OBJECTIVE. The purpose of this article is to review the structure of bone marrow and the differential diagnosis of bone marrow pathology on the basis of T1-weighted MRI patterns.
CONCLUSION. Bone marrow is an organ that is evaluated routinely during MRI of the spine, particularly lumbar spine evaluation. Thus, it is one of the most commonly performed MRI examinations. T1-weighted MRI is a fundamental sequence in evaluating spinal marrow, and an understanding of T1-weighted MR signal abnormalities is important for the practicing radiologist.
MRI of the spine is a commonly used diagnostic tool in patients with back pain and requires an understanding of not only the findings of common degenerative changes but also of the normal appearance of bone marrow and common benign lesions.
Because the majority of people will experience back pain at some point in their lives, it is not surprising that back pain results in 2.8% of all physician visits . Most patients are treated conservatively without need for imaging; however, patients with persistent back pain, radiculopathy, or a history of cancer routinely undergo MRI . Although the frequency of malignancy or infection is very low in the primary care population (< 1%) , distinguishing normal spinal marrow from pathology on MRI is essential to avoid missing pathology or misinterpreting normal changes, either of which may result in unnecessary additional testing. MRI can detect early bone marrow deposits because it is the only clinical imaging technique that allows direct visualization of bone marrow with high spatial resolution.
Bone Marrow Structure and Function
Microstructure and Function
The bone marrow is a surprisingly large organ that is responsible for normal hematopoiesis and accounts for approximately 5% of body weight in an adult human [3, 4]. The cellular structure of bone marrow is complex, containing stem cells responsible for the production of erythrocytes, granulocytes, monocytes, lymphocytes, and platelets . The supportive cellular environment, including macrophages, adipocytes, osteoblasts, osteoclasts, and adventitial reticular cells, provides the nutrients and cytokines that allow the proliferation, differentiation, and maturation of the hematopoietic cells . A rich vascular supply of venous sinuses supplies nutrients and provides ready access to release blood cells into circulation [3, 4].
Macroscopic Appearance of Marrow
The bone marrow microenvironment provides the components that constitute the macroscopic bone marrow, which gives rise to the terms red marrow and yellow marrow. Red marrow is more cellular, containing the hematopoietic stem cells and blood cell progenitors that give rise to the peripheral blood, whereas yellow marrow contains more fat and is less cellular . Red marrow contains approximately 40% fat, whereas yellow marrow contains 80% fat . This difference is important for understanding the normal and abnormal appearance of marrow on T1-weighted MRI.
Differential Diagnosis of Bone Marrow Pathology
Differential signal intensity (SI) can be used to characterize bone marrow cellular content, which is useful in differentiating pathology. Whereas a routine nonselective iliac crest bone marrow biopsy provides important cellular and structural information, imaging can provide a noninvasive and more global picture of the bone marrow cellular composition [3, 5]. A quantitative assessment of particular cell types is not possible using MRI; however, the relative proportion of active and nonactive cellular components can be determined. The relative SI of lesions can raise suspicion for malignant cells. That is, bone marrow infiltration or replacement with malignant cells tends to produce focal or diffuse areas of T1-weighted signal that are equal to or lower than muscle . Because red marrow contains intermixed fat, it typically has T1-weighted SI that is higher in intensity than muscle. However, in cases of profound red marrow reconversion, red marrow may be difficult to differentiate from malignancy . Additional descriptive considerations of the lesions include the distribution (e.g., diffuse vs infiltrative, focal, or multifocal), location (e.g., body, endplate, or posterior elements), and morphology (e.g., discrete border vs aggressive margin). MRI may serve to guide biopsy of areas of abnormal SI . The remaining sections will discuss the differential diagnosis of abnormal marrow signal within the spinal bone marrow on T1-weighted imaging (Table 1).
Focal T1-Weighted Signal Increase
T1-hyperintense bone marrow lesions are usually benign. The location and character of the focal fatty lesion will help determine the cause. Differential considerations for focal T1 hyperintensity include normal variant, focal fatty marrow, solitary hemangioma, lipoma, Paget disease, bone marrow hemorrhage, melanoma, and Modic type 2 discogenic degenerative endplate changes and other postinflammatory focal marrow atrophy .
Vertebral hemangiomas are relatively common, occurring in 11% of patients in a large autopsy series . The majority of hemangiomas in the spine have the classic appearance of coarsened trabeculae that have a corduroy pattern on sagittal CT or radiography and a polka-dot appearance on axial CT . These are characterized by increased T1- and T2-weighted SI corresponding to the increased fat content .
