scholarly journals High glucose improves healing of periodontal wound by inhibiting proliferation and osteogenetic differentiation of human PDL cells

2014 ◽  
Vol 13 (1) ◽  
pp. 39-43 ◽  
Author(s):  
Min Li ◽  
Cheng-Zhang Li
Keyword(s):  
High Glucose ◽  
Human Pdl Cells ◽  
Pdl Cells

Induction of IL-6 and IL-8 by activation of thermosensitive TRP channels in human PDL cells

2015 ◽  
Vol 60 (4) ◽  
pp. 526-532 ◽  
Author(s):  
Ga-Yeon Son ◽  
Jeong Hee Hong ◽  
Inik Chang ◽  
Dong Min Shin
Keyword(s):  
Trp Channels ◽  
Human Pdl Cells ◽  
Pdl Cells

scholarly journals Induction of Apoptotic Cell Death by Oral Streptococci in Human Periodontal Ligament Cells

2021 ◽  
Vol 12 ◽  
Author(s):  
Ok-Jin Park ◽  
A Reum Kim ◽  
Yoon Ju So ◽  
Jintaek Im ◽  
Hyun Jung Ji ◽  
...  
Keyword(s):  
Cell Death ◽  
Infectious Diseases ◽  
Periodontal Ligament ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Ros Production ◽  
Oral Streptococci ◽  
Human Pdl Cells ◽  
Pdl Cells ◽  
Induced Apoptosis

Initiation and progression of oral infectious diseases are associated with streptococcal species. Bacterial infection induces inflammatory responses together with reactive oxygen species (ROS), often causing cell death and tissue damage in the host. In the present study, we investigated the effects of oral streptococci on cytotoxicity and ROS production in human periodontal ligament (PDL) cells. Streptococcus gordonii showed cell cytotoxicity in a dose- and time-dependent manner. The cytotoxicity might be due to apoptosis since S. gordonii increased annexin V-positive cells, and the cytotoxicity was reduced by an apoptosis inhibitor, Z-VAD-FMK. Other oral streptococci such as Streptococcus mitis, Streptococcus sanguinis, and Streptococcus sobrinus also induced apoptosis, whereas Streptococcus mutans did not. All streptococci tested except S. mutans triggered ROS production in human PDL cells. Interestingly, however, streptococci-induced apoptosis appears to be ROS-independent, as the cell death induced by S. gordonii was not recovered by the ROS inhibitor, resveratrol or n-acetylcysteine. Instead, hydrogen peroxide (H2O2) appears to be important for the cytotoxic effects of streptococci since most oral streptococci except S. mutans generated H2O2, and the cytotoxicity was dramatically reduced by catalase. Furthermore, streptococcal lipoproteins are involved in cytotoxicity, as we observed that cytotoxicity induced by the lipoprotein-deficient S. gordonii mutant was less potent than that by the wild-type and was attenuated by anti-TLR2-neutralizing antibody. Indeed, lipoproteins purified from S. gordonii alone were sufficient to induce cytotoxicity. Notably, S. gordonii lipoproteins did not induce H2O2 or ROS but cooperatively induced cell death when co-treated with H2O2. Taken together, these results suggest that most oral streptococci except S. mutans efficiently induce damage to human PDL cells by inducing apoptotic cell death with bacterial H2O2 and lipoproteins, which might contribute to the progression of oral infectious diseases such as apical periodontitis.

Strontium promotes cell proliferation and suppresses IL-6 expression in human PDL cells

2012 ◽  
Vol 194 (2) ◽  
pp. 208-211 ◽  
Author(s):  
Piero Römer ◽  
Benjamin Desaga ◽  
Peter Proff ◽  
Andreas Faltermeier ◽  
Claudia Reicheneder
Keyword(s):  
Cell Proliferation ◽  
Human Pdl Cells ◽  
Pdl Cells

scholarly journals Collagen synthesis from human PDL cells following orthodontic tooth movement

1997 ◽  
Vol 19 (1) ◽  
pp. 29-37 ◽  
Author(s):  
A. Bumann ◽  
R. S. Carvalho ◽  
C. L. Schwarzer ◽  
E. H. K. Yen
Keyword(s):  
Collagen Synthesis ◽  
Tooth Movement ◽  
Orthodontic Tooth Movement ◽  
Human Pdl Cells ◽  
Pdl Cells

scholarly journals The Topographical Optimization of 3D Microgroove Pattern Intervals for Ligamentous Cell Orientations: In Vitro

