Extra! Extra! Read all about it! In a newly published paper in the American Journal of Sports Medicine, a group of PhDs and Surgeons used our F-CHPs to evaluate the collagen turnover after a complete ACL tear. They visualized the collagen turnover using CHPs (Panel D) and quantified the signal. They found that there was a statistically significant increase in dynamic collagen remodeling in the injured vastus lateralis muscle (outer quad muscle) vs the uninjured muscle in the opposite leg (Panel F). They compared these results with other upregulated cells and ECM biomarkers and concluded that there is an increase in collagen turnover after ACL tear leading to a decrease in muscle quality.
Background: Anterior cruciate ligament (ACL) tears result in significant quadriceps muscle atrophy that is resistant to recovery despite extensive rehabilitation. Recent work suggests an elevated fibrotic burden in the quadriceps muscle after the injury, which may limit recovery. Elucidating the mechanisms and cell types involved in the progression of fibrosis is critical for developing new treatment strategies.
Purpose: To identify factors contributing to the elevated fibrotic burden found after the injury.
Methods: After an ACL injury, muscle biopsy specimens were obtained from the injured and noninjured vastus lateralis of young adults (n = 14, mean ± SD: 23 ± 4 years). The expression of myostatin, transforming growth factor β, and other regulatory factors was measured, and immunohistochemical analyses were performed to assess turnover of extracellular matrix components.
Results: Injured limb skeletal muscle demonstrated elevated myostatin gene (P < .005) and protein (P < .0005) expression, which correlated (R2 = 0.38, P < .05) with fibroblast cell abundance. Immunohistochemical analysis showed that human fibroblasts express the activin type IIB receptor and that isolated primary human muscle-derived fibroblasts increased proliferation after myostatin treatment in vitro (P < .05). Collagen 1 and fibronectin, primary components of the muscle extracellular matrix, were significantly higher in the injured limb (P < .05). The abundance of procollagen 1–expressing cells as well as a novel index of collagen remodeling was also elevated in the injured limb (P < .05).
Conclusion: These findings support a role for myostatin in promoting fibrogenic alterations within skeletal muscle after an ACL injury.
Clinical Relevance: The current work shows that the cause of muscle quality decline after ACL injury likely involves elevated myostatin expression, and future studies should explore therapeutic inhibition of myostatin to facilitate improvements in muscle recovery and return to sport.
Check out the full article FULL ARTICLE HERE