Degenerative Disk Disease
Fatty degeneration of the marrow occurs in 16–23% of patients evaluated for disk disease [6, 9]. On MRI, Modic type 2 discogenic degenerative endplate changes exhibit hyperintense T1-weighted SI, isointense to hyperintense T2-weighted SI, and hypointense STIR SI. Type 1 change, in which there is destruction and fissuring of the endplate, progresses to type 2 changes with healing of subchondral bone . Ongoing inflammatory processes in some type 2 changes are thought to be the causes of the conversion of yellow to red marrow, resulting in mixed type 1/2 Modic change [9, 11].
Paget disease (osteitis deformans) affects 3.0–3.7% of the population over 40 years of age and increases with age [12, 13]. The spine is the second most commonly affected site after the pelvis and comprises 30–75% of cases. Paget disease is characterized by a disturbance in bone remodeling due to an increase in osteoblastic and osteoclastic activity, which results in trabecular disorganization, fatty marrow, and vertebral body expansion. Three phases are seen: lytic, mixed, and blastic. Marrow SI changes vary with the stage of disease . Low T1-weighted SI and mild high T2-weighted SI are seen in the mixed hypervascular phase. The vertebral body may show a thickened cortex, which can result in a picture-frame appearance on radiographs . The blastic or sclerotic phase shows low T1-weighted and T2-weighted SI because of increased trabecular thickness, sclerosis, and marrow fibrosis. This can give the ivory vertebrae manifestation on radiographs . In the fatty transformation later stage, there is hyperintensity on both T1-weighted and T2-weighted images. This fat SI can be helpful in guiding treatment; if there is fat SI in the presence of osteolysis in a pagetic vertebral body, malignant transformation is considered less likely and the patient may be treated conservatively .
Although T1-hyperintense lesions are typically benign, correlation with the appearance on other MR sequences and imaging modalities as well as with clinical history may suggest an alternative diagnosis. Melanoma metastases appear as well-circumscribed T1-hyperintense lesions because of the melanin or hemorrhage  (Fig. 1). The T1 hyperintensity may be due to the paramagnetic effects of melanin . These lesions show T2 shortening; however, the correlation between melanin content and T2 shortening is weaker than its association with T1 shortening . Contrast-enhanced T1-weighted imaging with fat saturation may increase the conspicuity of the lesions with the suppression of the background marrow signal.
Bone Marrow Hemorrhage
Vertebral marrow hemorrhage may present as areas of T1-weighted hyperintensity. In the setting of fracture, initially the edema and hemorrhage appear as T1-weighted hypointensity. As the edema resolves and blood products begin maturing, there is increased T1-weighted hyperintensity because of methemoglobin, resulting in variable T1-weighted signal with regions of T1-weighted hyperintensity mixed with foci of T1 hypointensity . In addition, evolving bone marrow necrosis may show T1-weighted and T2-weighted hyperintensity, which is attributed to blood and proteinaceous debris within hyperemic marrow .
Lipomas are rare T1-weighted hyperintense lesions within vertebral bodies, with a prevalence of less than 0.1–2.5% of primary bone tumors . Spinal lipomas represent 4% of intraosseous lipomas. Various stages of involution of intraosseous lipomas have been described: lipocytes forming solid tumor; mixture of lipocytes, fat necrosis, and focal calcification; and reactive bone formation admixed with necrotic adipose tissue . The lesions show signal intensities similar to fat on all MR sequences and would be expected to be hypointense on fat-suppressed images.
Diffuse or Multifocal Increase in T1-Weighted Signal
Diffusely increased T1-weighted hyperintensity indicates decreased cellularity of bone marrow. The differential diagnosis includes normal variant, irradiated marrow, osteoporosis, heterogeneous fatty marrow, and multiple hemangiomas. Rare diagnoses that may present with diffuse T1-weighted hyperintensity include anorexia and aplastic anemia.
Prior Radiation Treatment
Irradiated bone marrow undergoes characteristic time-dependent changes that ultimately result in increased T1-weighted signal with a sharp demarcation corresponding to the radiation port (Fig. 2). Radiation destroys the sinusoidal vasculature, with hematopoietic marrow being replaced by fatty marrow and results in hypocellular bone marrow . At doses above 36 Gy, fatty replacement is permanent, with little chance of hematopoietic recovery. Below doses of 30 Gy, these changes are likely reversible and generally occur within 12–24 months [24, 25].
On MRI, osteoporosis can have a heterogeneous appearance because of decreased cellular marrow components and increased fat content [26, 27]. T1-weighted images show heterogeneously hyperintense signal intensity, but the T2-weighted signal can be variable. Focal fatty marrow usually has rounded lesions that coalesce to involve the entire vertebral body. Because of the round morphology, differentiating multiple focal fatty marrow sites from osteoporosis or multifocal hemangiomas may sometimes be difficult. In these cases, comparison with radiography, CT, or dual-energy x-ray absorptiometry can help to elucidate the correct diagnosis.
