Decellularized extracellular matrix repair of volumetric muscle loss injury impairs adjacent bone healing in a rat model of complex musculoskeletal trauma. (November 2016)

• Record Type: Journal Article
• Authors: Pollot, Beth E.; Goldman, Stephen M.; Wenke, Joseph C.; Corona, Benjamin T.
• Is Part Of: Journal of trauma and acute care surgery. Volume 81(2016)Supplement 2
• Publication Date: 2016-11
• Subjects: Biological scaffold -- inflammation and resorption -- Lewis rats -- open fracture -- skeletal muscle injury; Surgical intensive care -- Periodicals; Surgical emergencies -- Periodicals; Wounds and injuries -- Surgery -- Periodicals; 617.026
• DOI: 10.1097/TA.0000000000001212
• Languages: English
• ISSNs: 2163-0755

Abstract

ABSTRACT: BACKGROUND: Traumatic muscle loss (i.e., volumetric muscle loss [VML] injury) impairs adjacent fracture healing but is often left untreated. A promising therapy for this application is a decellularized extracellular matrix (ECM) because of their capacity to regenerate a vascularized tissue bed. This study tested the hypothesis that repair of VML concomitant to fracture with a small intestine submucosa (SIS)–ECM improves musculoskeletal healing. METHODS: In male Lewis rats (~375 g), a 3-mm segmental bone defect (SBD) was created in concomitance with a 6-mm, full-thickness VML injury to the adjacent tibialis anterior (TA) muscle. For all rats (n = 10), the SBD was treated with internal plate fixation and delivery of recombinant human bone morphogenetic protein 2 (1 μg) on a collagen sponge. The VML either had no repair or SIS-ECM repair (n = 5/group). Bone regeneration within the SBD (BV/TV [bone volume as a fraction of total volume]) was assessed via in vivo micro–computed tomography at 2, 4, and 6 weeks and histology at 6 weeks after injury. Tibialis anterior muscle in vivo strength and histologic assessments were performed at 6 weeks after injury. RESULTS: Compared with no repair, SIS-ECM presented −21% ( p = 0.09) and −27% ( p = 0.004) BV/TV at 4 and 6 weeks after injury, respectively. At 6 weeks, the SBD gap length was shorter for the no repair than that for the SIS-ECM (2.64 ± 0.30 and 3.67 ± 0.41 mm, respectively; p = 0.09), whereas the distances from the end of each cortical segment to the center of the first stabilization screw were longer (1.86 ± 0.25 and 0.85 ± 0.30 mm, respectively; p = 0.035), indicating enhanced resorption in the SIS-ECM group. Both groups presented similar magnitude TA muscle strength deficits compared with their contralateral limbs (10–150 Hz: no repair, −58% to 67%; SIS-ECM, −51% to 74%). The TA muscle of the SIS-ECM group was remarkable for its presentation of fibrosis, edema, and immune cell presence. CONCLUSIONS: Small intestine submucosa–ECM VML repair impaired open fracture healing and failed to improve skeletal muscle strength.