Recent research has uncovered a cell mechanism that could help explain why smoking, alcohol, and other modifiable factors could raise the risk of developing the bone disease osteoporosis.

Share on Pinterest Scientists find a cell mechanism that could explain why certain lifestyle factors, such as smoking, increase the risk of osteoporosis.

The mechanism spurs a cell type in the immune system to turn into osteoclasts, which are a type of cell that resorbs, or dissolves, bone.

It appears that mitochondria, the tiny enclosures that produce energy in cells, send out a signal that triggers this process when under stress.

When this happens in the mitochondria of macrophages, the cells turn into osteoclasts. Macrophages are prolific immune cells that remove cell waste and foreign objects by swallowing and digesting them.

The researchers behind the discovery hail from the University of Pennsylvania (Penn) in Philadelphia and the Icahn School of Medicine at Mount Sinai in the city of New York. They write about their findings in a recent FASEB Journal study paper.

“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,” says senior study author Narayan G. Avadhani, who is a professor of biochemistry at Penn’s School of Veterinary Medicine.

Some of the environmental factors, such as smoking, drinking alcohol, and certain medications, that can impair the function of mitochondria, also appear to raise the risk of osteoporosis.

Prof. Avadhani and his colleagues suggest that the stress signaling pathway that they uncovered could be the reason.

They demonstrated their findings in laboratory-cultured macrophages and mice with dysfunctional mitochondria.