The goal of orthopaedic surgery is to help the entire musculoskeletal system function in harmony, but the preponderance of orthopaedic research focuses on the skeletal system instead of muscles and tendons. Bone is the only organ that can heal by regenerating tissue that is usually just as effective as the original structure. Consequently, we have focused on developing systems to hold bone intact as it heals so that postinjury function is maximized. Decades have been spent understanding the critical biologic pathways of bone healing and developing implantable, pharmacologic, and cell-based therapies to optimize it.
However, we sometimes overlook the fact that the skeleton can’t move without muscles. Only a few researchers have devoted their careers to understanding skeletal muscle’s response to injury and approaches to enhance muscle recovery after disuse and injury. In the August 15, 2018 issue of The Journal, Hara et al. report on experiments with the protein periostin in mice. Periostin is involved with the process of muscle fibrosis, during which fibroblasts proliferate in the injured area of the muscle and create “scar tissue” that eventually inhibits muscle function.
In one experiment, the authors found that “knockout” mice without the gene that encodes for periostin had improved recovery in a lacerated gastrocnemius muscle, less fibrosis in the muscle, and a significantly reduced number of infiltrating fibroblasts than “wild” mice with the same induced injury. In a similar experiment, they found reduced muscle fibrosis in injured muscles of mice whose production of periostin was neutralized by an antibody injected into the injured muscle. Although a sharp injury to muscle (the laceration model used in these mouse experiments) is not a common clinical scenario in patients seen by orthopaedists, the Hara et al. study represents a step forward in understanding muscle response to injury.
While these findings need to be replicated and then translated into clinical applications for humans, they shed new light on the importance of preventing periostin-induced fibroblast migration after skeletal muscle injury. This research hints at a potential therapeutic strategy to enhance muscle’s functional recovery, which is the most sought-after outcome for patients.
The clinical sports and orthopaedic communities are in need of approaches to limit scarring and atrophy in the setting of muscle disuse and injury. Any of us who unavoidably injure muscle during surgical approaches to bones and joints or for graft harvests and other procedures should be heartened by these findings. It is my hope that more early-career researchers will focus on the first half of the term “musculoskeletal” to advance therapeutic approaches to problems that impact function to a much more permanent degree than do most bone injuries.
Marc Swiontkowski, MD