Immobilization modulates macrophage accumulation in tendon-bone healing.

Abstract

Tendon-to-bone healing occurs by formation of a fibrous, scar tissue interface rather than regeneration of a normal insertion. Because inflammatory cells such as macrophages lead to formation of fibrous scar tissue, we hypothesized immobilization would allow resolution of acute inflammation and result in improved tendon-bone healing. We reconstructed the ACL of 60 Sprague-Dawley rats using a tendon autograft. An external fixation device was used to immobilize the surgically treated knee in 30 rats. We evaluated tendon-bone interface width, collagen fiber continuity, and new osteoid formation histologically. Immunohistochemistry was used to localize ED1+ and ED2+ macrophages at the tendon-bone interface at 2 and 4 weeks. Biomechanical testing was performed at 4 weeks. Interface width was smaller and collagen fiber continuity was greater in the immobilized group. Immobilized animals exhibited fewer ED1+ macrophages at the healing interface at 2 and 4 weeks. In contrast, there were more ED2+ macrophages at the interface in the immobilized group at 2 weeks. Failure load and stiffness were similar between groups at 4 weeks. The data suggest early immobilization diminishes macrophage accumulation and may allow improved tendon-bone integration.