Inflammation in bone marrow occurs rapidly after muscle paralysis, and this may promote the formation of large cells that break down bone, according to researchers from the University of Washington, Seattle, in a new study.
Researchers from the University of Washington, Seattle studied mice whose calf muscles were exposed to botulinum toxin A (BTxA), a protein that causes temporary muscle weakness and paralysis. The research team found that calf paralysis caused inflammation in the marrow of the adjacent tibia, the larger of the two lower leg bones. This inflammation was associated with an increase in the size of cells that break down bone tissue (osteoclasts) that occurred 3 days after BTxA exposure.
Breakdown of bone that is not replaced with new tissue results in osteopenia, a condition in which bones become weak and are more likely to break. Reduced bone mass is prevalent in older adults but also often affects people paralyzed by spinal cord injury and those who have other conditions of disuse, explains a media release from the American Physiological Society.
The findings of this study may have important implications for treating people with paralysis, according to the researchers.
“The identification of an acute inflammatory cascade in bone marrow leading to the formation of giant osteoclasts has potential to reveal novel therapeutic strategies for mitigating paralysis-induced bone loss following neuromuscular trauma,” they write, in their study, published in the American Journal of Physiology—Cell Physiology.
[Source(s): American Physiological Society, Newswise]
