Flexor tendon healing and restoration of the gliding surface. An ultrastructural study in dogs

Abstract

Healing canine flexor tendons were treated with either total immobilization or early controlled passive mobilization and were studied by light, scanning, and transmission electron microscopy at ten, twenty-one, and forty-two days. The immobilized tendons healed by ingrowth of connective tissue from the digital sheath and cellular proliferation of the endotenon. The ingrowth of reparative tissue from the digital sheath overwhelmed the epitenon response. At the ultrastructural level, collagen resorption was prominent whereas protein synthesis was limited. This was observed at all study-intervals. In contrast, the mobilized tendons healed by proliferation and migration of cells from the epitenon. Ingrowth of reparative tissue from the tendon sheath was notably lacking in this group. The epitenon cells exhibited greater cellular activity and collagen production at each interval compared with cells of the immobilized repairs. Clinical relevance: Early controlled passive motion was shown to stimulate an intrinsic healing response in a clinically relevant tendon-repair model. The gliding surface was restored at an early stage, and the tendon healed more rapidly than in the immobilized repairs. These data support the concept that a precise, limited immediate-mobilization program improves the quality of the biological repair response following flexor tendon repair within the digital sheath.