T1ρ relaxation was quantified and correlated with intervertebral disc degeneration and proteoglycan content in cadaveric human lumbar spine tissue.
To show the use of T1ρ-weighted magnetic resonance imaging (MRI) for the assessment of degeneration and proteoglycan content in the human intervertebral disc.
Loss of proteoglycan in the nucleus pulposus occurs during early degeneration. Conventional MRI techniques cannot detect these early changes in the extracellular matrix content of the disc. T1ρ MRI is sensitive to changes in proteoglycan content of articular cartilage and may, therefore, be sensitive to proteoglycan content in the intervertebral disc.
Intact human cadaveric lumbar spines were imaged on a clinical MR scanner. Average T1ρ in the nucleus pulposus was calculated from quantitative T1ρ maps. After MRI, the spines were dissected, and proteoglycan content of the nucleus pulposus was measured. Finally, the stage of degeneration was graded using conventional T2 images.
T1ρ decreased linearly with increasing degeneration (r = −0.76, P < 0.01) and age (r = −0.76, P < 0.01). Biochemical analysis revealed a strong linear correlation between T1ρ and sulfated-glycosaminoglycan content. T1ρ was moderately correlated with water content.
Results from this study suggest that T1ρ may provide a tool for the diagnosis of early degenerative changes in the disc. T1ρ-weighted MRI is a noninvasive technique that may provide higher dynamic range than T2 and does not require a high static field or exogenous contrast agents.
Quantitative measurement of T1ρ relaxation in the intervertebral disc was performed. T1ρ was strongly correlated with degenerative grade and sulfated-glycosaminoglycan content of the nucleus pulposus. Because early degenerative changes are marked by a loss of proteoglycan in the disc, this technique provides a potential tool for noninvasive diagnosis of early disc degeneration.
From the Departments of *Orthopaedic Surgery, McKay Orthopaedic Research Laboratory, and †Radiology, University of Pennsylvania, Philadelphia PA.
Acknowledgment date: June 2, 2005. First revision date: August 5, 2005. Acceptance date: August 23, 2005.
The manuscript submitted does not contain information about medical device(s)/drug(s).
Federal funds were received in support of this work. No benefits in any form have been or will be received from a commercial party related directly or indirectly to the subject of this manuscript.
Address correspondence and reprint requests to Dawn M. Elliott, PhD, University of Pennsylvania School of Medicine, Department of Orthopaedic Surgery, McKay Orthopaedic Research Laboratory, 424 Stemmler Hall, Philadelphia, PA 19104-6081; E-mail: email@example.com