scholarly journals 3D-Printed Collagen-Based Waveform Microfibrous Scaffold for Periodontal Ligament Reconstruction

2021 ◽  
Vol 22 (14) ◽  
pp. 7725
Author(s):  
Hsu-Hsiang Lin ◽  
Pen-Hsiu Grace Chao ◽  
Wei-Chiu Tai ◽  
Po-Chun Chang
Keyword(s):  
Shear Stress ◽  
Periodontal Ligament ◽  
Ligament Reconstruction ◽  
Cyclin D ◽  
Functional Requirement ◽  
Functional Load ◽  
Pdl Cells ◽  
3D Printed ◽  
Adhesion Pattern ◽  
Gene Expression Levels

Reconstruction of the periodontal ligament (PDL) to fulfill functional requirement remains a challenge. This study sought to develop a biomimetic microfibrous system capable of withstanding the functional load to assist PDL regeneration. Collagen-based straight and waveform microfibers to guide PDL cell growth were prepared using an extrusion-based bioprinter, and a laminar flow-based bioreactor was used to generate fluidic shear stress. PDL cells were seeded on the respective microfibers with 0 or 6 dynes/cm2 fluidic shear stress for 1–4 h. The viability, morphology, adhesion pattern, and gene expression levels of PDL cells were assessed. The results revealed that upon bioprinting optimization, collagen-based microfibers were successfully fabricated. The straight microfibers were 189.9 ± 11.44 μm wide and the waveform microfibers were 235.9 ± 11.22 μm wide. Under 6 dynes/cm2 shear stress, PDL cells were successfully seeded, and cytoskeleton expansion, adhesion, and viability were greater. Cyclin D, E-cadherin, and periostin were upregulated on the waveform microfibers. In conclusion, 3D-printed collagen-based waveform microfibers preserved PDL cell viability and exhibited an enhanced tendency to promote healing and regeneration under shear stress. This approach is promising for the development of a guiding scaffold for PDL regeneration.

scholarly journals Autophagy facilitates type I collagen synthesis in periodontal ligament cells

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Tomomi Nakamura ◽  
Motozo Yamashita ◽  
Kuniko Ikegami ◽  
Mio Suzuki ◽  
Manabu Yanagita ◽  
...  
Keyword(s):  
Periodontal Ligament ◽  
Collagen Synthesis ◽  
Type I Collagen ◽  
Periodontal Diseases ◽  
Polyacrylamide Gel Electrophoresis ◽  
Sodium Dodecyl ◽  
Physiological Role ◽  
Type I ◽  
Periodontal Tissue ◽  
Pdl Cells

AbstractAutophagy is a lysosomal protein degradation system in which the cell self-digests its intracellular protein components and organelles. Defects in autophagy contribute to the pathogenesis of age-related chronic diseases, such as myocardial infarction and rheumatoid arthritis, through defects in the extracellular matrix (ECM). However, little is known about autophagy in periodontal diseases characterised by the breakdown of periodontal tissue. Tooth-supportive periodontal ligament (PDL) tissue contains PDL cells that produce various ECM proteins such as collagen to maintain homeostasis in periodontal tissue. In this study, we aimed to clarify the physiological role of autophagy in periodontal tissue. We found that autophagy regulated type I collagen synthesis by elimination of misfolded proteins in human PDL (HPDL) cells. Inhibition of autophagy by E-64d and pepstatin A (PSA) or siATG5 treatment suppressed collagen production in HPDL cells at mRNA and protein levels. Immunoelectron microscopy revealed collagen fragments in autolysosomes. Accumulation of misfolded collagen in HPDL cells was confirmed by sodium dodecyl sulfate–polyacrylamide gel electrophoresis. E-64d and PSA treatment suppressed and rapamycin treatment accelerated the hard tissue-forming ability of HPDL cells. Our findings suggest that autophagy is a crucial regulatory process that facilitates type I collagen synthesis and partly regulates osteoblastic differentiation of PDL cells.

scholarly journals Genetic correlates of wall shear stress in a patient-specific 3D-printed cerebral aneurysm model

