Chelsey L Dunham1, Ryan M Castile1, Aaron M Chamberlain1, Spencer P Lake1. 1. Departments of Biomedical Engineering (C.L.D. and S.P.L.), Mechanical Engineering & Materials Science (R.M.C. and S.P.L.), and Orthopaedic Surgery (A.M.C. and S.P.L.), Washington University in St. Louis, St. Louis, Missouri.
Abstract
BACKGROUND: Elbow injuries disrupt the surrounding periarticular soft tissues, which include the muscles, tendons, capsule, ligaments, and cartilage. Damage to these tissues as a result of elbow trauma causes clinically significant contracture in 50% of patients. However, it is unclear which of these tissues is primarily responsible for the decreased range of motion. We hypothesized that all tissues would substantially contribute to elbow contracture after immobilization, but only the capsule, ligaments, and cartilage would contribute after free mobilization, with the capsule as the primary contributor at all time points. METHODS: Utilizing a rat model of posttraumatic elbow contracture, a unilateral soft-tissue injury was surgically induced to replicate the damage that commonly occurs during elbow joint dislocation. After surgery, the injured limb was immobilized for 42 days. Animals were evaluated after either 42 days of immobilization (42 IM) or 42 days of immobilization with an additional 21 or 42 days of free mobilization (42/21 or 42/42 IM-FM). For each group of animals, elbow mechanical testing in flexion-extension was completed post-mortem with (1) all soft tissues intact, (2) muscles/tendons removed, and (3) muscle/tendons and anterior capsule removed. Total extension was assessed to determine the relative contributions of muscles/tendons, capsule, and the remaining intact tissues (i.e., ligaments and cartilage). RESULTS: After immobilization, the muscles/tendons and anterior capsule contributed 10% and 90% to elbow contracture, respectively. After each free mobilization period, the muscles/tendons did not significantly contribute to contracture. The capsule and ligaments/cartilage were responsible for 47% and 52% of the motion lost at 42/21 IM-FM, respectively, and 26% and 74% at 42/42 IM-FM, respectively. CONCLUSIONS: Overall, data demonstrated a time-dependent response of periarticular tissue contribution to elbow contracture, with the capsule, ligaments, and cartilage as the primary long-term contributors. CLINICAL RELEVANCE: The capsule, ligaments, and cartilage were primarily responsible for persistent motion loss and should be considered during development of tissue-targeted treatment strategies to inhibit elbow contracture following injury.
BACKGROUND: Elbow injuries disrupt the surrounding periarticular soft tissues, which include the muscles, tendons, capsule, ligaments, and cartilage. Damage to these tissues as a result of elbow trauma causes clinically significant contracture in 50% of patients. However, it is unclear which of these tissues is primarily responsible for the decreased range of motion. We hypothesized that all tissues would substantially contribute to elbow contracture after immobilization, but only the capsule, ligaments, and cartilage would contribute after free mobilization, with the capsule as the primary contributor at all time points. METHODS: Utilizing a rat model of posttraumatic elbow contracture, a unilateral soft-tissue injury was surgically induced to replicate the damage that commonly occurs during elbow joint dislocation. After surgery, the injured limb was immobilized for 42 days. Animals were evaluated after either 42 days of immobilization (42 IM) or 42 days of immobilization with an additional 21 or 42 days of free mobilization (42/21 or 42/42 IM-FM). For each group of animals, elbow mechanical testing in flexion-extension was completed post-mortem with (1) all soft tissues intact, (2) muscles/tendons removed, and (3) muscle/tendons and anterior capsule removed. Total extension was assessed to determine the relative contributions of muscles/tendons, capsule, and the remaining intact tissues (i.e., ligaments and cartilage). RESULTS: After immobilization, the muscles/tendons and anterior capsule contributed 10% and 90% to elbow contracture, respectively. After each free mobilization period, the muscles/tendons did not significantly contribute to contracture. The capsule and ligaments/cartilage were responsible for 47% and 52% of the motion lost at 42/21 IM-FM, respectively, and 26% and 74% at 42/42 IM-FM, respectively. CONCLUSIONS: Overall, data demonstrated a time-dependent response of periarticular tissue contribution to elbow contracture, with the capsule, ligaments, and cartilage as the primary long-term contributors. CLINICAL RELEVANCE: The capsule, ligaments, and cartilage were primarily responsible for persistent motion loss and should be considered during development of tissue-targeted treatment strategies to inhibit elbow contracture following injury.
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