During a game in 2018, Alex Smith suffered a compound fracture that broke both the tibia and fibula in his right leg. The gruesome injury aside, the former 49ers quarterback soon developed life-threatening necrotizing fasciitis — a rare bacterial infection — that resulted in sepsis and required him to undergo 17 surgeries.
In a battle to save his life and avoid amputating his leg, doctors had to remove a great deal of his muscle tissue leading to volumetric muscle loss (VML). When Smith returned to the field after nearly two years of recovery, many called his comeback a “miracle”.
Skeletal muscle is one of the most dynamic tissues of the human body. It defines how we move and can repair itself after injury using stem cells. However, when significant chunks of muscle are destroyed through severe injury (e.g. gunshot wound) or excessive surgery (like that of Smith’s), VML overwhelms the regenerative capacity of the muscle stem cells.
Despite the prevalence of these injuries, no standardized evaluation protocol exists for the characterization and quantification of VML and little is understood about why it consistently overwhelms the body’s natural regenerative processes. Current treatment options include functional free muscle transfer and the use of advanced bracing designs.
However, new research from the University of Michigan (U-M) may have just discovered why tissues often fail to regenerate from traumatic muscle loss injuries.
When researchers from U-M collaborated with partners at Georgia Tech, Emory University and the University of Oregon to study VML injuries in mice, they found that that sometimes post-injury immune cells become dysregulated and prevent stem cell repair. In VML injuries that don’t heal, neutrophils — a type of white blood cell — remain at the injured site longer than normal meaning that they’re not doing their job properly.
In addition, researchers found that intercellular communication between neutrophils and natural killers cells impacted muscle stem cell-mediated repair. When neutrophils communicated with natural killer cells, they were essentially prompted to self-destruct.
The findings suggest that by altering how the two cell types communicate, different healing outcomes may be possible and could offer new treatment strategies that eventually restore function and prevent limb loss. The team of researchers hope that better treatments could mean that recovery from VML injuries is no longer considered a “miracle”.
To read the source release, click here.