Epilepsy drug could slow joint damage in osteoarthritis

In a new study, researchers at Yale School of Medicine identify a drug that could ease the joint degeneration caused by osteoarthritis. Treatment for this common, debilitating condition has long depended on pain relievers and lifestyle changes to manage symptoms in the absence of effective disease-modifying therapies.

Scientists in the Yale labs of Chuan-Ju Liu, PhD, and Stephen Waxman, MD, PhD, say a sodium channel called Nav1.7 plays a role in the joint damage seen in osteoarthritis and could provide a new therapeutic target.

Sodium channels are specialized proteins found in cell membranes, which produce electrical impulses in "excitable" cells in muscles, the nervous system, and the heart. Previous research from Dr. Waxman's lab has shown Nav1.7 plays a key role in the transmission of pain signals. In the new study, researchers found Nav1.7 channels were also present in non-excitable cells that produce collagen and help maintain the joints in the body.

“The function of sodium channels in non-excitable cells has been a mystery,” Waxman said. “This new study provides a window on how small numbers of sodium channels can powerfully regulate the behavior of non-excitable cells.”

By deleting Nav1.7 genes from collagen-producing cells, the team was able to significantly reduce joint damage from osteoarthritis in mouse models. Researchers also found Nav1.7 blockers, like the epilepsy drug carbamazepine, offered significant protection against joint damage in mouse models.

“The findings open new avenues for disease-modifying treatments,” says the study's lead author Wenyu Fu, PhD.