A Smart Window with Passive Radiative Cooling and Switchable Near-Infrared Light Transmittance via Molecular Engineering.

Smart windows with synergetic light modulation have heightened demands for applications in smart cars and novel buildings. However, improving the on-demand energy-saving efficiency is quite challenging due to the difficulty of modulating sunlight with a broad bandwidth in an energy-saving way. Herein, a smart window with switchable near-infrared light transmittance and passive radiative cooling is prepared via a monomer design strategy and photoinduced polymerization. The effects of hydrogen bonds and fluorine groups in acrylate monomers on the electro-optical properties as well as microstructures of polymer-dispersed liquid crystal films have been systematically studied. Some films show a high contrast ratio of 90.4 or a low threshold voltage (Vth) of 2.0 V, which can be roll-to-roll processed in a large area. Besides, the film has a superior indoor temperature regulation ability due to its passive radiative cooling and controllable near-infrared light transmittance properties. Its radiative cooling efficiency is calculated to be 142.69 W/m2 and NIR transmittance could be switched to below 10%. The introduction of a carboxylic monomer and fluorinated monomer into the system endows the film with a highly efficient temperature management capability. The film has great potential for applications in fields such as flexible smart windows, camouflage materials, and so on.

Circ_0087199 depletion attenuates lipopolysaccharides-induced human periodontal ligament cell injury through the miR-527/TLR4 axis.

BACKGROUND: Circular RNAs participate in the development of periodontitis. The present work aims to reveal the role and mechanism of circ_0087199 in human periodontal ligament cell (PDLC) injury during periodontitis. METHODS: PDLCs were treated with lipopolysaccharides (LPS) to establish a periodontitis cell model. Quantitative real-time polymerase chain reaction was used to detect the expression of circ_0087199, miR-527, toll-like receptor 4 (TLR4). Western blot analysis assay was performed to assess protein expression. Cell viability, proliferation, apoptosis and inflammation were investigated by cell counting kit-8, EdU assay, flow cytometry and enzyme-linked immunosorbent assay, respectively. Oxidative stress was evaluated by malondialdehyde assay kit and superoxide dismutase activity assay kit. The interaction between miR-527 and circ_0087199 or TLR4 was confirmed by a dual-luciferase reporter assay. RESULTS: Circ_0087199 and TLR4 expression levels were significantly increased, while miR-527 was decreased in the periodontal ligament tissues of periodontitis patients and LPS-stimulated PDLCs when compared with controls. LPS treatment inhibited cell viability and proliferation but induced cell apoptosis, inflammation and oxidative stress, whereas these effects were attenuated after circ_0087199 knockdown. Circ_0087199 bound to miR-527 and regulated LPS-caused PDLC damage by targeting miR-527. Additionally, the overexpression of TLR4, a target gene of miR-527, rescued miR-527 mimic-mediated effects on LPS-treated PDLCs. Further, the regulation of circ_0087199 toward TLR4 involved miR-527. CONCLUSION: Circ_0087199 knockdown attenuated LPS-induced apoptosis, inflammation and oxidative stress of PDLCs by regulating the miR-527/TLR4 pathway.

Knockdown of Bach1 protects periodontal bone regeneration from inflammatory damage.

Periodontal bone regeneration is a major challenge in the treatment of periodontitis. However, the regenerative vitality of periodontal ligament cells (PDLCs) declines in the environment of periodontitis and accompanying oxidative stress. This study aimed to investigate the functional mechanisms of Bach1, a transcriptional suppressor involved in oxidative stress response, and its regulation of PDLC osteogenesis under inflammatory conditions. We observed a significant elevation in Bach1 expression in periodontal tissues with periodontitis and PDLCs under inflammatory conditions. Knockdown of Bach1 alleviated the inflammation-induced oxidative stress level and partly offset the inhibitory effect of inflammatory conditions on osteogenesis, as well as the expression of osteogenic genes BMP6, OPG and RUNX2. Similarly, knockdown of Bach1 protects PDLCs from inflammatory damage to periodontal bone regeneration in vivo. Furthermore, we found that Bach1 could bind to the histone methyltransferase EZH2, and the binding increased under inflammatory conditions. Bach1 enhanced the ability of EZH2 to catalyse H3K27me3 on the promoter region of RUNX2 and BMP6, thus repressing the expression of osteoblastic genes. In conclusion, our study revealed that knockdown of Bach1 effectively rescued the osteogenesis and oxidative stress of PDLCs with inflammation. Bach1 could be a promising target for enhancing periodontal tissue regeneration under periodontitis conditions.

