Explore the vast range of titles available.

Regenerating periodontal ligament (PDL) tissue is a vital challenge in dentistry that aims to restore periodontal function and aesthetics. This study explores a tissue engineering strategy that combines polycaprolactone (PCL)/collagen/cellulose acetate electrospun scaffolds with collagen hydrogels to deliver curcumin-loaded ZIF-8 nanoparticles fand periodontal ligament stem cells (PDLSCs). Scaffolds were fabricated via electrospinningand collagen hydrogels incorporated PDLSCs and curcumin-loaded ZIF-8 nanoparticles (CURZIF-8) were developed using cross-linking. In vitro assays evaluated biocompatibility, anti-inflammatory, and antioxidative properties. In vivo efficacy was assessed in a rat PDL injury model using histological and ELISA analyses examining tissue regeneration and inflammatory cytokine modulation. In vitro studies demonstrated that the scaffolds effectively supported PDLSC viability and migration. CURZIF-8 hydrogels enhanced anti-inflammatory and antioxidative activities. In vivo study showed that the combined scaffold-hydrogel system significantly promoted PDL regeneration. Tissue levels of bFGF, HGF, and TGF-β that are crucial for tissue repair, angiogenesis, and cell proliferation were evaluated. Whereas, pro-inflammatory cytokines TNF-α and IL-6=were downregulated. Histological analysis confirmed the formation of organized PDL structures and improved bone-cementum integration that arekey indicators of successful periodontal regeneration. The developed scaffold-hydrogel system facilitates PDL regeneration by modulating inflammation and promoting pro-healing factor expression. This approach shows promise for advancing periodontal tissue engineering and warrants further investigation in clinical settings.

The selective in vitro expansion and differentiation of multipotent stem cells are critical steps in cell‐based regenerative therapies, while technical challenges have limited cell yield and thus affected the success of these potential treatments. The Rho GTPases and downstream Rho kinases are central regulators of cytoskeletal dynamics during cell cycle and determine the balance between stem cells self‐renewal, lineage commitment and apoptosis. Trans‐4‐[(1R)‐aminoethyl]‐N‐(4‐pyridinyl)cylohexanecarboxamidedihydrochloride (Y‐27632), Rho‐associated kinase (ROCK) inhibitor, involves various cellular functions that include actin cytoskeleton organization, cell adhesion, cell motility and anti‐apoptosis. Here, human periodontal ligament stem cells (PDLSCs) were isolated by limiting dilution method. Cell counting kit‐8 (CCK8), 5‐ethynyl‐2′‐deoxyuridine (EdU) labelling assay, cell apoptosis assay, cell migration assay, wound‐healing assay, alkaline phosphatase (ALP) activity assay, Alizarin Red S staining, Oil Red O staining, quantitative real‐time polymerase chain reaction (qRT‐PCR) were used to determine the effects of Y‐27632 on the proliferation, apoptosis, migration, stemness, osteogenic and adipogenic differentiation of PDLSCs. Afterwards, Western blot analysis was performed to elucidate the mechanism of cell proliferation. The results indicated that Y‐27632 significantly promoted cell proliferation, chemotaxis, wound healing, fat droplets formation and pluripotency, while inhibited ALP activity and mineral deposition. Furthermore, Y‐27632 induced PDLSCs proliferation through extracellular‐signal‐regulated kinase (ERK) signalling cascade. Therefore, control of Rho‐kinase activity may enhance the efficiency of stem cell‐based treatments for periodontal diseases and the strategy may have the potential to promote periodontal tissue regeneration by facilitating the chemotaxis of PDLSCs to the injured site, and then enhancing the proliferation of these cells and maintaining their pluripotency.

