Oxygen and reactive oxygen species in cartilage degradation: friends or foes?
OBJECTIVE
This review is focused on the influence of oxygen and derived reactive species on chondrocytes aging, metabolic function and chondrogenic phenotype.


METHODS
A systematic computer-aided search of the Medline database.


RESULTS
Articular cartilage is an avascular tissue, and consequently oxygen supply is reduced. Although the basal metabolic functions of the cells are well adapted to hypoxia, the chondrocyte phenotype seems to be oxygen sensitive. In vitro, hypoxia promotes the expression of the chondrogenic phenotype and cartilage-specific matrix formation, indicating that oxygen tension is probably a key parameter in chondrocyte culture, and particularly in the context of tissue engineering and stem cells transplantation. Besides the influence of oxygen itself, reactive oxygen species (ROS) play a crucial role in the regulation of a number of basic chondrocyte activities such as cell activation, proliferation and matrix remodeling. However, when ROS production exceeds the antioxidant capacities of the cell, an "oxidative stress" occurs leading to structural and functional cartilage damages like cell death and matrix degradation.


CONCLUSIONS
This paper is an overview of the in vitro and in vivo studies published on the influence of oxygen and derived reactive species on chondrocyte aging, metabolic function, and the chondrogenic phenotype. It shows, that oxygen and ROS play a crucial role in the control of cartilage homeostasis and that at this time, the exact role of "oxidative stress" in cartilage degradation still remains questionable.
Henrotin
Y
Y
Bone and Cartilage Research Unit, University of Liège, Institute of Pathology, Level +5, CHU Sart-Tilman, 4000 Liège, Belgium. yhenrotin@ulg.ac.be
Kurz
B
B
Aigner
T
T
D000375:Aging / Q000502:physiology; D000975:Antioxidants / Q000378:metabolism; D002358:Cartilage, Articular / Q000378:metabolism / Q000503:physiopathology*; D016923:Cell Death; D019902:Chondrocytes / Q000378:metabolism / Q000502:physiology; D006801:Humans; D010003:Osteoarthritis / Q000503:physiopathology*; D018384:Oxidative Stress / Q000502:physiology; D010100:Oxygen / Q000502:physiology*; D010641:Phenotype; D017382:Reactive Oxygen Species / Q000378:metabolism*
D000975:Antioxidants; D017382:Reactive Oxygen Species; D010100:Oxygen