Construction of biomimetic cell-sheet-engineered periosteum with a double cell sheet to repair calvarial defects of rats.

Background: The periosteum plays a crucial role in the development and injury healing process of bone. The purpose of this study was to construct a biomimetic periosteum with a double cell sheet for bone tissue regeneration. Methods: In vitro, the human amniotic mesenchymal stem cells (hAMSCs) sheet was first fabricated by adding 50 â€‹µg/ml ascorbic acid to the cell sheet induction medium. Characterization of the hAMSCs sheet was tested by general observation, microscopic observation, live/dead staining, scanning electron microscopy (SEM) and hematoxylin and eosin (HE) staining. Afterwards, the osteogenic cell sheet and vascular cell sheet were constructed and evaluated by general observation, alkaline phosphatase (ALP) staining, Alizarin Red S staining, SEM, live/dead staining and CD31 immunofluorescent staining for characterization. Then, we prepared the double cell sheet. In vivo, rat calvarial defect model was introduced to verify the regeneration of bone defects treated by different methods. Calvarial defects (diameter: 4 â€‹mm) were created of Sprague-Dawley rats. The rats were randomly divided into 4 groups: the control group, the osteogenic cell sheet group, the vascular cell sheet group and the double cell sheet group. Macroscopic, micro-CT and histological evaluations of the regenerated bone were performed to assess the treatment results at 8 weeks and 12 weeks after surgery. Results: In vitro, hAMSCs sheet was successfully prepared. The hAMSCs sheet consisted of a large number of live hAMSCs and abundant extracellular matrix (ECM) that secreted by hAMSCs, as evidenced by macroscopic/microscopic observation, live/dead staining, SEM and HE staining. Besides, the osteogenic cell sheet and the vascular cell sheet were successfully prepared, which were verified by general observation, ALP staining, Alizarin Red S staining, SEM and CD31 immunofluorescent staining. In vivo, the macroscopic observation and micro-CT results both demonstrated that the double cell sheet group had better effect on bone regeneration than other groups. In addition, histological assessments indicated that large amounts of new bone had formed in the calvarial defects and more mature collagen in the double cell sheet group. Conclusion: The double cell sheet could promote to repair calvarial defects of rats and accelerate bone regeneration. The translational potential of this article: We successfully constructed a biomimetic cell-sheet-engineered periosteum with a double cell sheet by a simple, low-cost and effective method. This biomimetic periosteum may be a promising therapeutic strategy for the treatment of bone defects, which may be used in clinic in the future.

Circ_0099630 Participates in SPRY1-Mediated Repression in Periodontitis.

