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Research Papers

Trabecular Bone Loss at a Distant Skeletal Site Following Noninvasive Knee Injury in Mice

[+] Author and Article Information
Blaine A. Christiansen

Department of Orthopaedic Surgery,
University of California-Davis Medical Center,
4635 2nd Avenue, Suite 2000,
Sacramento, CA 95817;
Biomedical Engineering Graduate Group,
University of California-Davis,
Davis, CA 95616
e-mail: bchristiansen@ucdavis.edu

Armaun J. Emami, Michael R. Hardisty

Department of Orthopaedic Surgery,
University of California-Davis Medical Center,
4635 2nd Avenue, Suite 2000,
Sacramento, CA 95817;
Biomedical Engineering Graduate Group,
University of California-Davis,
Davis, CA 95616

David P. Fyhrie

Department of Orthopaedic Surgery,
University of California-Davis Medical Center,
4635 2nd Avenue, Suite 2000,
Sacramento, CA 95817;
Biomedical Engineering Graduate Group,
University of California-Davis,
Davis, CA 95616

Patrick B. Satkunananthan

Department of Orthopaedic Surgery,
University of California-Davis Medical Center,
4635 2nd Avenue, Suite 2000,
Sacramento, CA 95817;
Biomedical Engineering Graduate Group,
University of California-Davis,
Davis, CA 95616

1Corresponding author.

Manuscript received June 17, 2014; final manuscript received September 9, 2014; accepted manuscript posted October 16, 2014; published online December 10, 2014. Assoc. Editor: Ara Nazarian.

J Biomech Eng 137(1), 011005 (Jan 01, 2015) Paper No: BIO-14-1271; doi: 10.1115/1.4028824 History: Received June 17, 2014; Revised September 09, 2014; Accepted October 16, 2014; Online December 10, 2014

Traumatic injuries can have systemic consequences, as the early inflammatory response after trauma can lead to tissue destruction at sites not affected by the initial injury. This systemic catabolism may occur in the skeleton following traumatic injuries such as anterior cruciate ligament (ACL) rupture. However, bone loss following injury at distant, unrelated skeletal sites has not yet been established. In the current study, we utilized a mouse knee injury model to determine whether acute knee injury causes a mechanically significant trabecular bone loss at a distant, unrelated skeletal site (L5 vertebral body). Knee injury was noninvasively induced using either high-speed (HS; 500 mm/s) or low-speed (LS; 1 mm/s) tibial compression overload. HS injury creates an ACL rupture by midsubstance tear, while LS injury creates an ACL rupture with an associated avulsion bone fracture. At 10 days post-injury, vertebral trabecular bone structure was quantified using high-resolution microcomputed tomography (μCT), and differences in mechanical properties were determined using finite element modeling (FEM) and compressive mechanical testing. We hypothesized that knee injury would initiate a loss of trabecular bone structure and strength at the L5 vertebral body. Consistent with our hypothesis, we found significant decreases in trabecular bone volume fraction (BV/TV) and trabecular number at the L5 vertebral body in LS injured mice compared to sham (−8.8% and −5.0%, respectively), while HS injured mice exhibited a similar, but lower magnitude response (−5.1% and −2.5%, respectively). Contrary to our hypothesis, this decrease in trabecular bone structure did not translate to a significant deficit in compressive stiffness or ultimate load of the full trabecular body assessed by mechanical testing or FEM. However, we were able to detect significant decreases in compressive stiffness in both HS and LS injured specimens when FE models were loaded directly through the trabecular bone region (−9.9% and −8.1%, and 3, respectively). This finding may be particularly important for osteoporotic fracture risk, as damage within vertebral bodies has been shown to initiate within the trabecular bone compartment. Altogether, these data point to a systemic trabecular bone loss as a consequence of fracture or traumatic musculoskeletal injury, which may be an underlying mechanism contributing to increased risk of refracture following an initial injury. This finding may have consequences for treatment of acute musculoskeletal injuries and the prevention of future bone fragility.

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Figures

Grahic Jump Location
Fig. 1

Mouse L5 vertebra orthogonal view (left). Trabecular bone structure of the L5 vertebral body was analyzed with microcomputed tomography in a volume excluding the endplates and posterior elements (right).

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Fig. 2

Representative L5 vertebral body (reconstructed from μCT scan) used for finite element analysis with parallel-cut ends and posterior elements trimmed at the pedicle (left). FE models were compressed with two different boundary conditions (center/right). Full specimen compression was simulated by loading to the entire cross section at the top and bottom, including both trabecular bone and the cortical shell. Trabecular bone compression was simulated by loading 1.002 mm (167 pixel) diameter circular areas axially aligned on the top and bottom of the models.

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Fig. 3

L5 vertebral body trabecular bone structural parameters. BV/TV was 8.8% lower in LS injured mice than sham mice. Similarly, trabecular number was decreased 2.5% and 5.0% for HS and LS injured mice, respectively, while trabecular separation was increased 3.4% and 5.3% in HS and LS injured mice, respectively, compared to sham mice. No significant differences were observed for trabecular thickness. * p < 0.05

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Fig. 4

Representative stress distribution in the direction of the principal loading axis at the top boundary of the model (top row) and midfrontal section (middle row). Full specimen compression (left column) did not predict any significant differences between HS injured, LS injured, or sham specimens (bottom left). However, trabecular bone loading (right column) predicted significantly lower compressive stiffness for HS injured (−9.9%) and LS injured (−8.1%) specimens compared to sham (bottom right). * p < 0.05

Grahic Jump Location
Fig. 5

Results for compressive mechanical testing of isolated mouse L5 vertebral bodies. No significant differences were observed between HS injured, LS injured, or sham specimens for stiffness or ultimate load.

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