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Abstract
The metabolism of cells in articular joint tissues in normal and pathological conditions
is subject to a complex environmental control. In addition to soluble mediators such
as cytokines and growth factors, as well as mechanical stimuli, reactive oxygen species
(ROS) emerge as major factors in this regulation. ROS production has been found to
increase in joint diseases, such as osteoarthritis and rheumatoid arthritis, but their
role in joint diseases initiation and progression remains questionable.
This review is focused on the role of ROS, mainly nitric oxide, peroxynitrite and
superoxide anion radicals, in the signaling mechanisms implied in the main cellular
functions, including synthesis and degradation of matrix components. The direct effects
of ROS on cartilage matrix components as well as their inflammatory and immunomodulatory
effects are also considered.
Some intracellular signaling pathways are redox sensitive and ROS are involved in
the regulation of the production of some biochemical factors involved in cartilage
degradation and joint inflammation. Further, ROS may cause damage to all matrix components,
either by a direct attack or indirectly by reducing matrix components synthesis, by
inducing apoptosis or by activating latent metalloproteinases. Finally, we have highlighted
the uncoupling effect of ROS on tissue remodeling and synovium inflammation, suggesting
that antioxidant therapy could be helpful to treat structural changes but not to relieve
symptoms.
This review of the literature supports the concept that ROS are not only deleterious
agents involved in cartilage degradation, but that they also act as integral factors
of intracellular signaling mechanisms. Further investigation is required to support
the concept of antioxidant therapy in the management of joint diseases.