BACKGROUND: Periodontitis is chronic inflammation that causes damage to periodontal tissues and cementum. It has been reported that circular RNA hsa_circ_0099630 (circ_0099630) was overexpressed in gingival samples from patients with periodontitis. However, the function of circ_0099630 on the osteogenic differentiation of periodontal ligament cells (PDLCs) in periodontitis remains unclear. METHODS: Periodontal ligaments from patients with periodontitis and third molars (termed wisdom teeth) were utilised to isolate inflamed PDLCs (iPDLCs) and healthy PDLCs (hPDLCs). Expression levels of circ_0099630 in isolated PDLCs were assessed using reverse transcription quantitative polymerase chain reaction (RT-qPCR). Effects of circ_0099630 overexpression and silencing on iPDLC viability, proliferation, and cycle progression were determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), 5-ethynyl-2'-deoxyuridine (EdU), and flow cytometry assays. The osteogenic differentiation was detected by analysing the alkaline phosphatase (ALP) activity, mineralisation amount, and osteogenic markers osterix (OSX), ALP, and RUNX2 in iPDLCs. The regulatory mechanism of circ_0099630 was predicted by bioinformatics analysis and validated by dual-luciferase reporter, RNA immunoprecipitation, and RNA pull-down assays. RESULTS: Circ_0099630 was underexpressed in iPDLCs compared to hPDLCs. Overexpression of circ_0099630 repressed iPDLC proliferation and osteogenic differentiation, but circ_0099630 silencing exerted an opposing effect. Mechanically, circ_0099630 sponged miR-212-5p to block the inhibiting effect of miR-212-5p on SPRY1. Elevated expression of SPRY1 partly reversed the promoting effect of circ_0099630 knockdown on iPDLC proliferation and osteogenic differentiation. CONCLUSIONS: Circ_0099630 curbed PDLC proliferation and osteogenic differentiation through elevating SPRY1 expression via sponging miR-212-5p in periodontitis.

The circular RNA circ_0099630/miR-940/receptor-associated factor 6 regulation cascade modulates the pathogenesis of periodontitis.

Background/purpose: Periodontitis is one of the highly prevalent chronic inflammatory conditions in adults. The importance of circular RNAs (circRNAs) in the regulation of inflammation has been gradually reported in recent years, but the role of circRNA circ_0099630 in periodontitis has not been reported. Materials and methods: The contents of circ_0099630, microRNA-940 (miR-940) and tumor necrosis factor (TNF) receptor-associated factor 6 (TRAF6) were measured using quantitative real-time polymerase chain reaction (qRT-PCR) or Western blot. Inflammatory factor secretion, cell proliferation, and apoptosis were analyzed under the application of Enzyme-linked immunosorbent assay (ELISA), Cell Counting Kit-8 (CCK8), 5-ethynyl-2'-deoxyuridine (EdU) and flow cytometry, respectively. The Western blot also analyzed the phosphorylation levels of RELA proto-oncogene (P65) and IkappaBalpha (IκBα), key molecules of the nuclear factor kappa-B (NF-κB) pathway. The relationship between miR-940 and circ_0099630 or TRAF6 was verified by luciferase reporter system and RNA immunoprecipitation (RIP) assay. Results: Higher abundance of circ_0099630 and TRAF6 and lower miR-940 expression were observed in periodontitis, and circ_0099630 knockdown attenuated the damage of human PDL cells (PDLCs) induced by lipopolysaccharides (LPS). The relationship between miR-940 and circ_0099630 or TRAF6 was evidenced, while miR-940 downregulation diminished the repair effect of si-circ_0099630 on overexpression LPS-induced damage in PDLCs. Similarly, TRAF6 upregulation impaired the mitigating effect of miR-940 overexpression on LPS-induced injury in PDLCs. Circ_0099630 silencing evidently curbed the phosphorylation levels of P65 and IκBα and thus attenuating the inflammatory response by acting on the miR-940/TRAF6 axis. Conclusion: Silencing circ_0099630 alleviates LPS-induced periodontal ligament cell injury via targeting miR-940/TRAF6/NF-κB in periodontitis.

Pluripotency of periodontal ligament and dental pulp cells is induced by intercellular communication via the CDX2/Oct-4/Sox2 pathway.

