In a trial on mice, an anti-epileptic drug helped limit joint degradation associated with osteoarthritis.
- Osteoarthritis causes progressive destruction of joint cartilage.
- Current medications cannot stop this process.
- According to an American study, anti-epileptic treatment could prevent this joint damage.
Osteoarthritis affects ten million people in France. This joint disease leads to cartilage destruction which is now inevitable. In fact, existing treatments act on the symptoms but do not prevent the progression of the disease. A new study could revolutionize the treatment of this pathology: according to its authors, an anti-epileptic drug would limit the deterioration of the joints. Their work appeared in the specialized journal Nature.
Osteoarthritis: the absence of drugs capable of preventing joint ruptures
“Linked to dysfunctions that involve all components of the joint, osteoarthritis is characterized by destruction of cartilage, inflammation of the membrane that lines the inside of the joint (synovial membrane), as well as remodeling of the layer of bone located directly beneath the cartilage (subchondral bone)”reminds himInserm. It causes pain and stiffness, but the destruction of the cartilage sometimes requires replacement of the joint with a prosthesis. “There is an urgent need for therapies that can prevent joint ruptures that occur in osteoarthritis.”estimates this team of scientists from Yale University, in the United States.
Osteoarthritis: a cellular structure involved in the maintenance of joints
In previous work, scientists noted that a sodium channel, a structure that transports sodium across cell membranes, is involved in transmitting pain signals in osteoarthritis. These structures also produce electrical impulses in cells.excitable“muscles, the nervous system and the heart. In this new research, the authors noticed that this channel, called Nav1.7, is also present in cells”non-excitable“, which produce collagen and help maintain the body’s joints.
An anti-epileptic drug to fight osteoarthritis?
In a trial on mice, researchers tested the impact of this channel on osteoarthritis. “Serial genetic ablation of Nav1.7 in several mouse models demonstrates that Nav1.7 expressed in dorsal root ganglion neurons is involved in pain, whereas Nav1.7 in chondrocytes regulates the progression of pain. osteoarthritis.” Concretely, deletion of Nav1.7 genes from these collagen-producing cells significantly reduces joint damage in mice with osteoarthritis. After that, they tried to block the canal with medication. To do this, they used carbamazepine, a sodium channel blocker currently prescribed in the treatment of epilepsy. This helped protect the mice from joint damage linked to osteoarthritis. “These results open new avenues for treatments to act on the disease“, concludes Wenyu Fu, lead author of the study.
