Targeted healing agent
It’s not fully known why some bones don’t heal the way they should — nor do scientists know whether a genetic component plays a role, Hankenson says.
This much is clear: People with metabolic dysfunction, such as diabetes, have greater odds of poor healing after a fracture. So do the elderly, who are also prone to more bone injuries because of lower bone mass, such as osteoporosis. Those suffering severe trauma, regardless of age or prior health status, also are likely to face problems.
What Hankenson and other research groups have studied for years, meanwhile, is the capacity of the Jagged-1 ligand to promote bone-forming cells.
The signaling is unique, Hankenson says, because this particular ligand typically binds to a delivery cell to activate bone healing in an adjacent cell — a vital trait to help ensure that a supplemental Jagged-1 dose, administered at the spot of injury, stays in place (and on task) to carry out its intended function.
As a result, “bone will only form where bone is supposed to form,” says Hankenson.
BMPs, by comparison, are soluble, so they can migrate from the site of delivery and settle elsewhere in the body, triggering other cells that aren’t supposed to form bone.
Because the body produces Jagged-1 on its own, this potential new therapy would require a synthetic version of the ligand to be produced and administered to a patient.
“We do not think there is necessarily a deficiency,” says Hankenson. “But when we think about biological molecules delivered for therapy, we’re usually identifying something that’s there normally and trying to promote more activity by giving more of it.”