The link between mitochondrial damage and osteoporosis

An image of mitochondria to illustrate mitochondrial damage and the link to osteoporosis
© iStock/wir0man

Possible mitochondrial damage from alcohol, cigarette smoke, and exposure to medications and toxins could lead to osteoporosis.

A new study from the University of Pennsylvania has assessed how these environmental factors which they have associated with mitochondrial damage could be linked to osteoporosis.

Risk factors for osteoporosis

The study notes that some risk factors for osteoporosis cannot be avoided, such as:

  • Being older;
  • Being female; and
  • Having a family history of the condition.

However, other factors can be avoided, including:

  • Smoking cigarettes,;
  • Consuming alcohol;
  • Taking certain medications; or
  • Being exposed to environmental pollutants.

Mitochondrial damage

The research found that mitochondrial damage, damage to the key cellular organelles and energy generators, leads to a surge in the creation of osteoclasts, cells which are responsible for breaking down bone.

The study assessed the link between mitochondrial damage and osteoporosis, through the work of macrophages. To do this, the team induced damage to a key enzyme called cytochrome oxidase C which is responsible for energy production in mitochondria in lab-grown mouse macrophages.

They found that the macrophages released signalling molecules associated with an inflammatory reaction and seemed to encourage them toward becoming osteoclasts.

How do environmental factors link to bone loss?

The research has gained a clearer picture of how these avoidable exposures link to the process of bone loss.

Narayan Avadhani, a biochemist at Penn Vet and senior author on the work, said: “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. 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.”

Avadhani added: “In some respects, mitochondrial stress signaling may even be replacing RANK-L. That we don’t know now, but we plan to look into that further.”

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