2020 ◽  
Vol 21 (24) ◽  
pp. 9358
Author(s):  
Min Guk Kim ◽  
Chan Ho Park
Keyword(s):  
Computer Aided Design ◽  
High Surface ◽  
Root Surface ◽  
3D Scaffold ◽  
High Surface Quality ◽  
Human Pdl Cells ◽  
Pdl Cells ◽  
Wax Printing ◽  
Optimal Surface

Specific orientations of periodontal ligaments (PDLs) to tooth-root surface play an important role in offering positional stabilities of teeth, transmitting and absorbing various stresses under masticatory/occlusal loading conditions, or promoting tissue remodeling by mechanical stimulations to periodontal cells. However, it is still challenging to spatially control PDL orientations and collective PDL cell alignments using 3D scaffold architectures. Here, we investigated the optimization of scaffold topographies in order to control orientations of human PDL cells with predictability in in vitro. The 3D PDL-guiding architectures were designed by computer-aided design (CAD) and microgroove patterns on the scaffold surfaces were created with four different slice intervals such as 25.40 µm (μG-25), 19.05 µm (μG-19), 12.70 µm (μG-12), and 6.35 µm (μG-6) by the digital slicing step. After scaffold design and 3D wax printing, poly-ε-caprolactone (PCL) was casted into 3D printed molds and human PDL cells were cultured for 7 days. In the results, μG-25 with low vertical resolution can angularly organize seeded cells predictably rather than μG-6 created by the highest resolution for high surface quality (or smooth surface). Moreover, nuclear orientations and deformability were quantitatively analyzed and a significant correlation between microgroove pattern intervals and cell alignments was calculated for the topographic optimization. In conclusion, controllable microgroove intervals can specifically organize human PDL cells by 3D printing, which can create various surface topographies with structural consistence. The optimal surface topography (μG-25) can angularly guide human PDL cells, but 6.35 µm-thick patterns (μG-6) showed random organization of cell collectivity.

Heat shock protein 70 dampens the inflammatory response of human PDL cells to mechanical loading in vitro

2019 ◽  
Vol 54 (5) ◽  
pp. 481-488 ◽  
Author(s):  
Jana Marciniak ◽  
Stefan Lossdörfer ◽  
Christian Kirschneck ◽  
James Deschner ◽  
Andreas Jäger ◽  
...  
Keyword(s):  
Heat Shock ◽  
Inflammatory Response ◽  
Heat Shock Protein ◽  
Mechanical Loading ◽  
Heat Shock Protein 70 ◽  
Human Pdl Cells ◽  
Pdl Cells

PR 34 Cytotoxicity of resin modified glass ionomers on human PDL cells

1997 ◽  
Vol 23 (4) ◽  
pp. 275
Author(s):  
H. Makkawy ◽  
M. Lavin ◽  
S. Koka ◽  
N. Ewoldsen
Keyword(s):  
Human Pdl Cells ◽  
Pdl Cells

Nicotine-upregulated miR-30a arrests cell cycle in G1 phase by directly targeting CCNE2 in human periodontal ligament cells

2020 ◽  
Vol 98 (3) ◽  
pp. 354-361
Author(s):  
Lizheng Wu ◽  
Kuan Yang ◽  
Yajie Gui ◽  
Xiaojing Wang
Keyword(s):  
Cell Cycle ◽  
Periodontal Ligament ◽  
Luciferase Reporter ◽  
Pcr Analysis ◽  
Periodontal Ligament Cells ◽  
Periodontal Tissues ◽  
Human Pdl Cells ◽  
Pdl Cells ◽  
Reporter Assays

The consumption of nicotine via smoking tobacco has been reported to stimulate the occurrence and progression of periodontitis. Many studies have demonstrated that nicotine prevents the regeneration of periodontal tissues primarily by inhibiting the proliferation of human periodontal ligament (PDL) cells. However, the mechanisms underlying this process are still unclear. Therefore, we investigated whether nicotine-upregulated miR-30a inhibited the proliferation of human PDL cells by downregulating cyclin E2 (CCNE2), in vitro. Quantitative real-time PCR analysis revealed that nicotine upregulated the expression of miR-30a in human PDL cells. In addition, nicotine inhibited the proliferation of human PDL cells by inducing cell cycle arrest. To support this hypothesis, we showed that nicotine downregulated the expression of CCNE2 in human PDL cells, whereas inhibition of miR-30a restored CCNE2 expression that had been downregulated by nicotine. Furthermore, using luciferase reporter assays, we found that miR-30a directly interacts with the CCNE2 3′UTR. In conclusion, these findings indicate that nicotine-upregulated miR-30a inhibits the proliferation of human PDL cells by downregulating the expression of CCNE2.

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