Background: Intercellular communication in the environments of mature or aged cells can restore and regenerate their function and promote the expression of pluripotency markers. The regeneration of dental tissue is stimulated by periodontal ligament cells (PDLCs) and dental pulp cells (DPCs). However, the communication networks between the cells and their microenvironments are poorly understood. Methods: In this study, gene expression was analyzed by polymerase chain reaction, and chromatin immunoprecipitation assays, dual-luciferase assays, and electrophoretic mobility shift assays were used to analyze the signaling pathways associated with pluripotency after the knockdown or overexpression of caudal-type homeobox transcription factor 2 (CDX2). Results: Elevated levels of SRY-box transcription factor 2 (Sox2) and octamer-binding transcription factor 4 (Oct-4) were observed in the co-culture system, while the levels of CDX2 were significantly reduced. The overexpression of CDX2 promoted cell apoptosis and reduced the synthesis stage of the cell cycle. CDX2 was shown to bind directly to the promoter regions of Sox2 and Oct-4. The silencing of CDX2 promoted calcium deposition, adipogenic differentiation, and elevated alkaline phosphatase (ALP) activity in the DPCs. Conclusions: These findings demonstrate the enhancement of DPC and PDLC pluripotency by intercellular communication. CDX2 plays a significant part in the regulation of DPC and PDLC pluripotency via its regulation of Oct-4 and Sox2 expression.

Osteogenic capacity and cytotherapeutic potential of periodontal ligament cells for periodontal regeneration in vitro and in vivo.

BACKGROUND: The periodontal ligament cells (PDLCs) contain heterogeneous cell populations and possess stem-cell-like properties. PDLCs have attracted considerable attention as an option for periodontal regeneration. However, the osteogenic differentiation of PDLCs remains obscure owing to variable osteo-inductive methods and whether PDLCs could be directly used for periodontal regeneration without stem cell enrichment is uncertain. The aim of the present study was to clarify the osteogenic differentiation capacity of PDLCs and test PDLCs as an alternative to stem cells for periodontal regeneration. METHODS: We tested the performance of human PDLCs in osteo-inductive culture and transplantation in vivo while taking human bone marrow derived mesenchymal stem cells (hMSCs) as positive control. Proliferation of PDLCs and hMSCs in osteo-inductive condition were examined by MTT assay and colony formation assay. The osteogenic differentiations of PDLCs and hMSCs were assessed by Alkaline phosphatase (ALP) activity measurement, von Kossa staining, Alizarin red S staining and quantitative RT-PCR of osteogenic marker gene including RUNX2, ALP, OCN, Col I, BSP, OPN. We transplanted osteo-inductive PDLCs and hMSCs with hydroxyapatite/tricalcium phosphate (HA/TCP) scaffolds to immunodeficient mice to explore their biological behaviors in vivo by histological staining and immunohistochemical evaluation. RESULTS: After 14 days of osteo-induction, PDLCs exhibited significantly higher proliferation rate but lower colony-forming ability comparing with hMSCs. PDLCs demonstrated lower ALP activity and generated fewer mineralized nodules than hMSCs. PDLCs showed overall up-regulated expression of RUNX2, ALP, OCN, Col I, BSP, OPN after osteo-induction. Col I level of PDLCs in osteo-inductive group was significantly higher while RUNX2, ALP, OCN were lower than that of hMSCs. Massive fiber bundles were produced linking or circling the scaffold while the bone-like structures were limited in the PDLCs-loaded HA/TCP samples. The fiber bundles displayed strong positive Col I, but weak OCN and OPN staining. The in vivo results were consistent with the in vitro data, which confirmed strong collagen forming ability and considerable osteogenic potential of PDLCs. CONCLUSION: It is encouraging to find that PDLCs exhibit higher proliferation, stronger collagen fiber formation capacity, but lower osteogenic differentiation ability in comparison with hMSCs. This characteristic is essential for the successful periodontal reconstruction which is based on the synchronization of fiber formation and bone deposition. Moreover, PDLCs have advantages such as good accessibility, abundant source, vigorous proliferation and evident osteogenic differentiation capacity when triggered properly. They can independently form PDL-like structure in vivo without specific stem cell enrichment procedure. The application of PDLCs may offer a novel cytotherapeutic option for future clinical periodontal reconstruction.

