title: Chronic axial compression of the mouse tail segment induces MRI bone marrow edema changes that correlate with increased marrow vasculature and cellularity.
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.
authors.affiliation: The Center for Musculoskeletal Research, University of Rochester Medical Center, 601 Elmwood Avenue, Box 665, Rochester, New York 14642, USA.
authors.forename: M Owen
authors.initials: MO
authors.lastname: Papuga
authors.forename: Steven T
authors.initials: ST
authors.lastname: Proulx
authors.forename: Edmund
authors.initials: E
authors.lastname: Kwok
authors.forename: Zhigang
authors.initials: Z
authors.lastname: You
authors.forename: Paul T
authors.initials: PT
authors.lastname: Rubery
authors.forename: Paul E
authors.initials: PE
authors.lastname: Dougherty
authors.forename: Matthew J
authors.initials: MJ
authors.lastname: Hilton
authors.forename: Hani A
authors.initials: HA
authors.lastname: Awad
authors.forename: Edward M
authors.initials: EM
authors.lastname: Schwarz
mesh_terms: D000367:Age Factors; D000818:Animals; D001853:Bone Marrow / Q000000981:diagnostic imaging / Q000473:pathology* / Q000502:physiology*; D001854:Bone Marrow Cells / Q000473:pathology / Q000502:physiology; D002908:Chronic Disease; D019245:Compressive Strength / Q000502:physiology*; D004487:Edema / Q000000981:diagnostic imaging / Q000473:pathology* / Q000503:physiopathology*; D005260:Female; D008279:Magnetic Resonance Imaging; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D010010:Osteoclasts / Q000473:pathology / Q000502:physiology; D013131:Spine / Q000000981:diagnostic imaging / Q000473:pathology / Q000502:physiology; D025242:Spondylarthropathies / Q000000981:diagnostic imaging / Q000473:pathology* / Q000503:physiopathology*; D013623:Tail / Q000000981:diagnostic imaging / Q000473:pathology / Q000502:physiology; D016474:Weight-Bearing / Q000502:physiology; D055114:X-Ray Microtomography