Macrophage depletion following anterior cruciate ligament reconstruction resulted in significantly improved morphologic and biomechanical properties at the healing tendon-bone interface, which we hypothesize are due to diminished macrophage-induced TGF-beta production.

Further studies are needed to investigate the potential clinical application of enhancing healing and decreasing recovery time using bone morphogenetic proteins in soft tissue ligament reconstruction.

Osteoprotegerin significantly improves bone formation around the grafted tendon and improves the stiffness at the healing tendon-bone junction in a rabbit model.

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

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