Lidocaine cytotoxicity to the bovine articular chondrocytes in vitro: changes in cell viability and proteoglycan metabolism

2011 ◽  
Vol 19 (7) ◽  
pp. 1198-1205 ◽  
Author(s):  
Tsuyoshi Miyazaki ◽  
Shigeru Kobayashi ◽  
Kenichi Takeno ◽  
Takafumi Yayama ◽  
Adam Meir ◽  
...  
2014 ◽  
Vol 575 ◽  
pp. 219-222
Author(s):  
A.W. Tan ◽  
Belinda Pingguan-Murphy ◽  
Roslina Ahmad ◽  
Sheikh Akbar

Titania nanofiber (TiO2 NFs) arrays were fabricated in situ on a Ti-6Al-4V substrate by an oxidation process. Their surface morphology, crystallographic structure, surface roughness and wettability were characterized, as well as their in vitro interaction with bovine articular chondrocytes at different time points. Results showed that TiO2 NFs possessed greater surface roughness, hydrophilicity and degree of crystallinity. The in vitro cell studies revealed that TiO2 NFs substrate triggers enhanced cell adhesion, proliferation and extracellular matrix (ECM) formation compared to the untreated control sample. These results showed that chondrocytes have an affinity to the nanofibrous substrate surface and thus we suggest that such surfaces are suited to be used as an implant designed for cartilage growth.


Author(s):  
Constance R. Chu ◽  
Nicholas J. Izzo ◽  
Nicole E. Papas ◽  
Freddie H. Fu

1981 ◽  
Vol 22 (3) ◽  
pp. 499-511 ◽  
Author(s):  
D. Mitrovic ◽  
L. Lippiello ◽  
F. Gruson ◽  
F. Aprile ◽  
H.J. Mankin

2017 ◽  
Vol 44 (4) ◽  
pp. 1282-1294 ◽  
Author(s):  
Taitao Sun ◽  
Xianjun Li ◽  
Hua Song ◽  
Fei Gao ◽  
Guannan Zhou ◽  
...  

Background/Aims: Osteoarthritis (OA) as a degenerative disease is a major problem in ageing populations. To better understand the molecular mechanisms in the pathogenesis of OA, this study explored the role of microRNA (miR)-146a in the articular chondrocytes. Methods: The articular chondrocyte line ATDC5 was used to simulate inflammatory injury by LPS administration in vitro. Cell viability, apoptosis, mRNA expressions and productions of inflammatory factors were assessed, respectively. Mir-146a and Cxcr4 mRNA expressions were measured by qRT-PCR. Targeting effect of miR-146a on Cxcr4 3’UTR was assessed by luciferase activity analysis. Protein expression levels of CXCR4 and main factors in PI3K/AKT, Wnt/β-catenin signal pathways were measured by western blotting. Results: LPS exposure suppressed cell viability, prompted apoptosis of ATDC5 cells, and stimulated expression and release of inflammatory factors. MiR-146a was upregulated in LPS-induced cells. Overexpression of miR-146a further aggravated LPS-induced inflammatory injury, while it was reduced after miR-146a was knocked down. CXCR4 expression was negatively regulated by miR-146a. CXCR4 was a direct target of miR-146a and thus involved in regulatory effect of miR-146a on the injured chondrocytes, which was also related with phosphorylation levels of PI3K/AKT and expressions of Wnt/β-catenin signal factors. Conclusion: miR-146a promoted inflammatory response of articular chondrocytes via targeting CXCR4 and suppressing CXCR4 expression. Overexpression of CXCR4 could attenuate the inflammatory injury. Our findings provided novel evidence which might be useful for further studies exploring therapeutic approaches for OA via targeting miR-146a.


2007 ◽  
Vol 35 (10) ◽  
pp. 1622-1627 ◽  
Author(s):  
John C. Karpie ◽  
Constance R. Chu

Background Intra-articular lidocaine is commonly used. Purpose This study was conducted to determine whether short-term exposures to 1% and 2% lidocaine are toxic to articular chondrocytes, whether this is due to pH, and whether an intact articular surface is protective. Study Design Controlled laboratory study. Methods Fresh bovine articular chondrocytes in alginate bead cultures were treated with 1% or 2% lidocaine or buffered saline (pH 7.4, 7.0, and 5.0) for 15, 30, or 60 minutes. Chondrocytes were then analyzed for viability by flow cytometry 1 hour, 1 day, and 1 week later. Bovine osteochondral cores with and without the superficial 1 mm of cartilage removed were submerged in either 0.9% saline (pH 7.4) or in 1% or 2% lidocaine for 30 minutes and assessed for viability using fluorescent microscopy. Results Chondrocyte viability decreased after just 15-minute exposures to 1% lidocaine. Longer exposures to 1% and 2% lidocaine further reduced chondrocyte viability. Chondrotoxicity of 2% lidocaine was greater than 1% lidocaine. There was no difference in chondrocyte viability after exposures to saline solutions of pH 7.4, 7.0, or 5.0. An intact articular surface did not affect lidocaine's chondrotoxic effects. Conclusion Results show dose- and time-dependent cytotoxic effects of lidocaine on bovine articular chondrocytes. Reduction of pH alone did not decrease chondrocyte viability, and the intact articular surface was not protective. Clinical Relevance Although lidocaine chondrotoxicity was less than previously reported with bupivacaine, these observations suggest that local anesthetics as a class of drugs may negatively affect articular cartilage.


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