Metformin has shown outstanding anti-inflammatory and osteogenic abilities. Mesenchymal stem cell-derived extracellular vesicles (EVs) reveal promising therapeutic potency by carrying various biomolecules. This study explored the effects of metformin on the therapeutic potential of EVs derived from human periodontal ligament stem cells (PDLSCs) for periodontitis. PDLSCs were cultured in osteogenic medium with or without metformin, and the supernatant was then collected separately to extract EVs and metformin-treated EVs (M-EVs). After identifying the characteristics, we evaluated the anti-inflammatory and osteogenic effects of EVs and M-EVs in vivo and in vitro. Osteogenic differentiation of PDLSCs was markedly enhanced after metformin treatment, and the effect was dramatically inhibited by GW4896, an inhibitor of EVs’ secretion. Metformin significantly increased EVs’ yields and improved their effects on cell proliferation, migration, and osteogenic differentiation. Moreover, metformin significantly enhanced the osteogenic ability of EVs on inflammatory PDLSCs. Animal experiments revealed that alveolar bone resorption was dramatically reduced in the EVs and M-EVs groups when compared to the periodontitis group, while the M-EVs group showed the lowest levels of alveolar bone loss. Metformin promoted the osteogenic differentiation of PDLSCs partly through EVs pathway and significantly enhanced the secretion of PDLSCs-EVs with superior pro-osteogenic and anti-inflammatory potential, thus improving EVs’ therapeutic potential on periodontitis.

This study assessed the effects of photobiomodulation therapy (PBMT) with different laser wavelengths on the viability and differentiation of periodontal ligament mesenchymal stem cells (PDLMSCs) exposed to zoledronic acid (ZA). In this in vitro study, PDLMSCs were cultured with 5 µM ZA for 48 h and randomly assigned to 6 groups of positive and negative controls, and PBMT with 635 nm (2 and 4 J/cm 2 ) and 980 nm (2 and 4 J/cm 2 ) lasers. Cell viability was assessed by the methyl thiazolyl tetrazolium (MTT) assay after 24 and 72 h, and mineralized nodule formation was evaluated by Alizarin red staining. Mineralization was assessed by alkaline phosphatase (ALP) activity and expression analysis of osteocalcin (OCN), osteopontin (OPN), and RUNX2 by real-time polymerase chain reaction (PCR). Data were analyzed by one-way ANOVA and Tukey test (α = 0.05). ZA exposure in no-irradiation group decreased viability, ALP activity, mineralized nodule formation, and expression of osteogenic genes ( P  < 0.05). Cell viability in 980 nm (4 J/cm 2 ) group at 24 h and in 635 nm (4 J/cm 2 ) and 980 nm (2 and 4 J/cm 2 ) groups at 72 h was significantly higher than that in ZA group ( P  < 0.05). Mineralized nodule formation in both 980 nm groups was significantly higher than that in ZA group ( P  < 0.001). PBMT with 635 nm laser caused significant downregulation of OCN and OPN with 4 J/cm 2 and upregulation of OPN with 2 J/cm 2 ( P  < 0.05) energy density. PBMT with 980 nm laser (2 and 4 J/cm 2 ) caused significant upregulation of OCN, OPN, and RUNX2 ( P  < 0.05). PBMT with 980 nm laser (4 J/cm 2 ) in presence of ZA increased PDLMSC viability, ALP activity, mineralized nodule formation, and expression of osteogenic genes.

Fibroblast growth factor-2 (FGF-2) enhances the formation of new alveolar bone, cementum, and periodontal ligament (PDL) in periodontal defect models. However, the mechanism through which FGF-2 acts in periodontal regeneration in vivo has not been fully clarified yet. To reveal the action mechanism, the formation of regenerated tissue and gene expression at the early phase were analyzed in a beagle dog 3-wall periodontal defect model. FGF-2 (0.3%) or the vehicle (hydroxypropyl cellulose) only were topically applied to the defect in FGF-2 and control groups, respectively. Then, the amount of regenerated tissues and the number of proliferating cells at 3, 7, 14, and 28 days and the number of blood vessels at 7 days were quantitated histologically. Additionally, the expression of osteogenic genes in the regenerated tissue was evaluated by real-time PCR at 7 and 14 days. Compared with the control, cell proliferation around the existing bone and PDL, connective tissue formation on the root surface, and new bone formation in the defect at 7 days were significantly promoted by FGF-2. Additionally, the number of blood vessels at 7 days was increased by FGF-2 treatment. At 28 days, new cementum and PDL were extended by FGF-2. Moreover, FGF-2 increased the expression of bone morphogenetic protein 2 (BMP-2) and osteoblast differentiation markers (osterix, alkaline phosphatase, and osteocalcin) in the regenerated tissue. We revealed the facilitatory mechanisms of FGF-2 in periodontal regeneration in vivo. First, the proliferation of fibroblastic cells derived from bone marrow and PDL was accelerated and enhanced by FGF-2. Second, angiogenesis was enhanced by FGF-2 treatment. Finally, osteoblastic differentiation and bone formation, at least in part due to BMP-2 production, were rapidly induced by FGF-2. Therefore, these multifaceted effects of FGF-2 promote new tissue formation at the early regeneration phase, leading to enhanced formation of new bone, cementum, and PDL.

