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Updated: Aug 2, 2026
A Simple Critical-sized Femoral Defect Model in Mice
Published on: March 15, 2015
Congenital lack of COX-2 affects mechanical and geometric properties of bone in mice
1Department of Biomedical Engineering, University of Memphis, Memphis, Tennessee, USA.
Abstract:
We compared the mechanical properties of bones from mice lacking either a functional cycloxygenase-1 (C57BL6/DBA COX-1-/-; n = 9) or COX-2 (C57BL6/DBA COX-2-/-; n = 9) gene and wild type mice (C57BL6/DBA; n = 10). Twenty-eight right femora from 3-month-old male mice were used to determine bulk structural and material properties of bone by three-point bending. Bone matrix properties were also measured by nanoindentation to access the changes in bulk mechanical properties due to changes in bone matrix or bone geometry. The bulk material properties (elastic modulus, P < 0.05; ultimate stress, P < 0.01) of COX-2-/- bones were lower than those of wild-type mice whereas the bulk structural properties (stiffness, P > 0.2; breaking force, P > 0.1) were similar to those of the wild-type mice. COX-2-/- mice had a longer moment of inertia but their cortical bones were thinner and contained many more intra-cortical pores compared with the bones of the other two groups. Finally, the bone matrix properties of COX-1-/- mice, COX-2-/- mice and their heterozygous littermates were similar to those of C57BL6/DBA wild-type mice.
Insights
Cyclooxygenase-2 (COX-2) deficiency in mice significantly reduces bone material strength, impacting elastic modulus and ultimate stress. However, overall bone structure and matrix properties remain comparable to wild-type mice.
Area of Science:
- Biomechanical Engineering
- Skeletal Biology
- Pharmacology
Background:
- Cyclooxygenase enzymes (COX-1 and COX-2) play roles in inflammation and bone metabolism.
- Understanding the specific contributions of COX-2 to bone mechanical properties is crucial for skeletal health research.
Purpose of the Study:
- To investigate the impact of cyclooxygenase-2 (COX-2) gene deficiency on the mechanical properties of mouse femora.
- To compare bone mechanical properties between COX-2 knockout mice, COX-1 knockout mice, and wild-type controls.
Main Methods:
- Three-point bending tests were performed on femora from COX-2 knockout, COX-1 knockout, and wild-type mice.
- Nanoindentation was used to assess bone matrix properties.
- Bulk structural and material properties were analyzed.
Main Results:
- COX-2 knockout mice exhibited significantly lower bone material properties (elastic modulus and ultimate stress) compared to wild-type mice.
- Bulk structural properties (stiffness and breaking force) were similar across all groups.
- COX-2 knockout mice showed altered bone geometry, including thinner cortices and increased intra-cortical pores.
Conclusions:
- COX-2 deficiency primarily affects bone material quality rather than overall structural integrity.
- The findings suggest a specific role for COX-2 in maintaining bone matrix properties.
- Further research is needed to elucidate the mechanisms by which COX-2 influences bone material strength.