2019 ◽  
Vol 11 (10) ◽  
pp. 999-1003 ◽  
Author(s):  
Michael R Levitt ◽  
Christian Mandrycky ◽  
Ashley Abel ◽  
Cory M Kelly ◽  
Samuel Levy ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Wall Shear Stress ◽  
Cerebral Aneurysm ◽  
Cell Morphology ◽  
Patient Specific ◽  
Parent Vessel ◽  
3D Printed ◽  
Wall Shear ◽  
Dynamics Simulations

ObjectivesTo study the correlation between wall shear stress and endothelial cell expression in a patient-specific, three-dimensional (3D)-printed model of a cerebral aneurysm.Materials and methodsA 3D-printed model of a cerebral aneurysm was created from a patient’s angiogram. After populating the model with human endothelial cells, it was exposed to media under flow for 24 hours. Endothelial cell morphology was characterized in five regions of the 3D-printed model using confocal microscopy. Endothelial cells were then harvested from distinct regions of the 3D-printed model for mRNA collection and gene analysis via quantitative polymerase chain reaction (qPCR.) Cell morphology and mRNA measurement were correlated with computational fluid dynamics simulations.ResultsThe model was successfully populated with endothelial cells, which survived under flow for 24 hours. Endothelial morphology showed alignment with flow in the proximal and distal parent vessel and aneurysm neck, but disorganization in the aneurysm dome. Genetic analysis of endothelial mRNA expression in the aneurysm dome and distal parent vessel was compared with the proximal parent vessels. ADAMTS-1 and NOS3 were downregulated in the aneurysm dome, while GJA4 was upregulated in the distal parent vessel. Disorganized morphology and decreased ADAMTS-1 and NOS3 expression correlated with areas of substantially lower wall shear stress and wall shear stress gradient in computational fluid dynamics simulations.ConclusionsCreating 3D-printed models of patient-specific cerebral aneurysms populated with human endothelial cells is feasible. Analysis of these cells after exposure to flow demonstrates differences in both cell morphology and genetic expression, which correlate with areas of differential hemodynamic stress.

scholarly journals STORAGE MEDIUM FOR AVULSED TEETH: A LITERATURE REVIEW

2021 ◽  
Vol 9 (08) ◽  
pp. 874-886
Author(s):  
Navpreet Kaur ◽  
Nikhil Srivastava ◽  
Vivek Rana ◽  
Noopur Kaushik ◽  
Tushar Pruthi
Keyword(s):  
Literature Review ◽  
Periodontal Ligament ◽  
Storage Medium ◽  
Avulsion Injury ◽  
Storage Media ◽  
Pdl Cells ◽  
Traumatic Dental Injuries ◽  
Dental Injuries

Avulsion injury is one of the most severe types of traumatic dental injuries. Following avulsion, periodontal ligament tissues are injured and the vessels and nerves of the pulp rupture at the apical foramen which causes pulp necrosis. In studies it was reported that the key to retention of the knocked-out teeth was to maintain the viability of the periodontal ligament. Storage media plays an important role in preserving the viability of PDL cells during extra alveolar time. This article highlights the different storage medias available for avulsed teeth, along with their merits and demerits.

scholarly journals Assessment of platelet-rich fibrin in the maintenance and recovery of cell viability of the periodontal ligament

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Lorena Bortolini Navarro ◽  
Fabiane Barchiki ◽  
Wilson Navarro Junior ◽  
Everdan Carneiro ◽  
Ulisses Xavier da Silva Neto ◽  
...  
Keyword(s):  
Cell Viability ◽  
Periodontal Ligament ◽  
Trypan Blue ◽  
Enzymatic Digestion ◽  
Type Ii ◽  
Platelet Rich Fibrin ◽  
Pdl Cells ◽  
Autologous Platelet ◽  
Number Of Cells ◽  
Group 1

