A shot in the arm for people with bad knees

knee

Almost every day I get an email or phone call from someone asking if we have a stem cell therapy for bad knees. The inquiries are from people who’ve been told they need surgery to replace joints damaged by age and arthritis. They’re not alone. Every year around 600,000 Americans get a knee replacement. That number is expected to rise to three million by 2030.

Up till now my answer to those calls and emails has been ‘I’m sorry, we don’t have anything’. But a new CIRM-funded study from USC stem cell scientist Denis Evseenko says that may not always be the case.

JointCartilege_nancy_liu-824x549

The ability to regenerate joint cartilage cells instead of surgically replacing joints would be a big boon for future patients. (Photo/Nancy Liu, Denis Evseenko Lab, USC Stem Cell)

Evseenko and his team have discovered a molecule they have called Regulator of Cartilage Growth and Differentiation or RCGD 423. This cunning molecule works in two different ways. One is to reduce the inflammation that many people with arthritis have in their joints. The second is to help stimulate the regeneration of the cartilage destroyed by arthritis.

When they tested RCGD 423 in rats with damaged cartilage, the rats cartilage improved. The study is published in the Annals of Rheumatic Diseases.

In an article in USC News, Evseenko, says there is a lot of work to do but that this approach could ultimately help people with osteoarthritis or juvenile arthritis.

“The goal is to make an injectable therapy for an early to moderate level of arthritis. It’s not going to cure arthritis, but it will delay the progression of arthritis to the damaging stages when patients need joint replacements, which account for a million surgeries a year in the U.S.”

3 thoughts on “A shot in the arm for people with bad knees

  1. Human adult articular cartilage has almost no chance of repairing and join surface injuries always results on osteoarthritis which is characterised by loss of matrix, hypertrophy and condrocyte apoptosis. Inflammation mediated by IL-6 family cytokine triggers the expression of matrix degradating enzymes and IL-6 itelf. RCGD423, a small molecule gp130 regulator of cartilage growth and differentiation that promote signalling of receptor. In adult, in vitro work showed that RCGD423 inducing proliferation of chondrocyte but reducing cell apoptosis and hypertrophy response. In rat, RCGD423 improved cartilage healing by enhancing regeneration of cartilage while inhibiting inflammation. Injection of RCGD423 into the knees of rats with damaged cartilage speed up the healing of injuries. Therefore, RCG423 was able to amplify the gp130 receptor to stimulate cartilage degeneration while blocking the inflammatory response.

    The safety and efficacy of RCGD423 treatment of osteoarthritis are very depended on the affinity of RCGD423 bind to gp130 receptor in compare to IL-6. In addition, the stability of RCGD423 in vivo before interacting with targeted region must be carefully monitored to avoid the unnecessary adverse effects and toxicity happening in patient due to the breaking down or secondary reaction of drug. The poor binding of drug to its gp130 receptor may easily replace with IL-6, which is harmful to the patient. Although the drug might show excellent results in vitro and in vivo of mice but the result of treatment in human may sometime turn out to be disapointed. Therefore, the complexity of pharmacology reactions in human which is greatly different from animals require closely monitored. There are 3 approaches to improve the binding of drug to its receptor: 1. pH of buffer changes the ionic strength of drug to its binding site. 2.Protein carrier such as BSA may stabilize the binding of drug to its receptor. 3.The temperature may influence the binding affinity and stability of drug.

  2. I would like to take part in clinical trials of this treatment please contact me with more details in layman’s terms if such trials are needed.

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