Emerging evidence has indicated that oxidative stress (OS) contributes to periodontitis. Periodontal ligament cells (PDLCs) are important for the regeneration of periodontal tissue. Quercetin, which is extracted from fruits and vegetables, has strong antioxidant capabilities. However, whether and how quercetin affects oxidative damage in PDLCs during periodontitis remains unknown. The aim of this study was to assess the effects of quercetin on oxidative damage in PDLCs and alveolar bone loss in periodontitis and underlying mechanisms. The tissue block culture method was used to extract human PDLCs (hPDLCs). First, a cell counting kit 8 (CCK-8) assay was used to identify the optimal concentrations of hydrogen peroxide (H O ) and quercetin. Subsequently, a 2,7-dichlorodihydrofluorescein diacetate (DCFH-DA) probe, RT-qPCR, Western blotting and other methods were used to explore the effects of quercetin on OS in hPDLCs and the underlying mechanism. Finally, quercetin was administered to mice with periodontitis through gavage, and the effect of quercetin on the level of OS and alveolar bone resorption in these mice was observed by immunofluorescence, microcomputed tomography (micro-CT), hematoxylin and eosin staining (H&E) staining and so on. Quercetin at 5 μM strongly activated NF-E2-related factor 2 (NRF2) signaling, alleviated oxidative damage and enhanced the antioxidant capacity of hPDLCs. In addition, quercetin reduced cellular senescence and protected the osteogenic ability of hPDLCs. Finally, quercetin activated NRF2 signaling in the periodontal ligaments, reduced the OS level of mice with periodontitis, and slowed the absorption of alveolar bone in vivo. Quercetin can increase the antioxidant capacity of PDLCs and reduce OS damage by activating the NRF2 signaling pathway, which alleviates alveolar bone loss in periodontitis.

This study aimed to investigate the cytotoxicity and apoptotic activity of different endodontic sealers: Sealapex, Apexit Plus, AH Plus, MTA-Fillapex and TotalFill BC Sealer in the culture of human periodontal ligament fibroblast (HPDLF) cells. The sealers were mixed, set for 24 h, and then covered with culture medium to obtain extracts, which were diluted to 1:0, 1:1, 1:2, 1:4, and 1:8. Simultaneously, HPDLF cells (1 × 10 4 ) were seeded in 96-well plates and incubated for 24 h at 37 °C 5% CO 2 conditions. The cells were then exposed to 100 µL of diluted extract medium. Cytotoxicity was evaluated using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay to check cell viability, while apoptosis was assessed by TUNEL assay. Statistical analyses were performed using Kruskal-Wallis and Dunn post hoc tests with Mann Whitney U. In MTT and TUNEL assay cells were treated with sealers both 24 and 72 h. All materials showed higher toxicity at 72 h compared to 24 h. AH Plus exhibited the highest cytotoxicity, followed by MTA-Fillapex, Apexit Plus, Sealapex, while TotalFill BC Sealer had the lowest cytotoxicity. Consuquently, it was considered that TotalFill BC Sealer had the lowest cytotoxic potency when compared to other sealers, so it can be considered biocompatible.

