Porphyromonas gingivalis can invade periodontal ligament stem cells

Chen

Journal of Applied Biomaterials & Functional Materials

et al. 2020

Simvastatin (SIM) has been documented to induce the osteogenic differentiation of periodontal ligament stem cells (PDLSCs). To establish an efficient release system for periodontal regeneration, a polycaprolactone (PCL) membrane scaffold containing SIM was electrospun and evaluated. The obtained PCL–SIM membrane scaffold showed sustained release up to 28 days, without deleterious effect on proliferation of PDLSCs on the scaffolds. PDLSCs were seeded onto scaffolds and their osteogenic differentiation was evaluated. After 21 days, expressions of collagen type I, alkaline phosphatase and bone sialoprotein genes were significantly upregulated and mineralized matrix formation was increased on the PCL–SIM scaffolds compared with the PCL scaffolds. In a heterotopic periodontal regeneration model, a cell sheet–scaffold construct was assembled by placement of multilayers of PDLSC sheets on PCL or PCL–SIM scaffolds, and these were then placed between dentin and ceramic bovine bone for subcutaneous implantation in athymic mice. After 8 weeks, the PCL–SIM membrane showed formation of significantly more ectopic cementum-like mineral on the dentin surface. These findings demonstrated that the PCL–SIM membrane scaffold promotes cementum-like tissue formation by sustained drug release, suggesting the feasibility of its therapeutic use with PDLSC sheets to improve periodontal regeneration.

Section: Resultssupporting

confidence: 86%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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A simvastatin-releasing scaffold with periodontal ligament stem cell sheets for periodontal regeneration

Chen

Journal of Applied Biomaterials & Functional Materials

et al. 2020

“…hPDLCs were prepared according to previously published protocols. 22 In brief, the extracted teeth were placed immediately (within 2 h) in phosphate-buffered saline (PBS) (HyClone, South Logan, UT, USA) with 2% penicillin/streptomycin, and the periodontal ligament tissue in 1/3 of the root was scraped with a scalpel and cut into small pieces of 1 mm 3 in a 25 mL cell culture flask. The flask was turned upside down with 5 mL of α-MEM (HyClone) medium containing 10% fetal bovine serum (FBS) and 1% penicillin/streptomycin at 37°C in a 5% CO 2 humidified incubator for 4 h, and then the flask was turned over and cultured.…”

Section: Methodsmentioning

confidence: 99%

Quercetin Prevents Oxidative Stress-Induced Injury of Periodontal Ligament Cells and Alveolar Bone Loss in Periodontitis

Yu¹,

Fu²,

Wu³

et al. 2021

DDDT

Purpose 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. Materials and Methods 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 2 O 2 ) 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. Results 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. Conclusion 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.

“…TEM images show that P. gingivalis adheres to the hGF cell membrane and induces clear invagination and ruffles ( Figure 2C ), which is a precursor of endocytosis. 30 This change was barely observed in the 15-P-S+ P. g group, but structures resembling endocytic vesicles (yellow arrows) were observed. These data suggest that PSC-SPIONs prevent the entry of P. gingivalis into hGFs.…”

Section: Resultsmentioning

confidence: 93%

Superparamagnetic Iron Oxide Nanoparticles Protect Human Gingival Fibroblasts from Porphyromonas gingivalis Invasion and Inflammatory Stimulation

Chen

Zhang

Qin

et al. 2022

IJN

Introduction:Modulating the inflammatory response of human gingival fibroblasts (hGFs) is important for the control of periodontal inflammation because it is a key event in the pathogenesis of periodontitis. Here, we aimed to determine whether polyglucose sorbitol carboxymethyl ether (PSC)-coated superparamagnetic iron oxide nanoparticles (SPIONs) protect hGFs against invasion and inflammatory stimulation by Porphyromonas gingivalis (P. gingivalis). Methods: First, we determined the cytotoxicity and antimicrobial activity of PSC-SPIONs. Then, their effects on invasion of hGFs by P. gingivalis were evaluated by counting invading P. gingivalis, fluorescence staining, and transmission electron microscopy. The effect of PSC-SPIONs on inflammation in hGFs induced by P. gingivalis lipopolysaccharide was evaluated by measurement of reactive oxygen species (ROS), and enzyme-linked immunosorbent assays, quantitative reverse transcription-polymerase chain reaction, and Western blotting of key indicator molecules. The effects of dimercaptosuccinic acid (DMSA)-coated SPIONs and the free form of PSC alone were also tested and compared with those of PSC-SPIONs. Results: PSC-SPIONs (25 μg/mL) are cytocompatible with hGFs and exhibit no antimicrobial effects on P. gingivalis. However, they inhibit invasion of hGFs by P. gingivalis at 15 μg/mL. They also decrease ROS production and inflammatory cytokine secretion by hGFs at 5, 15, and 25 μg/mL, by downregulating activation of the nuclear factor-kappa B signaling pathway. Furthermore, PSC alone does not inhibit inflammation, while DMSA-SPIONs do. This indicates that the nanosize effects of PSC-SPIONs, rather than their coating material, play the dominant role in their anti-inflammatory activity. Conclusion: PSC-SPIONs protect hGFs against P. gingivalis invasion and inflammatory stimulation. Thus, they have potential for clinical application in control of periodontal inflammation.