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Última actualización:
21 de mayo de 2013
BIOIBERICA NEWS

June 8, 2012
A new research paper proves that chondroitin sulphate inhibits angiogenesis, a mechanism of action involved in the rapid progression of osteoarthritis
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 disease.

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. 




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