Bone marrow inflammation that leads to bone loss
Bone Marrow Inflammation and Bone Resorption
This work looks at how nerve-driven inflammation in bone marrow causes quick bone loss after muscle paralysis, with the goal of helping people who lose muscle use or have paralysis.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of Washington NIH-funded |
| Lab location | 1 site (Seattle, United States) |
| Project ID | NIH-11162382 on NIH RePORTER |
What this research studies
Researchers use a mouse model where calf muscles are temporarily paralyzed with botulinum toxin A to recreate rapid bone loss after neuromuscular dysfunction. They measure early inflammatory signals in the tibia bone marrow, including neuropeptides like Substance P and activation markers of mast cells. The team traces how these signals lead to RANKL-driven osteoclast formation and bone resorption and tests whether blocking mast cell or neurogenic pathways reduces bone loss. Findings will guide potential treatments to protect bone when nerves or muscles stop working properly.
Who could benefit from this research
Good fit: People with recent or ongoing neuromuscular weakness, paralysis, or conditions that cause rapid loss of muscle use would be the ideal future candidates for related interventions.
Not a fit: Patients whose bone loss is driven mainly by chronic age-related osteoporosis or purely mechanical disuse without neurogenic inflammation may not benefit from the specific mechanisms studied here.
Why it matters
Potential benefit: If successful, this work could point to new ways to prevent or reduce rapid bone loss after paralysis or severe muscle weakness.
How similar studies have performed: Prior mouse studies from this group showed early increases in Substance P and reduced bone loss in mast-cell–deficient mice, so the pathway has promising preclinical support though clinical application is still novel.
Where this research is happening
Seattle, United States
- University of Washington — Seattle, United States (Active)
Researchers
- Principal investigator: Gross, Ted S. — University of Washington
- Study coordinator: Gross, Ted S.
About this research
- This is an active NIH-funded research project — typically early-stage science, not a clinical trial accepting patient enrollment.
- Some NIH-funded labs run parallel clinical studies or seek volunteers for related work. To check, contact the principal investigator or institution listed above.
- For full project details, budget, and progress reports, visit the official NIH RePORTER page below.