AbstractThis study analyzed the efficacy of autologous platelet-rich fibrin (PRF) in maintaining and recovering cell viability of the periodontal ligament (PDL). The PDL cells were isolated from 45 extracted teeth randomly distributed among 6 groups: 5 min, 1 h, 2 h, PRF 30 min, PRF 1 h and PRF 2 h. In the groups 5 min, 1 h and 2 h (n = 5), the teeth were kept dry in extra-alveolar times of 5 min, 1 h and 2 h respectively. The teeth of the groups PRF 30 min, PRF 1 h and PRF 2 h (n = 10) were kept dry at extra-alveolar times of 30 min, 1 and 2 h followed by immersion in PRF for 45 min. PDL cells were isolated by enzymatic digestion with type II collagenase and dispase, counted and analyzed for viability with Trypan blue vital dye in Neubauer chamber. The variables total number of cells and cell viability demonstrated that in the 5 min, 1 h and 2 h groups there was a decrease after the extra-alveolar dry times of 1 and 2 h. In comparison with the total number of cells, group 1 h, considered immediate reimplantation, did not present statistical difference when compared to the groups PRF 30 min, PRF 1 h and 2 h, a result that demonstrates that PRF assists in cell maintenance and recovery. PRF provided increased cell viability in relation to the different dry extra-alveolar times analyzed (p < 0.001). Autologous PRF presented effectiveness in maintaining and recovering PDL cells from extracted teeth and kept dry for up to 2 h.

scholarly journals Extracellular Matrix Induces Periodontal Ligament Reconstruction In Vivo

2019 ◽  
Vol 20 (13) ◽  
pp. 3277 ◽  
Author(s):  
Naoko Nakamura ◽  
Ai Ito ◽  
Tsuyoshi Kimura ◽  
Akio Kishida
Keyword(s):  
Periodontal Ligament ◽  
Tooth Extraction ◽  
Ligament Reconstruction ◽  
Treatment Approach ◽  
Host Cells ◽  
The Matrix ◽  
Subrenal Capsule ◽  
Implant Treatment ◽  
Artificial Tooth

One of the problems in dental implant treatment is the lack of periodontal ligament (PDL), which supports teeth, prevents infection, and transduces sensations such as chewiness. The objective of the present study was to develop a decellularized PDL for supporting an artificial tooth. To this end, we prepared mouse decellularized mandible bone with a PDL matrix by high hydrostatic pressure and DNase and detergent treatments and evaluated its reconstruction in vivo. After tooth extraction, the decellularized mandible bone with PDL matrix was implanted under the subrenal capsule in rat and observed that host cells migrated into the matrix and oriented along the PDL collagen fibers. The extracted decellularized tooth and de- and re-calcified teeth, which was used as an artificial tooth model, were re-inserted into the decellularized mandible bone and implanted under the subrenal capsule in rat. The reconstructed PDL matrix for the extracted decellularized tooth resembled the decellularized mandible bone without tooth extraction. This demonstrates that decellularized PDL matrix can reconstruct PDL tissue by controlling host cell migration, which could serve as a novel periodontal treatment approach.

scholarly journals LPS fromP. gingivalisand Hypoxia Increases Oxidative Stress in Periodontal Ligament Fibroblasts and Contributes to Periodontitis

2014 ◽  
Vol 2014 ◽  
pp. 1-13 ◽  
Author(s):  
L. Gölz ◽  
S. Memmert ◽  
B. Rath-Deschner ◽  
A. Jäger ◽  
T. Appel ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Periodontal Ligament ◽  
Inflammatory Diseases ◽  
Periodontal Pathogen ◽  
Oral Diseases ◽  
Redox Systems ◽  
Periodontal Ligament Fibroblasts ◽  
Prolonged Incubation ◽  
Periodontal Tissues ◽  
Pdl Cells

Oxidative stress is characterized by an accumulation of reactive oxygen species (ROS) and plays a key role in the progression of inflammatory diseases. We hypothesize that hypoxic and inflammatory events induce oxidative stress in the periodontal ligament (PDL) by activating NOX4. Human primary PDL fibroblasts were stimulated with lipopolysaccharide fromPorphyromonas gingivalis(LPS-PG), a periodontal pathogen bacterium under normoxic and hypoxic conditions. By quantitative PCR, immunoblot, immunostaining, and a specific ROS assay we determined the amount of NOX4, ROS, and several redox systems. Healthy and inflamed periodontal tissues were collected to evaluate NOX4 and redox systems by immunohistochemistry. We found significantly increased NOX4 levels after hypoxic or inflammatory stimulation in PDL cells (P<0.001) which was even more pronounced after combination of the stimuli. This was accompanied by a significant upregulation of ROS and catalase (P<0.001). However, prolonged incubation with both stimuli induced a reduction of catalase indicating a collapse of the protective machinery favoring ROS increase and the progression of inflammatory oral diseases. Analysis of inflamed tissues confirmed our hypothesis. In conclusion, we demonstrated that the interplay of NOX4 and redox systems is crucial for ROS formation which plays a pivotal role during oral diseases.