Extracellular matrix derived from periodontal ligament cells maintains their stemness and enhances redifferentiation via the wnt pathway.

Large numbers of viable cells cannot be obtained from periodontal ligament tissues of patients with periodontitis. Therefore, it is imperative to establish an ex vivo environment that can support cell proliferation and delay senescence. Here, we have successfully reconstructed a native extracellular matrix (ECM), derived from early-passage human periodontal ligament cells (PDLCs) using the NH4 OH/Triton X-100 protocol. The ECM was investigated by scanning electron microscopy and immunostaining for specific ECM proteins (collagen I and fibronectin). Late-passage ECM-expanded PDLCs exhibited a much higher proliferation index and lower levels of reactive oxygen species (ROS), confirmed by the increased expression of pluripotent markers and enhanced osteogenic capacity. Interestingly, the Wnt pathway was suppressed during the ECM expansion-mediated increase in pluripotency, but was activated in an osteogenic differentiation environment, as confirmed by treatment with the XAV-939 ß-catenin inhibitor or the SP600125 c-Jun N-terminal kinase (JNK) inhibitor. Cell sheets formed by ECM-expanded PDLCs exhibited an enhanced periodontal tissue regeneration capacity compared to those formed on tissue culture polystyrene (TCP) surfaces in vivo. Taken together, the cell-free ECM provides a tissue-specific cell niche for the ex vivo expansion of PDLCs while retaining stemness and osteogenic potential, partially via the Wnt pathway. This represents a promising matrix for future applications in periodontal tissue regeneration therapy. © 2017 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 106A: 272-284, 2018.

C4orf7 modulates osteogenesis and adipogenesis of human periodontal ligament cells.

Periodontal ligament cells (PDLCs), which have potential for multilineage differentiation, are candidates for use in regeneration of periodontal tissue defects; however, our understanding of the mechanisms underlying the lineage commitment of PDLCs remains limited. C4orf7, which is specifically expressed in the periodontal ligament (PDL) tissue, may be crucial in deciding the fate of PDLCs and regulating the periodontal bone balance. In this study, we examined the expression of C4orf7 in PDL tissue, using immunohistochemical staining. We transfected PDLCs with lentiviral vectors expressing C4orf7 and examined the effect of C4orf7 on the balance of PDLC osteogenic and osteoclastogenic differentiation. Osteogenic induction resulted in the downregulation of mRNA and protein expression levels of the osteogenic/cementoblastic markers: ALP, RUNX2, COL1, OPN, OPG, OSX, IBSP, CAP, and CEMP1. Transfected cells also exhibited an increased RANKL/OPG ratio, which is an indicator of osteoclastogenic differentiation. ALP activity assays and Alizarin red staining confirmed the negative effect of C4orf7 on PDLC osteogenic differentiation. Finally, we investigated the effect of C4orf7 on the lineage commitment of PDLCs to adipocytes. We observed increased expression levels of PPARγ2, GLUT4, ZFP423, FABP4, and LPL mRNAs, as well as a gradual accumulation of lipid droplets in the C4orf7-overexpressing group compared with controls. In summary, our data confirm that C4orf7 has an important role in the regulation of periodontal bone remodeling through promotion of the adipogenic/osteoclastogenic, and inhibition of the osteogenic/cementoblastic, differentiation of PDLCs. Therefore, C4orf7 is a potential therapeutic target for the treatment of periodontal disease and other bone metabolic disorders.

MicroRNA expression profile of human periodontal ligament cells under the influence of Porphyromonas gingivalis LPS.

