The Clinic for Molecular Orthopedics

German Doctors Have OA on the Run

The Clinic for Molecular Orthopedic’s Treatment Stops Joint Disease in Its Tracks

by Justin Handley

Orthopedic doctors in Germany have just taken a giant lead in the race for a cure for human osteoarthritis (OA) – and they have a stable of million-dollar racehorses to thank for it.

Over the past 10 years, the speedy steeds have provided researchers with a jackpot of knowledge about a new treatment that is now able to halt moderate-to-severe OA in human patients.

Called IRAP, this new biological therapy has eliminated crippling joint pain and inflammation in thousands of OA sufferers, as well as their need for drugs and even joint replacement and/or spinal surgery.

How Racehorses Helped Doctors Solve the Riddle of Human OA

“Racehorses are the ideal research model because OA is so common among them,” explains Dr. Axel Baltzer of The Center for Molecular Orthopaedics, Königsallee Clinic (Gemeinschaftspraxis Königsallee) in Düsseldorf, Germany, one of the early pioneers in IRAP research on both horses and humans.

“Because of the horses’ high monetary value — and because standard treatments for equine OA are so ineffective — owners permitted us to experiment with IRAP, producing great results for them, along with valuable insights into human applications,” Dr. Baltzer explained.

More than 60% of lameness in horses is due to OA. And with 95% of their body mass (not including a rider) compressing the joints in their thin legs with crushing force as they run, it’s easy to understand why.

After years of clinical studies, IRAP has emerged as the cutting-edge treatment for equine OA. But the bigger news is how this has paved the way for official approval of IRAP for human treatment in Europe.

In clinical use now in Europe for the past eight years, IRAP is proving to be one of the most impressive weapons against human OA; the joint-destroying disease that is the second leading cause of disability globally.

How OA Happens

“IRAP” may sound like a vanity license plate on a hip-hop celebrity’s limousine, but in the world of molecular orthopedics, it stands for interleukin-l receptor antagonist (IL-1Ra), a super-hero protein with the ability to clobber the inflammatory bad guys that determine who will get OA and who won’t.

Normally, an injury to a joint or cartilage triggers the immune system to create inflammation, the first step in the healing process. In such cases, pain and immobility are temporary as the damage heals itself.

But if the injury is repetitive (like accumulated wear-and-tear friction) – and if there is a genetic tendency to develop OA — a state of chronic inflammation ensues in which a cascade of nasty inflammatory enzymes (called cytokines) can flood the joint and begin to permanently damage it.

Unchecked, the worst of these cytokine villains — interleukin-l (IL-1) and tumor necrosis factor-alpha (TNF) – “burn” into the smooth surface of cartilage that covers the ends of the bones in joints so they no longer glide freely against each other. The cytokines also increase sensitivity of nerve endings in the joint, causing intense pain.

As it is damaged, the cartilage surface becomes rough and uneven like sandpaper, which continues to wear away existing cartilage and perpetuates chronic inflammation. This dual assault of friction and cytokine erosion rapidly destroys existing cartilage — and ultimately the bone — until joint replacement is a patient’s only alternative.

OA is a vicious, downward cycle of progressive joint deterioration with increasing pain and immobility. Constant painkillers and anti-inflammatory drugs are needed to control the discomfort – and more desperate measures like steroid injections of cortisone are sometimes used before joint replacement or back surgery become inevitable.

Ironically, these drugs actually accelerate joint destruction by inhibiting the natural process by which the body repairs damaged cartilage.