Purpose: Tendon-to-bone repair remains a surgical challenge. Although bone tunnel fixation is a common surgical technique whereby soft tissue is expected to heal against a bone tunnel interface, contemporary methods have yet to recapitulate biomechanical similarity to the native enthesis. In this study, we aimed to understand how inside-out longitudinal tendon inversion affects bone tunnel healing with the hypothesis that inversion removes the gliding epitenon surface to facilitate interface healing.
Methods: Forty male Sprague-Dawley rats underwent either native tendon tenodesis (control group) or tendon inversion tenodesis (experimental group). Interface tissue was harvested 8 weeks after surgery. Biomechanical testing was performed to assess tensile strength and modes of failure. Histology was performed to assess tissue architecture, and immunohistochemistry confirmed the disruption of epitendinous lubricin from interface tissues.
Results: Maximum tensile strength increased after tendon inversion compared with control surgery. The extracellular matrix protein lubricin was reduced with tendon inversion, and specimens with tendon inversion had greater healing scores and collagen fibril alignment at the healing interface.
Conclusions: Tendon inversion has the potential to improve bone tunnel healing in rats.
Clinical relevance: Our findings suggest that longitudinal tendon inversion, or inverse tubularization, in a rat biceps model improves tendon-to-bone healing in part because of disruption of the epitendinous surface at the bone healing interface. This work provides molecular insight into future improvements for tendon-to-bone repair surgical techniques.
Keywords: Lubricin; rat model; surgical technique; tendon; tendon-to-bone repair; tenodesis.
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