The Addition of a Krackow Rip Stop Suture Augment After Achilles Tendon Debridement for Insertional Achilles Tendinopathy: A Biomechanical Study

Background In the operative treatment of insertional Achilles tendinopathy, the Achilles tendon is often released from its insertion to allow for adequate debridement of pathologic tissue. The use of a double row suture anchor construct has become increasingly favorable among surgeons after Achilles tendon debridement. This study hypothesized that the addition of a Krackow rip stop suture augment to the double row suture anchor construct would increase the repair’s maximum load to failure. A biomechanically stronger repair would potentially decrease the risk of catastrophic failure with early weight-bearing or accidental forced dorsiflexion after operative management for insertional Achilles tendinopathy. Methods Fourteen cadaveric specimens were used to compare the 2 repair techniques. Achilles tendons were debrided and repaired using either a double row suture anchor with and without the additional Krackow rip stop suture augment. The 2 repair techniques were compared using an axial-torsion testing system to measure average load to failure. Results The average load to failure for the double row suture anchor repair alone was 152.00 N. The average load to failure for the tendons with the double row suture anchor with the Krackow rip stop augment was 383.08 N. An independent-samples Mann-Whitney U-test was conducted and the suture anchor plus Krackow augment group had a significantly higher load to failure ( P = .011, Mann-Whitney U = 5.00, n1 = n2 = 7, P < .05, 2-tailed). Conclusion This study confirmed that the addition of a Krakow rip stop augment to the double row suture anchor is able to increase the maximum load to failure when compared to the double row suture anchor alone. These results suggest the potential of this added technique to decrease the risk of catastrophic failure.

Evaluation of Therapeutic Effects of Quercetin Against Achilles Tendinopathy in Rats via Oxidative Stress, Inflammation, Apoptosis, Autophagy, and Metalloproteinases

Background: Achilles tendinopathy, seen in athletes and manual labor workers, is an inflammatory condition characterized by chronic tendon pain. Owing to the toxicity that develops in various organs attributed to the use of anti–inflammatory drugs, there is a need for new therapeutic agents. Purpose: In the present study, the effects of quercetin (Que), the one that attracted the most attention of researchers studying this group of flavonoids, were investigated against collagenase–induced tendinopathy. Study Design: Controlled laboratory study. Methods: A total of 35 Sprague-Dawley rats were used in the study. Tendinopathy was created by injecting a single dose of collagenase (10 μL; 10 mg/mL) into the tendons of rats. Thirty minutes after the injection, Que was administered at doses of 25 or 50 mg/kg. Que administration was carried out for 7 days. Animals underwent a motility test at the end of the study. In addition, markers of oxidative stress, inflammation, apoptosis, and autophagy, as well as the expression levels of matrix metalloproteinases (MMPs 2, 3, 9, and 13), ICAM-1, and STAT3, were measured in tendon tissues with biochemical, molecular, and Western blot techniques. Results: The results showed that oxidative stress, inflammation, apoptosis, and autophagy were triggered by the injection of collagenase. In addition, MMPs, ICAM-1, and STAT3 were activated to participate in the development of tendinopathy. Que was found to reduce ICAM-1 levels in tendon tissue. Moreover, Que showed antioxidant, anti–inflammatory, antiapoptotic, and antiautophagic effects on tendons against tendinopathy. More important, Que suppressed the expression of MMPs in the tendon tissues. Conclusion: Que has protective properties against collagenase–induced tendon damage in rats. Clinical Relevance: We believe that with further study, Que may be shown to be an alternative treatment option for athletes or others who experience tendon injuries.