Dr. Steve Yoon weighs in on a study underway may be a new way to treat osteoarthritics.
The current study focused on a way to slow the joint damage caused by osteoarthritis rather than focusing on pain relief alone. Researchers noted that osteoarthritis involves cartilage breakdown and pain. At the cellular level, this involves chondrocytesTrusted Source, or cartilage cells and neurons, which are involved in the pain response from osteoarthritis.
Researchers were particularly interested in understanding the presence and work of voltage-gated sodium channelsTrusted Source in the cartilage cells. These sodium channels are a specific type of protein found in cell types.
To start, researchers examined chondrocytes in people with osteoarthritis. They found that the Nav1.7 sodium channels are present in chondrocytes and that the amount is increased in osteoarthritis.
Using mouse models, researchers genetically deleted Nav1.7 and studied the results. They found that in dorsal root ganglia neurons, the junction boxes for nerves as they exit the spinal column, this deletion contributed to pain reduction. In the chondrocyte cells in mice, the deletion contributed to much less structural damage and progression of osteoarthritis and less pain-related behavior from the osteoarthritis.
The results concluded that inhibiting these channels could be the key to slowing osteoarthritis progression and minimizing pain. Researchers looked at several components to test this hypothesis and some of the underlying mechanisms involved.
Dr. Yoon noted the following: “The study investigating Nav1.7 is important to create disease modifying medicines for osteoarthritis. Understanding the cellular mechanisms underlying osteoarthritis and creating targeted therapies to address both pain and the actual disease itself will be necessary to modify the impact of this disease.”