With the support of National Institutes of Health funding, Johns Hopkins Medicine investigators, led by pathologist Aaron W. James, M.D., Ph.D., previously discovered that sensory neurons in skeletal tissue are constantly sensing their environment and are quick to respond to injuries. Through new research published in Science Translational Medicine, they describe how this response profoundly affects growth plates, the soft cartilage at the end of bones in children that support normal growth and development, and how it responds to targeted treatment in mice.

Following a growth plate injury, a rapid invasion of nerve fibers and blood vessels triggers the formation of an unwanted “bony bar,” a rigid bone-like structure that can ultimately impede recovery and lead to stunted or altered bone growth. Through this new research, the team found inhibiting TrkA+ sensory neurons with long-acting bupivacaine, an FDA-approved nerve-numbing anesthetic, reduced this abnormal growth by up to 60%.

Spinal cord injuries affect an estimated 15 to 20 million people worldwide, often causing lasting impairments in movement, sensation, and independence. Such injuries can be especially devastating when they occur at the level of the neck, where damaged spinal circuits disrupt signals that control the diaphragm, the main muscle used for breathing. Despite advances in emergency care and rehabilitation, no approved therapies exist to rebuild the neurons and connections lost after a spinal cord injury. But new research from scientists at Gladstone Institutes offers hope for a regenerative treatment in the future.