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A new research paper proves that chondroitin sulphate inhibits angiogenesis, a mechanism of action involved in the rapid progression of osteoarthritis

8 Jun 2012

The uncontrolled formation of new blood vessels in the synovial membrane (angiogenesis) may increase joint inflammation. Inflammation is associated to loss of cartilage tissue and pain, which causes rapid progression of the disease.

Osteoarthritis has been perceived for many years as an
aging-associated disease. However, recent studies such as the research paper
published in Arthritis Research and Therapy journal whose main author is
Professor Yves Henrotin, (Director of the Bone and Cartilage Research Unit at
the University of Liège, Belgium), confirmed that inflammation of synovial
membrane (synovitis) is directly involved in the onset and progression of
osteoarthritis. A high degree of inflammation has been linked to an increase in
pain and loss of cartilage, and therefore to a rapid progression of the

To be more precise, explains profesor Henrotin, “the novel
aspect of our research is that we observed that uncontrolled formation of new
blood vessels in the synovial membrane leads to a more accelerated progression
of the disease”. The in vitro study compared inflammation and
angiogenesis in knee osteoarthritis and synovitis patients. There were
extracted synovial tissue samples from 16 patients undergoing prosthetic
surgery. Some of these samples were cultured in a growth medium containing
chondroitin sulphate.

The results, presented for the first time during the
European Congress of Rheumatology that has been held recently in Berlin,
Germany, concluded that chondroitin sulphate inhibit angiogenesis, and
therefore reduce inflammation. Researchers have therefore confirmed the results
of the GAIT clinical test published in 2006 by the prestigious New England
Journal of Medicine
, which suggested that chondroitin sulphate reduce
synovial membrane inflammation in knee osteoarthritis patients.

Since angiogenesis is a critical mechanism for the
progression of osteoarthritis, this paper opens the way to the design of new and
efficient treatments for that disease. These new treatments will be translated,
in clinical practice, into improved pain and mobility of the affected joints.

Also during the EULAR 2012 Congress, professor
Jean-Pierre Pelletier, Director of the Unit in Osteoarthritis research at the
University of Móntréal (Canada) contributed an additional insight which lend further
support to Professor Henrotin findings. Professor Pelletier ensured that
chondroitin sulphase “protects from cartilage volume loss, thus reducing the
need for prostatic surgery for knee osteoarthritis and synovitis patients”

Professor Pelletier based his opinion in the results
of a clinical test (published in 2011 by Annals of the Rheumatic Diseases)
which consisted of giving osteoarthritis patients chondroitin sulphate or
placebo. Nuclear Magnetic Imaging scans have proved that chondroitin sulphate
protect from loss of cartilage volume as well as from subchondral bone
injuries. After a four-year-long initial monitoring phase, researchers observed
that the placebo group underwent prostatic surgery much more often (71%) than
the group receiving chondroitin sulfate (29%).

These new scientific findings were presented at the “Progression
of osteoarthritis: predictors and treatment” symposium hosted by Bioibérica
Farma during the EULAR 2012 congress being held these days in Berlin.