Abstract
Introduction and Aims: In order to evaluate the hypothesis that the ‘temporary and controlled reduction of muscle force protects repair sites come from its safe, active, and passive range of motion and diminishes complications’, a tendon repair model was evaluated.
Method: After heel cord tenotomy, Sprague-Dawley rats (n=36) were randomised to Botulinum A Toxin at six units per kilogram or saline and the tendon repaired with a two-strand core suture and a peritenon running suture. The ankles were pinned in equinus for two days, and then the animals were allowed to move freely within their cages. Analysis included gap, rupture rates, electrophysiologic measurements and mechanical testing.
Results: The treatment group had a statistically significant lower spontaneous partial or total rupture rate than the control (P=0.38). Tendon electrophysiologic testing showed that the toxin group had lower twitch and tetanus values than the control group (evidence of effective denervation). The toxin group also had better histologic healing and better strength of repair (higher rupture strength values). Histologic assessment showed that the toxin-treated group had more normal histology with less scar.
Conclusion: Chemoprotection decreases significantly spontaneous tendon rupture rates following repair in active versus control groups. The active toxin group demonstrated better healing. Decreasing tension across repair sites is equally effective in increasing inastamotic strength and permits active range of motion without rupture.
These abstracts were prepared by Editorial Secretary, George Sikorski. Correspondence should be addressed to Australian Orthopaedic Association, Ground Floor, The William Bland Centre, 229 Macquarie Street, Sydney, NSW 2000, Australia.
At least one of the authors is receiving or has received material benefits or support from a commercial source.
