Musculoskeletal diseases and injuries are a major burden on society, representing the most common cause of pain and impaired function worldwide. Composite injuries involving bone and the surrounding soft tissue comprise one of the most challenging musculoskeletal conditions to return to normal function. During repair of these injuries there is a loss of the synergistic interactions between adjacent tissues resulting in impaired bone regeneration. Additionally, local soft tissue ischemia may also be a contributing factor to increased infection rates observed in severe composite tissue injuries. Muscle has been implicated as a source for re-vascularization, osteoprogenitor cells and osteogenic factors, as well as a contributor to the biomechanical stimuli; however, associated studies have mostly been qualitative in nature, offering little insight into the mechanistic nature of the relationship of soft tissue to bone regeneration. Small animal models of critically sized bone defects are an efficient means to test engraftment strategies of novel constructs and therapeutics particularly in terms of functional restoration of a limb. Our lab previously developed a critically-sized rat segmental defect model with which we have quantitatively assessed bone regeneration using numerous constructs and therapeutic treatments [1]. Our objective was to develop a composite injury model by combining this segmental defect model with a muscle injury adjacent to the bone defect. We hypothesized that animals with a composite injury would have attenuated BMP-2 mediated tissue regeneration as compared to animals with a single tissue injury.

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