Osteoarthritis Discovery Could Lead to New Treatment Approach
A new osteoarthritis discovery suggests scientists have been looking at the disease from the wrong angle. If researchers at Johns Hopkins University School of Medicine (JHUSM) are correct, the finding could lead to a new treatment approach for osteoarthritis and a way to stop progression of the disease.
What does the new discovery mean?
For years, clinicians and researchers believed that osteoarthritis was mainly a problem involving the cartilage, the spongy material that acts as a shock absorber between the ends of bones at the joints and prevents them from grinding together. In fact, that’s a reason why this degenerative condition is often referred to as a wear-and-tear disease.
But what if this theory is wrong, or at least misguided? What if the mechanisms involved in osteoarthritis come from somewhere else? Does that mean the treatments currently used to manage the disease need to be changed?
These are all good questions, and they were tackled by a team at Johns Hopkins, who discovered evidence that the bone under the cartilage has an important role in osteoarthritis and pain and makes the damage associated with the disease worse. The good news is that in their proof-of-concept experiment, they discovered they could stop progression of osteoarthritis by interfering with the activity of a specific protein.
Here’s a brief explanation of what the scientists discovered. They used mice with anterior cruciate ligament (ACL) tears, which is a known cause of osteoarthritis of the knee, to make their findings.
Within one week of the ACL injury, the investigators noted the bone underneath the cartilage, called subchondral bone, had been eaten away by cells called osteoclasts. This action in turn triggered high amounts of a protein called TGF-beta 1 to summon stem cells to the damaged area to build new bone.
Although this may sound like a good action, the scientists observed that the bone building exceeded the bone destruction process, and the extra bone formation placed excessive stress on the cartilage. According to Xu Cao, PhD, director of the Center for Musculoskeletal Research in the Department of Orthopaedic Surgery at JSUSM) and his colleagues, “We think that the problem in OA is not just the cartilage ‘cushion,’ but the bone underneath.”
In other words, the development of this extraneous bone, and not a problem with the cartilage, is the core cause of osteoarthritis. The exciting news is that when the scientists treated the mice with a TGF-beta1 inhibitor directly into the subchondral bone, they were able to stop progression of the disease.
The new discovery could lead to new ways to treat osteoarthritis, a disease that affects an estimated 27 million Americans and will affect half of all Americans during their lifetime. Osteoarthritis is not just a disease of older adults; in fact, research indicates that children and teens who participate in vigorous sports can develop abnormal bone formations that may result in early osteoarthritis of the hip.
Currently, osteoarthritis is typically treated with pain medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), cortisone injections, hyaluronic acid injections, acetaminophen, and narcotics, with surgery to replace damaged knees and hips as a last resort, although such surgeries are common.