Periodontitis is a chronic inflammatory disease which is caused by bacterial infection and leads to the destruction of periodontal tissues and resorption of alveolar bone. Thus, special attention should be paid to the mechanism under lipopolysaccharide (LPS)-induced periodontitis because LPS is the major cause of periodontitis. However, to date, miRNA expression in the LPS-induced periodontitis has not been well characterized. In this study, we investigated miRNA expression patterns in LPS-treated periodontal ligament cells (PDLCs). Through miRNA array and differential analysis, 22 up-regulated miRNAs and 28 down-regulated miRNAs in LPS-treated PDLCs were identified. Seven randomly selected up-regulated (miR-21-5p, 498, 548a-5p) and down-regulated (miR-495-3p, 539-5p, 34c-3p and 7a-2-3p) miRNAs were examined by qRT-PCR, and the results proved the accuracy of the miRNA array. Moreover, targets of these deregulated miRNAs were analysed using the miRWalk database. Database for Annotation, Visualization and Integration Discovery software were performed to analyse the Gene Ontology and Kyoto Encyclopaedia of Genes and Genomes pathway of differential expression miRNAs, and the results shown that Toll-like receptor signalling pathway, cAMP signalling pathway, transforming growth factor-beta signalling pathway, mitogen-activated protein kinase (MAPK) signalling pathway and other pathways were involved in the molecular mechanisms underlying LPS-induced periodontitis. In conclusion, this study provides clues for enhancing our understanding of the mechanisms and roles of miRNAs as key regulators of LPS-induced periodontitis.

Osteogenesis induction of periodontal ligament cells onto bone morphogenic protein-2 immobilized PCL fibers.

The purpose of this study was to develop bone morphogenic protein-2 (BMP-2) immobilized PCL fibers to induce osteogenic differentiation of periodontal ligament cells (PDLCs). The PCL fiber surface was modified with heparin-dopamine (Hep-DOPA) (Hep-PCL) and further immobilized with BMP-2 (BMP-2/Hep-PCL). PCL fibers and surface-modified PCL fibers (Hep-PCL and BMP-2/Hep-PCL) were characterized by X-ray photoelectron spectroscopy (XPS) and contact angle. Osteogenic differentiation of PDLCs was demonstrated by alkaline phosphatase (ALP) activity, calcium deposition, and gene expression. The results of XPS and contact angle revealed that Hep-DOPA and BMP-2 were successfully immobilized onto the PCL surface and that the BMP-2/Hep-PCL fibers have more hydrophilic surface properties than PCL fibers alone. ALP activity, calcium deposition, and gene expression on BMP-2/Hep-PCL fibers showed significantly induced osteogenic differentiation relative to PCL fibers. Therefore, we suggest that BMP-2/Hep-PCL fibers have the potential to effectively induce osteogenic differentiation of PDLCs.

Transplantation of stem cell-preseeded dentin slices incorporated with periodontal ligament cell sheets from beagle dog into nude mice / 实用口腔医学杂志

Objective:To observe the effects of dentin proseeded with BMSCs or PDLCs incorporated with PDLCs sheets and calci-nated ceramic bovine bone(CBB)in the reconstruction of periodontal tissue.Methods:Root dentin slices were prepared and pre-seeded with BMSCs or PDLCs from beagle dog.After cultivated in osteoinduction medium(OST groups)orα-modified eagle's medi-um(MEM groups)for 3 weeks,the dentin slices observed by scanning electron microscope (SEM).Then the slices were wrapped successively with PDLCs sheets and CBB as new constructs(BMSCs or PDLCs/dentin/PDLCs sheets/CBB).The new constructs were transplanted into nude mice subcutaneously,8 week after transplantation,samples were havested and examined by HE staining.Re-sults:Enough cells and extracellular matrices were detected on the dentin slices by SEM in vitro.A little new immature cementum-like tissue without periodontal-like tissue on the surface of the new construcs was observed in OST groups.By contrast,in MEM groups,periodontal-like without immature cementum-like tissue formation was observed.Conclusion:Dentin proseeded with BMSCs or PDLCs incorporated with PDLCs sheets and CBB cultured by MEM can promote periodontal-like tissue regeneration.Cultured with osteooinduction medium can promote cementum-like tissue regeneration.