Aim Periodontitis can impair the osteogenic function of periodontal ligament stem cells (PDLSCs), thereby compromising their capacity for periodontal tissue regeneration. In this study, we explored the impact of a synthetic small molecule, DS96432529 (DS), on the osteogenic differentiation potential of PDLSCs and its underlying mechanism. Methods The viability of DS was assessed by cell proliferation assays and apoptosis analysis. Osteogenic potential was evaluated through alkaline phosphatase (ALP) activity staining and Alizarin Red S (ARS) staining for mineralized nodule formation. Inflammatory injury was induced using recombinant tumor necrosis factor-alpha (TNF-α). RNA sequencing analyzed signaling pathways involved in DS-enhanced osteogenic differentiation. Western blotting quantified key pathway protein expression. Specific small molecule inhibitors and agonists modulated relevant signaling pathways. Therapeutic efficacy was evaluated in a ligature-induced rat periodontitis model. Results DS inhibited cell proliferation at lower concentrations but did not induce significant apoptosis at concentrations up to 250 nM. Across tested concentrations, DS significantly enhanced ALP activity and accelerated mineralized nodule formation in PDLSCs. DS upregulated mitophagy-related protein expression under both inflammatory and non-inflammatory conditions. Additionally, DS restored TNF-α-inhibited ALP activity and attenuated TNF-α-induced activation of the RIG-I-like receptor (RLR) signaling pathway. The RIG-I activator Poly(I: C) counteracted DS-mediated repair of inflammatory injury during osteogenesis. Mitophagy inhibition diminished DS’s beneficial effects on osteogenic differentiation under inflammation and reduced its suppression of RIG-I expression. DS alleviated ligation-induced alveolar bone loss in rats with periodontitis. Conclusions DS enhances the osteogenic potential of PDLSCs in association with the activation of mitophagy-related processes. It mitigates inflammation-impaired osteogenesis, potentially via modulation of the RIG-I-mediated RLR signaling pathway, in association with increased mitophagy-related activity. DS represents a potent therapeutic small molecule for ameliorating periodontitis-induced bone loss.

Objective To explore the effects and underlying biological mechanisms of tetrahedral DNA nanostructures (TDNs) on the proliferation and osteogenic differentiation of periodontal ligament stem cells (PDLSCs). Materials and methods Real‐time cell analysis (RTCA) and CCK8 were used to screen the best concentration of TDN for PDLSCs. Cell proliferation and osteogenic differentiation were assessed after PDLSCs were treated with TDN. Data were analysed using one‐way ANOVA. Results Tetrahedral DNA nanostructures could play a crucial role in accelerating the proliferation of PDLSCs and had the strongest promotive effect on PDLSCs at a concentration of 250 nmol/L. Simultaneously, the osteogenic differentiation of PDLSCs could be promoted significantly by TDNs and the finding displayed that the Wnt/β‐catenin signalling pathway might be the underlying biological mechanisms of TDNs on promoting the osteogenic differentiation of PDLSCs. Conclusion Tetrahedral DNA nanostructure treatment facilitated the proliferation of PDLSCs, significantly promoted osteogenic differentiation by regulating the Wnt/β‐catenin signalling pathway. Therefore, TDNs could be a novel nanomaterial with great potential for application to PDLSC‐based bone tissue engineering.

Oral biofilms contribute to apical periodontitis, a major cause of tooth loss. This study evaluated the potential of an on-demand aqueous chlorine dioxide solution, “matching transformation system” (MA-T), as a safer alternative to conventional root canal irrigants. The antibacterial activity of MA-T was assessed against mono-species biofilms ( Enterococcus faecalis , Parvimonas micra , Fusobacterium nucleatum ), polymicrobial biofilms derived from human supragingival plaque, and an in vitro infected root canal model using E. faecalis . Antibacterial efficacy was evaluated using viable cell counting and confocal laser scanning microscopy (CLSM) to quantify the reduction in bacterial load. Biofilm mass was assessed by crystal violet (CV) staining. Cytotoxicity was evaluated by treating rat osteoblasts and human periodontal ligament fibroblasts with MA-T or NaOCl, followed by assessment of ATP levels and morphological integrity. MA-T eradicated planktonic bacteria, inhibited biofilm formation, and significantly reduced viable bacteria in established biofilms without affecting the total amount of biofilm biomass time-dependently. The infected root canal model showed a substantial decrease in bacterial load. Compared with NaOCl, MA-T-treated cells retained higher ATP levels and normal morphology. MA-T could be a promising root canal irrigant offering effective disinfection and superior biocompatibility, making it a potential alternative to traditional root canal irrigants as NaOCl.