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Updated: Jun 15, 2026
Longitudinal Evaluation of Mouse Hind Limb Bone Loss After Spinal Cord Injury using Novel, in vivo, Methodology
Published on: December 7, 2011
Chronic axial compression of the mouse tail segment induces MRI bone marrow edema changes that correlate with
M Owen Papuga1, Steven T Proulx, Edmund Kwok
1The Center for Musculoskeletal Research, University of Rochester Medical Center, 601 Elmwood Avenue, Box 665, Rochester, New York 14642, USA.
Abstract:
Magnetic resonance imaging (MRI) of bone marrow edema (BME) has been found to be helpful in the diagnosis of back pain attributed to degenerative disk disease (DDD) and spondyloarthropathy (SA), but its interpretation is limited by a lack of knowledge of its nature and natural history. We assessed effects of compressive forces to mouse tail segments of WT and TNF-Tg mice with SA, via contrast enhanced-MRI and histology. Normalized marrow contrast enhancement (NMCE) of uninstrumented WT vertebrae significantly decrease, threefold (p < 0.01) from 8 to 12 weeks of age, while the NMCE of TNF-Tg vertebrae remained elevated. Compressive loading (6x body weight) increased NMCE twofold (p < 0.02) within 2 weeks in WT tails, which was equal to 6x loaded TNF-Tg tails within 4 weeks. Histology confirmed degenerative changes and that load-induced NMCE corresponded to increased vascular sinus tissue (35 +/- 3% vs. 19 +/- 3%; p < 0.01) and cellularity (4,235 +/- 886 vs.1,468 +/- 320 cells/mm(2); p < 0.01) for the loaded versus unloaded WT, respectively. However, micro-computed tomography (CT) analyses failed to detect significant load-induced changes to bone. While the bone marrow of loaded WT and TNF-Tg vertebrae were similar, histology demonstrated mild cellular infiltrate and increased osteoclastic resorption in the WT tails versus severe inflammatory-erosive arthritis in TNF-Tg joints. Significant (p < 0.05) decreases in cortical and trabecular bone volume in uninstrumented TNF-Tg versus WT vertebrae were confirmed by micro-CT. Thus, chronic load-induced DDD causes BME signals in vertebrae similar to those observed from SA, and both DDD and SA signals correlate with a conversion from yellow to red marrow, with increased vascularity.
Insights
Chronic loading causes bone marrow edema (BME) signals in vertebrae, mimicking spondyloarthropathy (SA). This BME, seen in degenerative disk disease (DDD), involves marrow conversion and increased vascularity, impacting back pain diagnosis.
Area of Science:
- Orthopedics
- Radiology
- Pathology
Background:
- Bone marrow edema (BME) on MRI aids in diagnosing back pain from degenerative disk disease (DDD) and spondyloarthropathy (SA).
- The precise nature and natural history of BME remain incompletely understood, limiting diagnostic interpretation.
Purpose of the Study:
- To investigate the effects of compressive forces on bone marrow in mouse models of DDD and SA.
- To correlate MRI findings with histological changes and assess bone microarchitecture.
Main Methods:
- Contrast-enhanced MRI and histology were used to assess mouse tail segments under compressive loading.
- Wild-type (WT) and TNF-transgenic (TNF-Tg) mice with SA were studied.
- Micro-computed tomography (micro-CT) analyzed bone microarchitecture.
Main Results:
- Compressive loading significantly increased normalized marrow contrast enhancement (NMCE) in WT mice, indicating BME.
- Load-induced BME in WT mice correlated with increased vascular sinus tissue and cellularity, suggesting marrow conversion.
- While MRI showed BME, micro-CT detected no significant load-induced changes in bone structure, but revealed reduced bone volume in uninstrumented TNF-Tg mice.
- Histology showed inflammatory changes in TNF-Tg mice, distinct from the degenerative changes in loaded WT mice.
Conclusions:
- Chronic loading-induced DDD can generate BME signals in vertebrae similar to those seen in SA.
- Both DDD and SA are associated with a conversion of yellow to red bone marrow, characterized by increased vascularity.
- MRI detection of BME in DDD and SA reflects underlying marrow changes rather than significant structural bone alterations.
