Health

Scientists Race To Regrow Lost Knee Cartilage

November 27, 2017   ·   0 Comments

Nov. 27, 2017 — Bad knees sideline athletes and mere mortals alike.

About 14 million Americans have osteoarthritis of the knees severe enough to cause pain and inflammation, according to the Arthritis Foundation, and more people are getting the condition — also known as OA — as they age.

As the knee’s natural cushioning — the cartilage — wanes, inflammation and pain rise, and people can’t get around as well.

Building knee cartilage has been a dream of researchers, and now several methods are under study. None has yet shown it can prevent or cure osteoarthritis, and all are in early phases, caution the scientists who presented their findings at the recent annual meeting of the American College of Rheumatology in San Diego, CA.

Stopping Excess Bone Breakdown

A treatment known as MIV-711 targets an enzyme called cathepsin K that is thought to play a role in the destruction of cartilage and the breakdown of too much bone.

Stimulating Cartilage

Another treatment, sprifermin, is a type of human fibroblast growth factor, which plays a role in cell growth and tissue repair. “It stimulates the cells in the cartilage to make more cartilage,” says Marc Hochberg, MD, primary investigator of the study and head of rheumatology and clinical immunology at the University of Maryland School of Medicine.

He reported on the 2-year results of what will be a 5-year study. “The cartilage becomes thicker, and it will do a better job of shock absorption and it will slow the progression of already established knee OA,” he says.

Stopping Cartilage Breakdown

Another treatment works with tissue regeneration and stops an enzyme from breaking down cartilage in the knee, says Yusuf Yazici, MD, chief medical officer of Samumed, a medical research and development

Perspective

Choosing which of the new treatments is most promising is difficult, says Brian Feeley, MD, an associate professor of sports medicine and orthopedic surgery at the University of California, San Francisco. He was not involved in the studies but reviewed the findings.

“The studies are all done slightly differently, so it’s hard to compare.” But, he says, so far, the improvement in some cases is very small.

Bottom line, for now? “Although the data does not show that these treatments are going to prevent or cure arthritis, the agents may be able to slow the progression of arthritis, which we don’t yet have the ability to do,” Feeley says.

Sources

American College of Rheumatology 2017 annual meeting, San Diego, CA, Nov. 3-8, 2017.

Philip Conaghan, MD, PhD, professor of musculoskeletal medicine, University of Leeds, UK; consults for Novartis Pharmaceuticals Corporation, Flexion Therapeutics, AbbVie, Infirst, Medivir, Merck Serono, and ONO Pharmaceutical Co.

Marc Hochberg, MD, head of rheumatology and clinical immunology, University of Maryland School of Medicine; consults for Merck, Bioiberica SA, Bristol-Myers Squibb, EMD Serono, Galapagos, IBSA SA, Eli Lilly, Novartis Pharma AG, Pfizer Inc., Plexxikon, Samumed LLC, Theralogix LLC, and TissueGene.

Yusuf Yazici, MD, clinical associate professor of medicine, New York University School of Medicine; is chief medical officer for Samumed LLC.

Brian Feeley, MD, associate professor, sports medicine and orthopedic surgery, University of California, San Francisco.

Arthritis Foundation: “Arthritis Facts.”

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