Purpose: Adhesion formation is closely related to tendon-gliding function. We aimed to investigate apoptosis (programmed cell death) in adhesions and tendons and study its relationship to the mechanics of adhesions and healing tendons.
Methods: The flexor digitorum profundus tendons of 30 long toes in 15 chickens were completely transected and repaired surgically. At postoperative weeks 4, 6, and 8, tendon-gliding excursions were tested and adhesion scores were recorded. Tendons and surrounding adhesions were then harvested for analysis of apoptosis using in situ terminal deoxynucleotidyl transferase dUTP (deoxyuridine triphosphate) nick end labeling assay. Three-dimensional image reconstruction was used to provide an overall view of cellular distribution in tendons and adhesions. Finally, we analyzed the correlation between the apoptotic index measured at the adhesions and the gliding excursions. Ten uninjured tendons served as normal controls.
Results: Apoptosis was found to be a dominant cellular event in the adhesion tissues at both the adhesion-tendon gliding interface and the adhesion core. The apoptotic index in the adhesions was generally above 20% to 50%. The apoptotic index was significantly higher in the adhesions than in the junction region of the cut tendon ends at weeks 4, 6, and 8. A higher apoptotic index in the adhesions significantly correlated to lower tendon excursions at week 6.
Conclusions: Apoptosis in adhesions and at the adhesion-tendon interface is a prominent event in the tendon-healing process. The tendons exhibiting a lower tendon-gliding amplitude, meaning more severe adhesions, tended to have a greater apoptotic index in their adhesions during a certain period of the tendon-remodeling process.
Clinical relevance: Apoptosis in the adhesions and at the adhesion-tendon interface may contribute remarkably to the fate of adhesions and the restoration of the tendon gliding surface, which may be closely related to the tendon function.
Copyright © 2013 American Society for Surgery of the Hand. Published by Elsevier Inc. All rights reserved.