A segmental defect adaptation of the mouse closed femur fracture model for the analysis of severely impaired bone healing.

Autor: Kaur A; Musculoskeletal Disease Center Research Service (151) Jerry L. Pettis Memorial Veterans Administration Medical Center Loma Linda CA USA., Mohan S; Musculoskeletal Disease Center Research Service (151) Jerry L. Pettis Memorial Veterans Administration Medical Center Loma Linda CA USA.; Department of Medicine Loma Linda University Loma Linda CA USA.; Department of Orthopedic Surgery Loma Linda University Loma Linda CA USA., Rundle CH; Musculoskeletal Disease Center Research Service (151) Jerry L. Pettis Memorial Veterans Administration Medical Center Loma Linda CA USA.; Department of Medicine Loma Linda University Loma Linda CA USA.
Jazyk: angličtina
Zdroj: Animal models and experimental medicine [Animal Model Exp Med] 2020 May 01; Vol. 3 (2), pp. 130-139. Date of Electronic Publication: 2020 May 01 (Print Publication: 2020).
DOI: 10.1002/ame2.12114
Abstrakt: Objective: To better characterize nonunion endochondral bone healing and evaluate novel therapeutic approaches for critical size defect healing in clinically challenging bone repair, a segmental defect model of bone injury was adapted from the three-point bending closed fracture technique in the murine femur.
Methods: The mouse femur was surgically stabilized with an intramedullary threaded rod with plastic spacers and the defect adjusted to different sizes. Healing of the different defects was analyzed by radiology and histology to 8 weeks postsurgery. To determine whether this model was effective for evaluating the benefits of molecular therapy, BMP-2 was applied to the defect and healing then examined.
Results: Intramedullary spacers were effective in maintaining the defect. Callus bone formation was initiated but was arrested at defect sizes of 2.5 mm and above, with no more progress in callus bone development evident to 8 weeks healing. Cartilage development in a critical size defect attenuated very early in healing without bone development, in contrast to the closed femur fracture healing, where callus cartilage was replaced by bone. BMP-2 therapy promoted osteogenesis of the resident cells of the defect, but there was no further callus development to indicate that healing to pre-surgery bone structure was successful.
Conclusions: This segmental defect adaptation of the closed femur fracture model of murine bone repair severely impairs callus development and bone healing, reflecting a challenging bone injury. It is adjustable and can be compared to the closed fracture model to ascertain healing deficiencies and the efficacy of therapeutic approaches.
Competing Interests: None.
(Published 2020. This article is a U.S. Government work and is in the public domain in the USA. Animal Models and Experimental Medicine published by John Wiley & Sons Australia, Ltd on behalf of The Chinese Association for Laboratory Animal Sciences.)
Databáze: MEDLINE
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