Quantitative susceptibility mapping (QSM) has enabled MRI of tissue magnetic susceptibility to advance from simple qualitative detection of hypointense blooming artifacts to precise quantitative measurement of spatial biodistributions. QSM technology may be regarded to be sufficiently developed and validated to warrant wide dissemination for clinical applications of imaging isotropic susceptibility, which is dominated by metals in tissue, including iron and calcium. These biometals are highly regulated as vital participants in normal cellular biochemistry, and their dysregulations are manifested in a variety of pathologic processes. Therefore, QSM can be used to assess important tissue functions and disease. To facilitate QSM clinical translation, this review aims to organize pertinent information for implementing a robust automated QSM technique in routine MRI practice and to summarize available knowledge on diseases for which QSM can be used to improve patient care. In brief, QSM can be generated with postprocessing whenever gradient echo MRI is performed. QSM can be useful for diseases that involve neurodegeneration, inflammation, hemorrhage, abnormal oxygen consumption, substantial alterations in highly paramagnetic cellular iron, bone mineralization, or pathologic calcification; and for all disorders in which MRI diagnosis or surveillance requires contrast agent injection. Clinicians may consider integrating QSM into their routine imaging practices by including gradient echo sequences in all relevant MRI protocols.

This study demonstrates the dependence of non-local susceptibility effects on object orientation in gradient echo MRI and the reduction of non-local effects by deconvolution using quantitative susceptibility mapping (QSM). Imaging experiments were performed on a 3T MRI system using a spoiled 3D multi-echo GRE sequence on phantoms of known susceptibilities, and on human brains of healthy subjects and patients with intracerebral hemorrhages. Magnetic field measurements were determined from multiple echo phase data. To determine the QSM, these field measurements were deconvolved through a dipole inversion kernel under a constraint of consistency with the magnitude images. Phantom and human data demonstrated that the hypointense region in GRE magnitude image corresponding to a susceptibility source increased in volume with TE and varied with the source orientation. The induced magnetic field extended beyond the susceptibility source and varied with its orientation. In QSM, these blooming artifacts, including their dependence on object orientation, were reduced and material susceptibilities were quantified.

Purpose To investigate the magnetic susceptibility of intracerebral hemorrhages (ICH) at various stages by applying quantitative susceptibility mapping (QSM). Materials and Methods Blood susceptibility was measured serially using QSM after venous blood withdrawal from healthy subjects. Forty-two patients who provided written consent were recruited in this institutional review board approved study. Gradient echo MRI data of the 42 patients (17 females; 64±12 yrs) with ICH were processed with QSM. The susceptibilities of various blood products within hematomas were measured on QSM. Results Blood susceptibility continually increased and reached a plateau 96 hours after venous blood withdrawal. Hematomas at all stages were consistently hyperintense on QSM. Susceptibility was 0.57 ± 0.48, 1.30 ± 0.33, 1.14 ± 0.46, 0.40 ± 0.13, and 0.71 ± 0.31 parts per million (ppm) for hyperacute, acute, early subacute, late subacute and chronic stages of hematomas respectively. The susceptibility decrease from early subacute (1.14ppm) to late subacute (0.4ppm) was significant (p<0.01). Conclusion QSM reveals positive susceptibility in hyperacute hematomas, indicating that even at their hyperacute stage, deoxyhemoglobin may exist throughout the hematoma volume, not just at its rim as seen on conventional T2* imaging. QSM also reveals reduction of susceptibility from early subacute to late subacute ICH, suggesting that methemoglobin concentration decreases at the late subacute stage.

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Purpose To validate a chemical shift‐encoded (CSE) water–fat imaging for quantifying marrow fat fraction (FF), using proton magnetic resonance spectroscopy (MRS) as reference. Materials and Methods Multiecho T2‐corrected MRS and CSE imaging with eight‐echo gradient‐echo acquisitions at 3T were performed to calculate marrow FF in 83 subjects, including 41 with normal bone mineral density (BMD), 26 with osteopenia, and 16 with osteoporosis (based on DXA). Eight participants were scanned three times with repositioning to assess the repeatability of CSE FF map measurements. Pearson correlation coefficient, Bland–Altman 95% limit of agreement, and Lin's concordance correlation coefficient were calculated. Results The Pearson correlation coefficient was 0.979 and Lin's concordance correlation coefficient was 0.962 between CSE‐based FF and MRS‐based FF. All data points, calculated using the Bland–Altman method, were within the limits of agreement. The intra‐ and interrater agreement for average CSE‐based FF was excellent (intrarater, intraclass correlation coefficient [ICC] = 0.993; interrater, ICC = 0.976–0.982 for different BMD groups). In the subgroups of varying BMD, inverse correlations were observed to be very similar between BMD (r = –0.560 to –0.710), T‐score (r = –0.526 to –0.747), and CSE‐based FF, and between BMD (r = –0.539 to –0.706), T‐score (r = –0.501 to –0.742), and MRS‐based FF even controlling for age, years since menopause, and body mass index. The repeatability for CSE FF map measurements expressed as absolute precision error was 1.45%. Conclusion CSE imaging is equally accurate in characterizing marrow fat content as MRS. Given its excellent correlation and concordance with MRS, the CSE sequence could be used as a potential replacement technique for marrow fat quantification. Level of Evidence: 1 J. Magn. Reson. Imaging 2017;45:66–73.

Marrow adipogenesis is synchronized with bone loss in the development of GIOP, which was characterized by a significant increase in the number of small-sized marrow adipocytes in the relatively early stage and concomitant volume increase later on. MR spectroscopy appears to be the most powerful tool for detecting the sequential changes in marrow lipid content.

Early icariin treatment restores marrow adiposity in the estrogen-deficient rat model.

Although the primary target cell of bisphosphonates is the osteoclast, increasing attention is being given to other effector cells influenced by bisphosphonates, such as osteoblasts and marrow adipocytes. Early zoledronic acid (ZA) treatment to ovariectomized (OVX) rats has been found to fully preserve bone microarchitecture over time. However, little is known regarding the influence of ZA on marrow adipogenesis. The purpose of this study was to monitor the ability of early administration of ZA in restoring marrow adiposity in an estrogen-deficient rat model. Thirty female Sprague-Dawley rats were randomly divided into sham-operated (SHAM), OVX + vehicle, and OVX + ZA groups (n=10/group). Dual-energy x-ray absorptiometry and water/fat magnetic resonance imaging were performed at baseline, 6 weeks, and 12 weeks after treatment to assess bone mineral density and marrow fat fraction. Serum biochemical markers, bone remodeling, and marrow adipocyte parameters were analyzed using biochemistry, histomorphometry, and histopathology, respectively. The expression levels of osteoblast, adipocyte, and osteoclast-related genes in bone marrow were assessed using RT-PCR. The OVX rats showed marked bone loss, first detected at 12 weeks, but estrogen deficiency resulted in a remarked increase in marrow fat fraction, first detected at 6 weeks compared with the SHAM rats (all P < .001). Similarly, the OVX rats had a substantially larger percent adipocyte area (+163.0%), mean diameter (+29.5%), and higher density (+57.3%) relative to the SHAM rats. Bone histomorphometry, levels of osteoclast-related gene expression, and a serum resorption marker confirmed that ZA significantly suppressed bone resorption activities. Furthermore, ZA treatment returned adipocyte-related gene expression and marrow adipocyte parameters toward SHAM levels. These data suggest that a single dose of early ZA treatment acts to reverse marrow adipogenesis occurring during estrogen deficiency, which may contribute to its capacity to reduce bone loss.