Flexor Hallucis Longus Transfer Improves Achilles Tendon Load to Failure in Surgery for Non-Insertional Tendinopathy: A Biomechanical Study.

Background: Non-insertional Achilles tendinopathy is a common disorder that may be treated with surgical debridement. A flexor hallucis longus (FHL) transfer is recommended if debridement of >= 50% is performed; however, there are no biomechanical data to support this. The purpose of this study was to assess the added biomechanical strength provided by an FHL transfer with incrementally sized non-insertional Achilles tendon defects. Methods: Thirty matched-pair below-the-knee cadaveric specimens (n = 60) (mean age at the time of donor death, 67 years; range, 36 to 74 years) were obtained and randomly divided into 3 groups according to whether the defect was 25%, 50%, or 75% of the tendon width. One specimen of each pair was then randomly selected to undergo FHL transfer using interference screw fixation. All specimens then underwent cyclic loading of 100 N, and elongation of the medial and lateral limbs of the tendon defect was recorded. The constructs were then loaded to failure to measure stiffness, ultimate strength, and peak elongation before failure. Results: The specimens with a 75% defect had significantly less elongation of the medial and lateral tendon-defect limbs when an FHL transfer had been done (p < 0.05). Ultimate load to failure was significantly increased in all groups (by 242 to 270 N depending on the defect size) following FHL transfer. Failures usually occurred through the tendon defect in the 75% and 50% defect groups, whereas all failures occurred at the Achilles tendon insertion when a 25% defect had been created. No significant differences were found in peak elongation with the addition of an FHL transfer. FHL augmentation resulted in significantly greater stiffness in the 25% and 75% defect groups (p < 0.05). Conclusions: This study showed that an FHL transfer significantly increased load to failure of Achilles tendons with a non-insertional defect involving 25%, 50%, and 75% of the tendon width. The mechanism of failure was usually through the defect in the specimens with a 50% or 75% defect, supporting the use of FHL augmentation with debridement of >= 50%.