Comparison of the properties of human CD146+ and CD146- periodontal ligament cells in response to stimulation with tumour necrosis factor α.

OBJECTIVES: Periodontal ligament stem cells (PDLSCs) can be used in periodontal regeneration. Tumour necrosis factor-alpha (TNF-α) participates in the regulation of cell proliferation, apoptosis, differentiation, and migration. However, whether TNF-α can affect the biological features of PDLSCs is still unclear. The objective of this study was to illustrate the biological effects (proliferation, apoptosis, osteogenesis and migration) of TNF-α on human CD146 positive periodontal ligament cells (CD146+PLDCs) and CD146 negative periodontal ligament cells (CD146-PDLCs). METHODS: CD146±PDLCs were isolated from human PDLCs and analyzed using a fluorescence-activated cell sorter. The biological effects of TNF-α on CD146±PDLCs were evaluated by CCK-8 assay (proliferation), DAPI staining (apoptosis), alizarin red staining and alkaline phosphatase activities assay (osteogenesis), and wounding assay and transwell assay (migration). RESULTS: CD146+PDLCs, which expressed MSC surface markers CD105, CD90, CD73, CD44, and Stro-1, showed higher proliferative and osteogenic potential than CD146-PDLCs. TNF-α at a dose of 2.5ng/ml was found to enhance both proliferation and osteogenesis in CD146+PDLCs. At 5ng/ml, TNF-α promoted proliferation, osteogenesis, and apoptosis in CD146+PDLCs and enhanced osteogenesis in CD146-PDLCs. At 10ng/ml, TNF-α only aggravated apoptosis in CD146+PDLCs. The migratory ability of both CD146+PDLCs and CD146-PDLCs was not altered by TNF-α. CONCLUSIONS: CD146+PDLCs were subpopulation of MSC. It showed greater proliferative and osteogenic potential than CD146-PDLCs. At low concentration, TNF-α was beneficial to CD146+PDLCs on proliferation and osteogenesis, and at high concentration it was detrimental. CD146-PDLCs were found to be less sensitive to TNF-α.

Advances in cytomechanics in orthodontic tooth movement / 医用生物力学

In recent years, great development has been made in cytomechanics in orthodontic tooth movement（OTM）.The essential role of periodontal ligament in OTM has been widely accepted. The in vitro models have become an important way to reveal the biological mechanism in OTM,largely based on periodontal ligament cells(PDLCs), as well as other cells, including bone marrow mesenchymal stem cells, osteoblast, cementoblast and myoblast.The in vitro models have been renovated from the traditional ways stressing the 2D cultured cells by deformation of the bottom,gravity, hydrostatic pressure or centrifugation, to the establishment of various novel models loading mechanical stimulation on cells 3D cultured in bioscaffolds. The molecular expression involved in the osteoblastic differentiation and osteoclastogenesis induction in the bone remodeling cycle has drawn great attention, and will continue to be a focus of study. Furthermore, with the identification of periodontal ligament stem cells(PDLSCs), the cytomechanics involved in OTM and periodontitis, will undoubtedly be a promising new direction.

The effects of nicotine on the proliferation and fibronectin synthesis of human periodontal ligament cells cultured in vitro / 实用口腔医学杂志

Objective:To observe the effects of nicotine on the proliferation and fibronectin(Fn) synthesis of human periodontal ligament cells(PDLCs) cultured in vitro,and to investigate the mechanism of the effects of smoking on the periodontitis.Methods:PDLCs were cultured in the presence of nicotine at various concentrations,the proliferation of cells was measured by MTT chromatometry,and the synthesis of Fn was measured by ELISA and reverse transcription-polymerase chain reaction(RT-PCR).Results:①MTT chromatometry:Nicotine inhibited the proliferation of PDLCs obviously(P