Some risk factors for osteoporosis such as being older and female or having a family history of the condition cannot be avoided. But others can, like smoking cigarettes, consuming alcohol, taking certain medications, or being exposed to environmental pollutants. But until now researchers haven’t gained a firm picture of how these exposures link up with bone loss.
A new study led by researchers from Penn’s School of Veterinary Medicine reveals a mechanism by which these factors and osteoporosis may be linked. Damage to mitochondria—key cellular organelles and energy generators—leads to a surge in the creation of cells called osteoclasts, which are responsible for breaking down bone, the researchers report in FASEB Journal. They uncovered these effects in cells in culture as well as in an animal model.
“In a normal individual, the process of bone degradation and rebuilding proceeds in a very balanced way, but in some people they somehow produce a lot more osteoclasts, and this leads to bone loss and osteoporosis,” said Narayan Avadhani, a biochemist at Penn Vet and senior author on the work. “We show in this paper that, when mitochondrial function is affected, it not only affects energy production but also triggers a type of stress signaling that induces the overproduction of osteoclasts.”