Issue: June 2012
May 15, 2012
2 min read
Save

Insights into cartilage damage mechanisms paving way to new osteoarthritis treatments

Issue: June 2012
You've successfully added to your alerts. You will receive an email when new content is published.

Click Here to Manage Email Alerts

We were unable to process your request. Please try again later. If you continue to have this issue please contact customerservice@slackinc.com.

MONTREAL — Understanding how the loss of articular cartilage is influenced by mechanical forces and the way joint remodeling can be promoted by alerting joint loading is key to developing new mechanical and biologic approaches to osteoarthritis prevention and treatment, Joseph A. Buckwalter, MD, said in an honorary lecture, here.

“This is one of the unsolved problems in orthopedics,” Buckwalter, professor and head of the department of orthopedics and rehabilitation and Arthur A. Steindler Chair in Orthopaedic Surgery at the University of Iowa, said at the International Cartilage Repair World Congress 2012. “We know that all sorts of joint injuries — be it a meniscal tear, a cartilage injury or a ligament injury — increase the risk of osteoarthritis (OA). But we do not know why.”

He went on to discuss a series of studies in which he and his team demonstrated that more than 12% of all osteoarthritis in the lower extremity is secondary to a joint injury. This affects nearly 6 million people in the United States and occurs in patients an average of 10 years younger than patients with age-related OA.

Joseph A. Buckwalter 

Joseph A. Buckwalter

“If you look at the results of [anterior cruciate ligament (ACL)] reconstruction over time, the risk of [OA] has not decreased significantly in the last 20 years,” Buckwalter said. “Now you could say maybe some of that is because we are doing such a good job of repairing the ACL that people go back to full activity and therefore are at increased risk of subsequent injury, but certainly the risk is high.”

Buckwalter shared research he and colleagues conducted that analyzed the amount of energy it takes to cause articular cartilage damage severe enough to become a predictive factor for OA development.

“It turns out — with at least pilon fractures — even in the very short term, just 2 years, those people with low fracture energy did not develop osteoarthritis,” he said. “Those people with high fracture energy all developed osteoarthritis within 2 years. So now we have a way of actually measuring the severity of injury and showing it actually relates to osteoarthritis.”

Buckwalter also noted that he and others found joint remodeling can be promoted through distraction and motion of osteoarthritic articular surfaces, which helps improve joint function and decrease pain in patients with end-stage post-traumatic OA.

“We have so many promising therapies,” he noted. “We are showing that altered motion and loading can really make a difference in treating even end-stage osteoarthritis — and maybe even the acute interarticular injury.”

Reference:

  • Buckwalter J. Advances in understanding of post-traumatic osteoarthritis: Implications for treatment of joint injuries. Paper #5.10. Presented at the International Cartilage Repair Society World Congress 2012. May 12-15. Montreal.