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MRI of bone and bone marrow in osteoarthritis

, medical expert
Last reviewed: 06.07.2025
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The cortex and trabeculae of bone contain few hydrogen protons and much calcium, which greatly reduces TR, and therefore do not give any specific MR signal. On MR tomograms, they have an image of curved lines with no signal, i.e. dark stripes. They create a silhouette of medium-intensity and high-intensity tissues, outlining them, for example, bone marrow and adipose tissue.

Bone pathology associated with osteoarthritis includes osteophyte formation, subchondral bone sclerosis, subchondral cyst formation, and bone marrow edema. MRI, because of its multiplanar tomographic capabilities, is more sensitive than radiographic or CT scanning for visualizing most of these types of changes. Osteophytes are also better visualized on MRI than on plain radiography, especially central osteophytes, which are particularly difficult to detect radiographically. The causes of central osteophytes are somewhat different from those of marginal osteophytes and therefore have a different significance. Bone sclerosis is also well visualized on MRI and has low signal intensity in all pulse sequences due to calcification and fibrosis. Enthesitis and periostitis can also be detected on MRI. High-resolution MRI is also the primary MR technology for studying trabecular microarchitecture. This may be useful for monitoring trabecular changes in subchondral bone to determine their significance in the development and progression of osteoarthritis.

MRI is a unique imaging capability of the bone marrow and is usually a very sensitive, although not very specific, technology for the detection of osteonecrosis, osteomyelitis, primary infiltration, and trauma, especially bone contusion and nondisplaced fractures. Evidence of these diseases is not apparent on radiographs unless the cortical and/or trabecular bone is involved. Each of these conditions results in increased free water, which appears as low signal intensity on T1-weighted images and high signal intensity on T2-weighted images, showing high contrast with normal bone fat, which has high signal intensity on T1-weighted images and low signal intensity on T2-weighted images. An exception is T2-weighted FSE (fast spin echo) images of fat and water, which require fat suppression to obtain contrast between these components. GE sequences, at least at high field strengths, are largely insensitive to bone marrow pathology because the magnetic effects are attenuated by bone. Areas of subchondral bone marrow swelling are frequently seen in joints with advanced osteoarthritis. Typically, these areas of focal bone marrow swelling in osteoarthritis develop at sites of articular cartilage loss or chondromalacia. Histologically, these areas are typical fibrovascular infiltration. They may be due to mechanical damage to the subchondral bone caused by changes in joint contact points at sites of biomechanically weak cartilage and/or loss of joint stability, or perhaps due to leakage of synovial fluid through a defect in exposed subchondral bone. Occasionally, epiphyseal bone marrow swelling is seen at some distance from the articular surface or enthesis. It remains unclear what magnitude and extent of these marrow changes contribute to local joint tenderness and weakness and when they are a precursor to disease progression.

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MRI of the synovial membrane and synovial fluid

Normal synovial membrane is generally too thin to be visualized with conventional MRI sequences and is difficult to distinguish from adjacent synovial fluid or cartilage. In most cases of osteoarthritis, a slight thickening may be observed for monitoring the response to treatment in patients with osteoarthritis or for studying the normal physiological function of synovial fluid in the joint in vivo, this technique is very useful.

The MP signal of nonhemorrhagic synovial fluid is low on T1-weighted images and high on T2-weighted images due to the presence of free water. Hemorrhagic synovial fluid may contain methemoglobin, which has a short T1 and gives a high-intensity signal on T1-weighted images, and/or deoxyhemoglobin, which appears as a low-intensity signal on T2-weighted images. In chronic recurrent hemarthrosis, hemosiderin is deposited in the synovium, which gives a low-intensity signal on T1- and T2-weighted images. Hemorrhages often develop in popliteal cysts, they are located between the gastrocnemius and soleus muscles along the posterior surface of the leg. Synovial fluid leakage from a ruptured Baker's cyst may resemble a feather shape when enhanced with gadolinium-containing contrast agents. When administered intravenously, KA is located along the surface of the fascia between the muscles behind the joint capsule of the knee joint.

Inflamed, edematous synovium usually has a slow T2, reflecting a high interstitial fluid content (has a high MR signal intensity on T2-weighted images). On T1-weighted images, thickened synovial tissue has a low to intermediate MR signal intensity. However, thickened synovial tissue is difficult to distinguish from adjacent synovial fluid or cartilage. Hemosiderin deposition or chronic fibrosis may decrease the signal intensity of hyperplastic synovial tissue on long-wavelength images (T2-weighted images) and sometimes even on short-wavelength images (T1-weighted images; proton density-weighted images; all GE sequences).

As noted previously, CA exerts a paramagnetic effect on nearby water protons, causing them to relax more rapidly on T1. Water-containing tissues that have accumulated CA (containing the Gd chelate) show an increase in signal intensity on T1-weighted images proportional to the tissue concentration of accumulated CA. When administered intravenously, CA is rapidly distributed throughout hypervascular tissues such as inflamed synovium. The gadolinium chelate complex is a relatively small molecule that rapidly diffuses inward even through normal capillaries and, as a disadvantage, over time into the adjacent synovial fluid. Immediately after a bolus of IV CA, the synovium of the joint may be seen separately from other structures because it is intensely enhanced. The contrast appearance of the high-intensity synovium and adjacent adipose tissue can be increased by fat suppression techniques. The rate at which contrast enhancement of the synovial membrane occurs depends on a number of factors, including: the rate of blood flow in the synovium, the volume of hyperplastic synovial tissue and indicates the activity of the process.

In addition, the determination of the amount and distribution of inflamed synovium and joint fluid in arthritis (and osteoarthrosis) provides an opportunity to establish the severity of synovitis by monitoring the rate of synovial enhancement with Gd-containing CA during the observation period of the patient. A high rate of synovial enhancement and a rapid peak enhancement following a bolus of CA are consistent with active inflammation or hyperplasia, whereas a slow enhancement corresponds to chronic synovial fibrosis. Although it is difficult to monitor subtle differences in the pharmacokinetics of Gd-containing CA in MRI studies at different stages of the disease in the same patient, the rate and peak of synovial enhancement can serve as criteria for the initiation or withdrawal of appropriate anti-inflammatory therapy. High values of these parameters are characteristic of histologically active synovitis.

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