Muscle response to leg lengthening during distraction osteogenesis.
Continuous lengthening of intact muscles during distraction osteogenesis leads to an increase of sarcomeres and enhances the regeneration of tendons and blood vessels. A high distraction rate leads to an excessive leg and muscle lengthening and might cause damages of muscle fibers with fibrosis, necrosis, and muscle weakness. Complications like muscle contractures or atrophy after postoperative immobilization emphazize the importance of muscles and their function in the clinical outcome. In an animal model of distraction osteogenesis, 18 sheep were operated with an external fixator followed by 4 days latency, 21 days distraction (1.25 mm per day) and 51 days consolidation. The anatomical location (gastrocnemius, peroneus tertius, and first flexor digitorum longus muscle), dimension and occurrence of muscular defects were characterized histologically. The callus formation and leg axis was monitored by weekly X-rays. Additionally, serum creatine kinase was analyzed during a distraction and consolidation period. Significant signs of muscle lesions in all three observed muscles can be found postoperatively, whereas normal callus formation and regular leg axis was observed radiologically. The peroneus tertius and first flexor digitorum longus muscles were found to have significantly more signs of fibrosis, inflammatory, and necrosis. Creatine kinase showed two peaks: 4 and 39 days postoperative as an indication of muscle damage and regeneration. The study implicates that muscle damages should be considered when a long-distance distraction osteogenesis is planned. The surgeon should consider these muscle responses and individually discuss a two-stage treatment or additional muscle tendon releases to minimize the risk of muscle damages.
Thorey
Fritz
F
Department of Orthopaedic Surgery, Hannover Medical School, Hannover, Germany. thorey@annastift.de
Bruenger
Jens
J
Windhagen
Henning
H
Witte
Frank
F
D000818:Animals; D003402:Creatine Kinase / Q000097:blood; D005355:Fibrosis; D018485:Muscle Fibers, Skeletal / Q000473:pathology; D018482:Muscle, Skeletal / Q000473:pathology*; D009133:Muscular Atrophy / Q000473:pathology; D009336:Necrosis; D019857:Osteogenesis, Distraction; D012756:Sheep
D003402:Creatine Kinase