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TNF-α accelerates bone fracture healing


Increasing longevity is creating a greater need for methods to enhance bone repair after injury or joint replacement, particularly in patients with osteoporosis. This study follows up on previous findings in a mouse model of slow healing fractures, which showed that covering bone fractures with muscle hastened healing and resulted in an increase in union strength.

Here, Glass et al. show that muscle-derived stromal cells (MDSCs) taken from a site adjacent to an experimentally induced fracture differentiate into osteoblasts in vitro; their osteogenic potential is similar to stromal cells from bone marrow. Tumor necrosis factor alpha (TNF-α) plays a key role, as it attracts MDSCs to the fracture site, and then induces MDSCs to differentiate into osteogenic cells.

Results from the same mouse model used previously by the authors also demonstrated that animals treated by local injection of recombinant human TNF-α (rhTNF-α) on the first two days after fracture-inducing surgery showed accelerated healing of their fracture. By day 28, rhTNF-α treated animals showed significantly higher callus mineralization compared to controls, as measured by microCT scanning.

Editor's comment: An interesting combination of in vitro work with human bone and an in vivo murine model. The potential clinical use of TNF-α – known as skeletal catabolic agent - to treat human fractures should be explored further.

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