In this study we aimed to develop a comprehensive quantitative UTE imaging package including UTE-Cones actual flip angle imaging (UTE-Cones-AFI) for accurate B1 mapping, UTE-Cones variable flip angle (UTE-Cones-VFA) for T1 mapping, 3D UTE-Cones-MT for MT modeling, UTE-Cones-AdiabT1rho for T1r mapping, and multi-echo UTE-Cones for T2* mapping. The techniques were evaluated on cadaveric human knee joints.
Six human knee joint samples from six donors (average age=52.5 y, 5 females and 1 male) were scanned on a clinical 3T MRI scanner (GE Healthcare) with an eight-channel knee coil for both signal transmission and receive. Clinical T2-weighted and PD-weighted images were used to identify osteoarthritis (OA) (Kellgren-Lawrence (KL) grade >1).
Quantitative MRI methods including CPMG-T2, UTE-Cones-MT modeling, UTE-Cones AdiabT1rho and UTE-Cones T2* were used to compare between the normal and OA groups. The conventional 3D UTE-Cones sequence (Figs. 1A and 1B) with a short rectangular pulse (duration of 26 to 52 µs) was used for non-selective signal excitation followed by 3D spiral trajectories with conical view ordering. 3D UTE-Cones-AFI was used for B1 mapping (Figs. 1C). The 3D UTE-Cones-MT (Figs. 1D) and UTE-Cones-AdiabT1rho (Figs. 1E) sequences were used for MT modeling and T1rho measurements, respectively.
The quantitative sequence parameters were shown as follows: A) 2D CMPG T2 measurement (TE=6.3, 12.7, 19.0, 25.4, 31.7, 38.0, 44.4, 50.8, 57.1, 63.4, 69.8, 76.1ms); B) 3D UTE-Cones-AFI: TR = 20/100 ms and flip angle = 45°; C) 3D UTE-Cones-VFA for T1 measurement: TR = 24 ms, flip angle = 4°, 8°, 16°, 24°, 32°; B) 3D UTE-Cones-MT with three saturation pulse powers (500°, 1000°, and 1500°) and five frequency offsets (2, 5, 10, 20 and 50 kHz), TR=102ms, flip angle=7°, number of spoke per-preparation (Nsp) = 9; C) 3D UTE-Cones-AdiabT1rho: spin-locking time (TSL) = 0, 6, 12, 24, 36, 48, 72 and 96 ms, TR=500ms, flip angle=10°, Nsp = 21; D) 3D UTE-Cones T2*: TE = 4, 8, 12, 16 and 20ms. Other imaging parameters included: FOV = 13×13×12 cm3, matrix=256×256×60. The measured B1 map will be used for both T1 and MT modeling correction. The derived T1 values were used for both MT modeling and AdiabT1rho calculation.
Figure 2 shows the quantitative results of a representative normal knee cartilage slice with T2 = 21.97±0.42 ms, T1rho= 27.56±3.73 ms and MT modeling: macromolecular proton fraction f = 18.83±1.52 %, proton exchange rate = 5.23±2.13 s-1 and macromolecular proton T2: T2b = 7.17±0.35 us.
Figure 3 shows the quantitative results of a representative OA knee cartilage slice with T2 = 40.00±2.90 ms, T1rho= 42.53±7.16 ms and MT modeling: macromolecular proton fraction f = 11.25±1.26%, proton exchange rate = 1.91±0.52 s-1 and T2b = 7.21±0.45 us.
Table 1 summarizes the T2,T2*, f and T1rho values between normal and abnormal groups of knee slices of the six ex vivo knees. Significant increase in AdiabT1rho (P=0.002) and T2 (P=0.003) and decrease in T2* (P=0.000) and macromolecular fraction f (P=0.000) are observed for the abnormal group. The increase in AdiabT1rho and decrease in macromolecular fraction reflect the loss of proteoglycan and collagen in advanced OA. The decrease in T2* might be related to chondrocalcinosis, although further research is needed.
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