scholarly journals Viability and volume of in situ bovine articular chondrocytes—changes following a single impact and effects of medium osmolarity

2005 ◽  
Vol 13 (1) ◽  
pp. 54-65 ◽  
Author(s):  
Peter G. Bush ◽  
Peter D. Hodkinson ◽  
Georgina L. Hamilton ◽  
Andrew C. Hall
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.


2006 ◽  
Vol 209 (2) ◽  
pp. 481-492 ◽  
Author(s):  
Mark J.P. Kerrigan ◽  
Corinne S.V. Hook ◽  
Ala' Qusous ◽  
Andrew C. Hall

2015 ◽  
Vol 656-657 ◽  
pp. 63-67
Author(s):  
Ai Wen Tan ◽  
Belinda Pingguan-Murphy ◽  
Roslina Ahmad ◽  
Sheikh Akbar

In situ TiO2 nanofiber arrays have been successfully produced directly on a Ti-6Al-4V substrate by using thermal oxidation under a limited supply of oxygen. Their morphology, elemental composition, crystal structure, surface roughness and surface wettability were characterized by field-emission scanning electron microscope (FESEM), energy-dispersive X-ray spectroscopy (EDX), X-ray diffractometer (XRD), atomic force microscope (AFM) and contact angle goniometer, respectively. The results of material characterization studies revealed that TiO2 nanofibers possessed greater surface roughness and wettability, as well as the degree of crystallinity. In vitro characterization have also been evaluated by using bovine articular chondrocytes on the resulting TiO2 nanofibrous surface at different time points. Cell adhesion was observed qualitatively by using FESEM and cell proliferation was determined quantitatively by using AlamarBlue reduction assay. The results showed that the TiO2 nanofibrous substrate triggers enhanced chondrocytes adhesion, proliferation, and production of extracellular matrix (ECM) fibrils compared to untreated substrate. These results suggest that the oxidation process produces a surface structure to which chondrocytes affinity, and thus this surface would has potential use in implants designed for cartilaginous applications.


1983 ◽  
Vol 212 (2) ◽  
pp. 517-520 ◽  
Author(s):  
D J Taylor ◽  
J R Yoffe ◽  
D E Woolley

The dose-response curve of histamine-induced cyclic AMP elevation in monolayer cultures of primary foetal-bovine articular chondrocytes was displaced to the right by cimetidine. In addition, H2 but not H1 antagonists prevented the histamine-induced cyclic AMP elevation, suggesting histamine activates chondrocyte adenylate cyclase through an H2 receptor.


2020 ◽  
Author(s):  
CR Coveney ◽  
L Zhu ◽  
J Miotla-Zarebska ◽  
B Stott ◽  
I Parisi ◽  
...  

AbstractMechanical forces are known to drive cellular signalling programmes in cartilage development, health, and disease. Proteins of the primary cilium, implicated in mechanoregulation, control cartilage formation during skeletal development, but their role in post-natal cartilage is unknown. Ift88fl/fl and AggrecanCreERT2 mice were crossed to create a cartilage specific inducible knockout mouse AggrecanCreERT2;Ift88fl/fl. Tibial articular cartilage thickness was assessed, through adolescence and adulthood, by histomorphometry and integrity by OARSI score. In situ cell biology was investigated by immunohistochemistry (IHC) and qPCR of micro-dissected cartilage. OA was induced by destabilisation of the medial meniscus (DMM). Some mice were provided with exercise wheels in their cage. Deletion of IFT88 resulted in a reduction in medial articular cartilage thickness (atrophy) during adolescence from 102.57μm, 95% CI [94.30, 119.80] in control (Ift88fl/fl) to 87.36μm 95% CI [81.35, 90.97] in AggrecanCreERT2;Ift88fl/fl by 8-weeks p<0.01, and adulthood (104.00μm, 95% CI [100.30, 110.50] in Ift88fl/fl to 89.42μm 95% CI [84.00, 93.49] in AggrecanCreERT2;Ift88fl/fl, 34-weeks, p<0.0001) through a reduction in calcified cartilage. Thinning in adulthood was associated with spontaneous cartilage degradation. Following DMM, AggrecanCreERT2;Ift88fl/fl mice had increased OA (OARSI scores at 12 weeks Ift88fl/fl = 22.08 +/− 9.30, and AggrecanCreERT2;Ift88fl/fl = 29.83 +/− 7.69). Atrophy was not associated with aggrecanase-mediated destruction or chondrocyte hypertrophy. Ift88 expression positively correlated with Tcf7l2 and connective tissue growth factor. Cartilage thickness was restored in AggrecanCreERT2;Ift88fl/fl by voluntary wheel exercise. Our results demonstrate that ciliary IFT88 regulates cartilage thickness and is chondroprotective, potentially through modulating mechanotransduction pathways in articular chondrocytes.


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