For Frances McKenzie, it was a pop in her left foot that told her it was broken and led to a diagnosis of osteoporosis or thinning bones. For her daughter, Lori, it was a seizure that led to a diagnosis of a thyroid condition that also left her with bone loss even though she was only in her early 30s.
“I had the bone age of an 85-year-old woman,” Lori McKenzie said as she waited at AU Health’s West Wheeler Parkway office with her mother. They are among the estimated 54 million in the U.S. who suffer from osteoporosis, a disease that causes one in two women over age 50 to suffer a fracture, according to the National Osteoporosis Foundation. Researchers at Augusta University are looking into why it develops and potentially if there are better ways to treat it.
Bones in the body are continuously built up and torn down and one of the ways the body maintains a healthy balance is in response to stress on them from things like walking or exercise, said Dr. Meghan McGee-Lawrence, an assistant professor of cellular biology and anatomy at AU.
“You don’t want to have a bone that doesn’t have the right amount of strength because then it is going to be prone to fracture but you also don’t want a bone that is overdesigned because then it’s metabolically expensive,” she said. “It is heavy it, it takes a lot of energy. You want to find the happy medium.”
It has long been known that osteocytes, the main cells in bone, respond to this stress but exactly how that happens has not been well defined. McGee-Lawrence and colleague Dr. Paul McNeil have come up with a simple and elegant explanation for it. The stress actually tears a tiny hole in the osteocyte cell wall that allows calcium outside it to come in and sets off a series of events that lead to bone formation, she said.
“What our work suggests is that initial rush of calcium that triggers all of the other downstream events that we know happen, we think that happens because the cell membrane gets a small tear in it and it allows that calcium to come rushing in,” McGee-Lawrence said.
It is also well known that bones lose osteocytes during aging and that leads to less density in the bones, and their work points to ways that might happen.
“Maybe the cell is more or less likely to experience a tear with (the stress),” McGee-Lawrence said. “And then after a tear happens we think there is a possibility that the cells might not repair as well with aging.”
Exercise is good for strengthening bone but older people don’t seem to get the same benefit as younger people do, she said.
“We’re hoping to come up with a new way to make bone more responsive in older individuals,” McGee-Lawrence said. “If we can use this mechanism to affect either how easily those membrane tears form or how well they repair or their rate of repair that gives us a new target for going after improving” the sensitivity of the bones to exercise.
The AU team has data in mice that show controlling how quickly or how slowly the tear is repaired can affect the response “so that makes us pretty excited about the possibilities for the future,” McGee-Lawrence said. Their work was funded by a $450,000 grant from the National Science Foundation but the hope is to eventually move on to human studies “to see if the same mechanism holds true in a human patient population,” she said.
Having tried some drugs that didn’t seem to work on her osteoporosis, Lori McKenzie, now 55, said she is ready for a new approach.
“That would be a great thing for women and everybody who has a problem with brittle bones,” she said.
Reach Tom Corwin at (706) 823-3213 or firstname.lastname@example.org