PURPOSE: To establish the specificity of T1rho with respect to fixed charge density (FCD) as a measure of proteoglycan (PG) content in cartilage during the onset of osteoarthritis (OA). MATERIALS AND METHODS: T1rho-weighted and sodium MRI were performed on cartilage samples of enzymatically degraded bovine explants and natural osteoarthritic human samples representing controlled and physiological models of OA, respectively. Spatial maps of T1rho and FCD (measured using the previously validated method of sodium MRI) were calculated from image data. Data were extracted from the maps and subjected to linear regression to compare changes in T1rho with changes in FCD in each model. Tissue samples were subjected to histological staining for a reduction in PG content. RESULTS: Plots of normalized T1rho rate vs. FCD were found to be strongly correlated (R2 > 0.75 and 0.85) in both models with nearly the same slope of approximately 1/2 (P > 0.51). Loss of PG in bovine and human tissue was confirmed by histology. CONCLUSION: The strong correlation of the FCD and T1rho data in both the controlled and physiological models demonstrates that changes in T1rho are due predominantly to changes in PG content. This work is a first step in establishing T1rho as a method of quantifying PG changes in early-stage OA. Copyright 2004 Wiley-Liss, Inc.
PURPOSE: To establish the specificity of T1rho with respect to fixed charge density (FCD) as a measure of proteoglycan (PG) content in cartilage during the onset of osteoarthritis (OA). MATERIALS AND METHODS: T1rho-weighted and sodium MRI were performed on cartilage samples of enzymatically degraded bovine explants and natural osteoarthritic human samples representing controlled and physiological models of OA, respectively. Spatial maps of T1rho and FCD (measured using the previously validated method of sodium MRI) were calculated from image data. Data were extracted from the maps and subjected to linear regression to compare changes in T1rho with changes in FCD in each model. Tissue samples were subjected to histological staining for a reduction in PG content. RESULTS: Plots of normalized T1rho rate vs. FCD were found to be strongly correlated (R2 > 0.75 and 0.85) in both models with nearly the same slope of approximately 1/2 (P > 0.51). Loss of PG in bovine and human tissue was confirmed by histology. CONCLUSION: The strong correlation of the FCD and T1rho data in both the controlled and physiological models demonstrates that changes in T1rho are due predominantly to changes in PG content. This work is a first step in establishing T1rho as a method of quantifying PG changes in early-stage OA. Copyright 2004 Wiley-Liss, Inc.
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