The Treatment of Complex Motorcycle Spoke Injuries in Children.

Motorcycle spoke injuries involving the soft tissue, Achilles tendon, and calcaneal defects are rare in children. Currently, calcaneal defects are very challenging to treat. Multiple methods have been used in clinical practice; however, an effective treatment has yet to be established, especially when Achilles tendon and soft-tissue defects are also present. It is important to address this condition, because the calcaneus plays a key role in standing and gait. Unsatisfactory treatment of calcaneal defects may significantly decrease patients' quality of life (eg, by limiting mobility). In this article, we report the effective treatment of calcaneal defects in four children using distraction osteogenesis with an external fixator framework designed by the authors. From May 2014 to May 2015, four children (age range, 6-11 years) with defects of the Achilles tendon, soft tissue, and calcaneus resulting from a motorcycle accident were treated at our hospital. The Achilles tendon and soft-tissue defects were treated with second-stage reconstruction. In the third-stage surgery, osteotomy of the residual calcaneus was performed. A customized external fixator was used to lengthen the calcaneus at a rate of 1.5 mm/day in the posterior direction and reposition it by 40° in the inferior direction. In all four children, the calcaneus was lengthened by 5 cm. Distraction osteogenesis through external fixation is effective for restoring the length, width, and height of the calcaneus in children.

Active exercise promotes Achilles tendon healing and is accompanied by the upregulation of collapsin response mediator protein­2 in rats.

Collapsin response mediator protein-2 (CRMP-2) is involved in neurite elongation and regeneration; however, its role in wound healing remains to be elucidated. The present study aimed to investigate the effects of active mobilization treatment on Achilles tendon healing and to determine the role of CRMP­2 in the healing process. Sprague Dawley rats were subjected to Achilles tendon injury, which was verified by hematoxylin and eosin staining and scanning electronic microscopy. Immobilization induced the disruption of collagen fibril arrangement and promoted collagen fibril damage. The average collagen fibril perimeter in the active mobilization group was significantly increased compared with in the immobilization group (125.6±0.8 nm vs. 119.9±1.7 nm; P<0.05). In addition, immunohistological analysis revealed that CRMP­2 expression was significantly upregulated, particularly in the ruptured site of Achilles tendon tissues derived from animals in the mobilization group compared with the immobilization group (0.32±0.00 vs. 0.08±0.00; P<0.05). The increased CRMP­2 levels were also confirmed by western blotting (active mobilization group, 0.71±0.03; immobilization group, 0.49±0.01 nm; P<0.05). These results indicated that active mobilization may promote Achilles tendon healing via upregulation of CRMP­2 protein expression.

Early Ankle Mobilization Promotes Healing in a Rabbit Model of Achilles Tendon Rupture.

The use of early mobilization of the ankle joint without orthosis in the treatment of Achilles tendon rupture has been advocated as the optimal management. The goal of this study was to compare outcomes in a postoperative rabbit model of Achilles tendon rupture between early mobilization and immobilized animals using a differential proteomics approach. In total, 135 rabbits were randomized into the control group (n=15), the postoperative cast immobilization (PCI) group (n=60), and the early mobilization (EM) group (n=60). A rupture of the Achilles tendon was created in each animal model and repaired microsurgically, and tendon samples were removed at 3, 7, 14, and 21 days postoperatively. Proteins were separated using 2-dimensional polyacrylamide gel electrophoresis and identified using peptide mass fingerprinting, tandem mass spectrometry, NCBI database searches, and bioinformatics analyses. A series of differentially expressed proteins were identified between groups, some of which may play an important role in Achilles tendon healing. Notable candidate proteins that were upregulated in the EM group were identified, such as CRMP-2, galactokinase 1, tropomyosin-4, and transthyretin. The healing of ruptured Achilles tendons appears to be affected at the level of protein expression with the use of early mobilization. The classic postoperative treatment of Achilles tendon rupture with an orthosis ignored the self-protecting instinct of humans. With a novel operative technique, the repaired tendon can persist the load that comes from traction in knee and ankle joint functional movement. In addition, kinesitherapy provided an excellent experimental outcome via a mechanobiological mechanism.

Active Achilles tendon kinesitherapy accelerates Achilles tendon repair by promoting neurite regeneration.

Active Achilles tendon kinesitherapy facilitates the functional recovery of a ruptured Achilles tendon. However, protein expression during the healing process remains a controversial issue. New Zealand rabbits, aged 14 weeks, underwent tenotomy followed immediately by Achilles tendon microsurgery to repair the Achilles tendon rupture. The tendon was then immobilized or subjected to postoperative early motion treatment (kinesitherapy). Mass spectrography results showed that after 14 days of motion treatment, 18 protein spots were differentially expressed, among which, 12 were up-regulated, consisting of gelsolin isoform b and neurite growth-related protein collapsing response mediator protein 2. Western blot analysis showed that gelsolin isoform b was up-regulated at days 7-21 of motion treatment. These findings suggest that active Achilles tendon kinesitherapy promotes the neurite regeneration of a ruptured Achilles tendon and gelsolin isoform b can be used as a biomarker for Achilles tendon healing after kinesitherapy.