Impact of nicotine on the interplay between human periodontal ligament cells and CD4+ T cells

2016 ◽  
Vol 35 (9) ◽  
pp. 983-990 ◽  
Author(s):  
Xin Ge ◽  
Ying-Feng Liu ◽  
Yong Wong ◽  
Li-Zheng Wu ◽  
Ling Tan ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cell Viability ◽  
Periodontal Ligament ◽  
Tobacco Consumption ◽  
Periodontal Ligament Cells ◽  
Nicotine Treatment ◽  
Pdl Cells ◽  
Induced Apoptosis ◽  
The Impact

Periodontitis is a common infectious disease associated with destruction of periodontal ligaments and alveolar bones. CD4+ T cell-mediated immune response is involved in the progression of periodontitis. Tobacco consumption increases the risk of periodontal disease. However, the impact of nicotine on the interaction between human periodontal ligament (PDL) cells and CD4+ T cells remains unrevealed. Our study aims to investigate the effect of nicotine on PDL cells and the cocultured CD4+ T cells. The PDL cell cultures were established by explants from healthy individuals, exposed to nicotine or α-bungarotoxin (α-BTX), and incubated solely or in combination with CD4+ T cells. Afterwards, cell viability, secreted cytokines, and matrix metalloproteinases (MMPs) were evaluated. In monoculture of PDL cells, nicotine dramatically repressed cell viability and increased apoptosis. Meanwhile, α-BTX largely reversed the nicotine-induced apoptosis and increased viability of PDL cells. Compared with the monoculture, MMP-1, MMP-3, interleukin (IL)-1β, IL-6, IL-17, and IL-21 in supernatant of cocultures were markedly elevated after treatment with nicotine. Moreover, α-BTX significantly attenuated nicotine-triggered production of these components either in mono- or co-cultures. In addition, PDL cell-derived CXCL12 following nicotine treatment recruited CD4+ T cells. Above all, nicotine deteriorated periodontitis partially by promoting PDL cell–CD4+ T cell-mediated inflammatory response and matrix degradation.

Clodronate Inhibits PGE2 Production in Compressed Periodontal Ligament Cells

2006 ◽  
Vol 85 (8) ◽  
pp. 757-760 ◽  
Author(s):  
L. Liu ◽  
K. Igarashi ◽  
H. Kanzaki ◽  
M. Chiba ◽  
H. Shinoda ◽  
...  
Keyword(s):  
Periodontal Ligament ◽  
Tooth Movement ◽  
Orthodontic Tooth Movement ◽  
Periodontal Ligament Cells ◽  
Prostaglandin E ◽  
Rankl Expression ◽  
Inhibitory Effects ◽  
Striking Increase ◽  
Pdl Cells ◽  
Cox 2

Periodontal ligament (PDL) cells play an essential role in orthodontic tooth movement. We recently reported that clodronate, a non-N-containing bisphosphonate, strongly inhibited tooth movement in rats, and thus could be a useful adjunct for orthodontic treatment. However, it is not clear how clodronate affects the responses of PDL cells to orthodontic force. In this study, we hypothesized that clodronate prevents the mechanical stress-induced production of prostaglandin E2 (PGE2), interleukin-1β (IL-1β), and nitric oxide (NO) in human PDL cells. A compressive stimulus caused a striking increase in PGE2 production, while the responses of IL-1β and NO were less marked. Clodronate concentration-dependently inhibited the stress-induced production of PGE2. Clodronate also strongly inhibited stress-induced gene expression for COX-2 and RANKL. These results suggest that the inhibitory effects of clodronate on tooth movement and osteoclasts may be due, at least in part, to the inhibition of COX-2-dependent PGE2 production and RANKL expression in PDL cells.

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