The term “bone marrow edema” was first introduced in 1988.1 It is characterized by ill-defined areas of decreased signal intensity on T1-weighted MRI and increased signal intensity on T2-weighted images.
Bone marrow edema is not the major component of histological anomalies in most situations. For this reason, some authors prefer “bone marrow edema-like” signal or abnormalities.2 Its physiopathology is unclear and varies with the underlying pathological condition.
Bone marrow edema may be apparent in a variety of anomalies that correspond to their etiologies (e.g., necrosis, fibrosis, hemorrhage, inflammation).
Cytokines play an important role in the formation of bone marrow edema. This could explain the link between bone marrow edema and pain, as well as the effect of treatments such as corticosteroids or anti-tumor-necrosis-factor-α (anti-TNFα) on the expression of cytokines. Peritumoral edema in bone tumors correlates with the level of prostaglandins and with the expression of cyclo-oxygenase-2, which is implicated in prostaglandin synthesis.3
Although bone marrow edema is defined using classic MRI sequences, it is better characterized with complementary sequences.
Classic sequences: Bone marrow edema is characterized by ill-defined medullary infiltration without bone lysis. It appears hypointense on T1-weighted images and hyperintense on T2-weighted/fat-saturated or STIR images and enhanced after injection of gadolinium contrast (Figure 1). Analysis of the trabeculae requires good spatial resolution. Identification of bone marrow edema on T2-weighted MRI may be difficult in the absence of fat-saturation techniques.
In-phase/opposed-phase imaging:Voxel signal intensity typically approaches zero on opposed-phase images when edema is present in the yellow marrow, reflecting equivalence in the quantities of water and fat. The signal is increased on in-phase images. Signal intensity reduction on opposed-phase acquisitions is lower when a tumoral process has infiltrated the bone marrow, owing to the reduced fat levels. There is no clear-cut threshold, however, to distinguish between benign and malignant processes.
Dynamic contrast-enhanced MRI: Bone marrow edema is characterized by a gradual increase in enhancement, which can be analyzed quantitatively using the enhancement factor and the enhancement gradient. This information is important because bone marrow edema is a sensitive marker of inflammatory activity and of response to treatment for rheumatoid arthritis or spondyloarthropathies.4 The examination can also help distinguish bone tumors (osteoid osteoma) from surrounding edema (Figure 2).
Diffusion-weighted MRI: Most pathologic processes affecting the bone marrow lead to an increase in apparent diffusion coefficient (ADC) and T2 values and appear bright on diffusion-weighted MRI. The calculation of ADC eliminates the T2 effect from diffusion images and provides a quantifiable value that is directly proportional to the degree of diffusion of water (Figure 3). Although ADC values for bone marrow edema and tumor overlap, the ADC calculation could still be used to quantify bone marrow edema and for follow-up (Figures 4 and 5). While diffusion-weighted imaging can reveal increased ADC values, STIR and T1-weighted spin-echo images show the disappearance of the classic BME pattern.
In summary, classic T1-weighted spin-echo and T2-weighted fast spin-echo imaging with fat saturation (or STIR) are usually sufficient to detect and diagnose bone marrow edema. Injection of gadolinium-based contrast is indicated when looking for extra-osseous anomalies, such as synovitis, for the detection of small bony lesions that can be hidden by edema, or for edema quantification. Dynamic-contrast MRI should be performed in such cases. Diffusion-weighted MRI is a promising tool for the quantification and follow-up of bone marrow edema.