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Deficiency in immunoadaptor protein DAP12 leads to altered fracture repair


Purpose: To determine if genetically deficient DAP12 mice demonstrate impaired fracture healing responses.

Methods: All studies were performed under IACUC approval. Genetically deficient DAP12 and age-matched C57BL/(6) (B6) control mice were used. The right tibia was cleaned and prepped for surgery and a closed, mid-diaphysis fracture was created. The fractures remained unstabilized to promote healing through the formation of a cartilage intermediate. Mice were sacrificed at 7, 10, 14, 21, and 28 days post fracture and processed for histology by decalcifying the tibia and embedding the samples into paraffin wax. Serial sections were collected through the callus and every tenth slide was stained with Milligan’s Trichrome, which stains for bone tissue. Using stereology, the volume of the fracture callus, cartilage, bone, bone marrow, and fibrous tissue was determined.

Results: Histological and stereological analysis demonstrated less trabecular bone percentage and volume, increased and delayed cartilage resorption, decreased bone marrow volume, and decreased overall callus volume in the DAP12-/-. Furthermore, DAP12-/- mice displayed elevated levels of fibrous tissue within the callus. Statistical significance was not observed in the callus volume between the DAP12-/- and control B6 mice.

Conclusion: Our data indicates that DAP12 deficiency disrupts the fracture healing process. Enhancing the understanding behind the mechanism of fracture repair can lead to improve healing strategies and potential therapeutics.

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