P<0.01) and on day 21 (2.231 ± 0.233 vs. 1.729 ± 0.229, P<0.01). RT-PCR and Real-time PCR assays showed that rhTNF-α augmented the expression of Cbfa1, Osx and OC of these cells.CONCLUSION:The findings indicate that 10 μg/L rhTNF-α can promote the osteogenic potential of osteogenetically induced hASCs in vitro.

OBJECTIVE:To investigate the proliferation and the secretion of vascular endothelial growth factor(VEGF), fibroblast growth factor-2(FGF-2) and insulin-like growth factor-1(IGF-1) of human adipose tissue-derived stromal cells(hADSCs) before and after osteogenic differentiation under the stimuli of recombinant human tumor necrosis factor alpha (rhTNF-alpha).METHODS:hADSCs were obtained from human lipoaspirates. All the cells used were at passage four. The proliferation of hADSCs was measured with MTT assays 48, 72, 96 hours after being treated with 0, 1, 5, 10, 50 or 100 microg/L rhTNF-alpha respectively. The secretion of VEGF, FGF-2 and IGF-1 of the undifferentiated hADSCs under stimuli of rhTNF-alpha with the above 5 concentration grades was observed and the secretion of these 3 growth factors of hADSCs at different stages of osteogenic differentiation under stimuli of 10 microg/L rhTNF-alpha was also observed. All the supernatants were harvested for measuring after 24 hours' incubation with rhTNF-alpha. The secretion of VEGF, FGF-2 and IGF-1 was measured with ELISA, and the values were normalized to the cell number of the corresponding wells.RESULTS:The effect of rhTNF-alpha on the proliferation of hADSCs varied with the concentration and time. Compared with the control(0 microg/L), 10 microg/L rhTNF-alpha showed no suppression or acceleration on proliferation of hADSCs at hour 48, but significantly promoted the proliferation at hour 96 (0.903+/-0.042 vs 0.810+/-0.011, P<0.01), 100 microg/L rhTNF-alpha seemed to suppress the proliferation at hour 48 (0.317+/-0.024 vs 0.458+/-0.046, P<0.01), but appeared to promote it (0.956+/-0.030 vs 0.810+/-0.011, P<0.01) at hour 96. rhTNF-alpha(1, 5, 10, 50 and 100 microg/L) significantly increased VEGF, FGF-2 and IGF-1 production of hADSCs versus the control (0 microg/L) (P<0.01). After osteogenic differention, the secretion of the three growth factors of hADSCs (without rhTNF-alpha treated) was elevated with the days increasing. Under the stimulus of 10 microg/L rhTNF-alpha, the hADSCs after 1 day of osteogenic differentiation significantly increased the secretion of VEGF (P<0.01) compared with the group without rhTNF-alpha treated; after 3 and 7 days of osteogenic differentiation, the hADSCs significantly increased the secretion of VEGF (P<0.01), FGF-2 (P<0.05)and IGF-1 (P<0.05). However, after 14 days of osteogenic differentiation, 10 microg/L rhTNF-alpha appeared to suppress the production of VEGF (P<0.01), FGF-2 (P<0.05) and IGF-1 (P<0.05) of the differentiated hADSCs.CONCLUSION:Within certain concentration range, rhTNF-alpha can promote the proliferation of hADSCs and the production of VEGF, FGF-2 and IGF-1. The effect of 10 microg/L rhTNF-alpha on the production of VEGF, FGF-2 and IGF-1 of the differentiated hADSCs varied at different stages of osteogenic differentiation.

OBJECTIVE:To investigate the distribution of antimicrobial agent STR-1 of nanometer level which was incorporated with ball-grinding method in the polymethylmethacrylate (PMMA) denture base, and to study the release mode of silver ions from the base.METHODS:The distribution of the antimicrobial agent in the PMMA denture base containing STR-1 at concentrations of 0 g/L, 5 g/L, and 10 g/L was examined with scanning electronic microscopy. Then, PMMA resin bases containing STR-1 at the three concentrations were respectively immersed in artificial saliva at 37 degrees C for 54 days. The release of silver ions from the resin bases was surveyed with inductively coupled plasma-mass spectroscopy (ICP-MS) every 24 hours.RESULTS:The antimicrobial agent incorporated by ball-grinding method was even-distributed with individual particles of nanometer level in the PMMA resin base. The release of silver ions from the PMMA resin with antimicrobial agent was extremely slow during the test, a very small fraction of the silver ions released. At the beginning of the test, the release speed was extremely slow, the speed increased rapidly in the middle of the test, and at the end of the test, the speed returned to slow and steady. The cumulative release curve of silver ions was of "S" type.CONCLUSIONS:STR-1 can be even-distributed in the denture base, and the silver ions release from the base with extremely slow speed. It also indicates that biological safety and long-term antimicrobial efficacy of denture base containing silver-supported antimicrobial agents of nanometer level are possibly obtained based on their slow release of silver ions.

Objective: To study the durability of the antimicrobial effect of polymethylmethacrylate (PMMA) denture base containing silver-supported antimicrobial agents of nanometer level against Streptococcus mutans and Candida albicans in vitro. Methods:The antimicrobial PMMA resin bases with the antimicrobial agent STR-1 at concentration of 5 mg/ml were prepared. Then the samples were divided into 4 groups: positive control group, the group immersed in distilled water at 57 ℃ for 14 days, the group irradiated by ultraviolet for 8 hours, and the group irradiated by ultraviolet for 8 hours after immersed in distilled water at 57 ℃ for 14 days. Then the inhibition ratios of the 4 groups against Streptococcus mutans and Candida albicans in vitro were tested. Results:The inhibition ratios of the 4 groups against Streptococcus mutans were 99%, 96%, 98%, and 90% in turn. The inhibition ratios of the 4 groups against Candida albicans were 91%, 82%, 90%, and 80% respectively. Conclusion: The antimicrobial effect of PMMA denture base containing silver-supported antimicrobial agents STR-1 of nanometer level at concentration of 5 mg/ml against Streptococcus mutans and Candida albicans in vitro is durable.