A recent study has discovered a mechanism operating at cell structure levels that explains why risks of osteoporosis increase with modifiable factors like smoking and alcohol. The mechanism causes cell types in a body’s immunity system to transform into osteoclasts. These can dissolve bone.
Mitochondrias of macrophages, which are cell waste removers, trigger this process under stress, causing formation of osteoclasts. Researchers from Pennsylvania University in Philadelphia & Icahn School in New York were behind this breakthrough, published in FASEB Journal. Narayan Avadhani, lead study author, energy production and osteoclasts were affected by mitochondrial functioning.
Factors like medications, alcohol and smoking can negatively affect mitochondrial function. The pathway for stress signaling uncovered by the team is a likely explanation for this. The findings were demonstrated in cultured macrophages in a laboratory and mice which had dysfunctional mitochondria.
Osteoporosis causes a fall in bone density levels and makes them brittle and porous. The risk increases with advancing age since bone generation-resorption levels vary with age. After their 30s, most people face declining bone density as the body chooses resorption instead of generation.
As per IOF, 33.33% of women and 20% of men will experience osteoporosis-related bone fractures in their lifetime.75 million people across Japan, Europe and US face osteoporosis with 8.9 million fractures being caused due to the condition worldwide.
MtRS pathway might help the cells adapt to the stress faced. However, several key mechanisms remain unknown. Experiments on mouse macrophages which were lab-cultured were conducted to estimate mitochondrial damage effects.
Enzymes like cytochrome oxidase C were disrupted, causing inflammation and overproduction of osteoclasts. Another molecule named RANK-L was also seen displaying unnatural behavior. RANK-L usually is used to trigger bone resorption. However, osteoclasts differentiation due to damaged mitochondrias turned out to further bone resorption, though there wasn’t enough RANK-L available. Further tests are to be conducted studying whether preservation of mitochondrial function can reduce osteoporosis risks.
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