Researchers at Henry Ford Hospital in Detroit have identified a gene that may offer a better understanding of how keloid scars develop, potentially opening the door to improved treatment for the often painful, itchy, and tender scars.
“This finding has great promise for better understanding how keloids function and offers a potential target for improved and novel treatments,” says Dr. Lamont R. Jones, vice chair for the department of otolaryngology-head and neck surgery at Henry Ford, as well as the study’s lead author. “We now have a better understanding of how this gene fits in the broader picture of the wound healing process, which may be important in preventing scars in general.”
In the Henry Ford Hospital study, researchers compared samples of keloid tissue with normal tissue and found that an altered AHNAK gene — a protein located on the cell membrane in epithelial cells and in the nucleus and cytoplasm of other cell types such as fibroblasts —may play a significant biological role in keloid development.
“Identifying AHNAK puts our translational research one step closer to moving from the bench to the bedside,” Jones says.
Keloid scars form raised, firm skin areas and most often occur on the chest, shoulders, earlobes (following ear piercing), upper arms, and cheeks. Unlike regular scars, keloids do not subside over time and often extend outside the wound site.
Current treatment for keloids includes cortisone injections, pressure dressings, silicone gels, surgery, freezing, laser treatment, or radiation therapy. A combination of treatments may be used, depending on the individual. In some cases, keloids return after treatment up to 50 to 100 percent of the time, Jones says.