Vertebral body hemangiomas are benign usually incidental lesions. Hemangiomas can rarely be aggressive with epidural involvement and cord compression [8, 28]. Multiple hemangiomas are seen as multiple T1-weighted hyperintense lesions in the vertebral bodies or posterior elements. Fast spin-echo T2-weighted MRI can be helpful in confirming the diagnosis because these lesions are most often T2-hyperintense. Depending on the balance of fat and vascular elements, they may or may not be hyperintense on STIR images.
Focal superior endplate T1-weighted hyperintensity, usually (but not exclusively) involving the anterior corners of the endplate, may be observed in the postinflammatory stage of ankylosing spondylitis because of fatty infiltration (Figs. 3A and 3B). These are termed Romanus lesions and are a delayed manifestation involving the edges of the vertebral endplates secondary to enthesitis of the anterior or posterior longitudinal ligamentous complexes . Later vertical bone outgrowths, or syndesmophytes, form between adjacent vertebrae and are the end stage of ankylosing spondylitis.
Marrow changes in patients with anorexia nervosa are attributable to early osteoporosis and premature conversion of red marrow to yellow marrow . Other studies have shown a waterlike SI pattern in the marrow spaces , which has been termed “serous atrophy.” This appearance has been attributed to the gelatinous transformation of the bone marrow, which is characterized by fat cell atrophy, loss of hematopoietic cells, and deposition of extracellular gelatinous substances, indicating increased severity of the disease  (Figs. 4A, 4B, and 4C). This waterlike signal intensity is a sign of a generalized severe illness and also can be visualized in patients with alcoholism, malignancies, chronic heart failure, and HIV/AIDS .
Focal T1-Weighted Signal Decrease
Focal low T1-weighted signal within spinal bone marrow provides a diagnostic dilemma because there are many causes of localized low T1-weighted SI. Therefore, it is useful to consider the location of the signal abnormality, including signal abnormality centered or confined to the endplate primarily in the vertebral body or centered in the posterior elements.
Degenerative endplate changes—Degenerative disk disease has been known to affect adjacent endplate bone marrow since the correlation of degenerative changes with histology by Modic et al. . Generally, the degenerative endplate changes are characteristic and unlikely to be confused with other pathology. Low T1-weighted signal in types 1 and 3 endplate change is due to edema and fibrovascular change and fibrotic change, respectively . Characteristic dorsal vertebral corner defects are sometimes visualized with disk herniations and should not be confused with other pathology . When the signal changes are early and more focal, they could be confused with metastatic disease or other pathology.
Osteomyelitis—Although the majority of cases of discitis-osteomyelitis will present with characteristic findings, early or atypical discitis-osteomyelitis could present with nonspecific findings. The typical imaging presentation of pyogenic discitis-osteomyelitis is low T1-weighted signal involving the vertebral body endplates and increased T2-weighted signal in the disk . Granulomatous discitis-osteomyelitis can spare the disk space, but there is usually paraspinal soft-tissue involvement . Occasionally in early discitis-osteomyelitis or in atypical cases, the imaging presentation may be that of a single vertebral body with low T1-weighted signal that could mimic a metastatic lesion or myeloproliferative disorder .
Amyloid—Rarely, focal decreased T1-weighted signal can be caused by amyloid deposition , which occurs in long-standing renal dialysis patients, who are usually elderly . The manifestations include low T1-weighted signal usually subjacent to the endplates within the lower cervical spine in the majority of cases . Less commonly, there is involvement of the thoracic or lumbar spine . Typically, the regional endplates show both low T1-weighted and T2-weighted signal; however, in some cases, the T2-weighted signal can be intermediate to high and those cases may be indistinguishable from discitis-osteomyelitis .
Primarily in the Vertebral Body
Hemangioma—Most hemangiomas present with the characteristic high T1-weighted and T2-weighted signal; however, some hemangiomas may appear low or intermediate in SI on T1-weighted images [37, 38]. This SI on T1-weighted MRI corresponds to less fat, which may indicate a more vascular and potentially a more aggressive hemangioma . These can be confused with malignant lesions, but fortunately CT often reveals the characteristic coarsened trabeculae unless the lesion is small .
Fracture—Fractures of vertebral bodies can present with focal decreased T1-weighted signal, usually in the acute setting [19, 40]. Fractures can occasionally be confused with an acute Schmorl node or pathologic compression fracture. A Schmorl node may not present with the typical undulated endplate appearance, and follow-up MRI or CT can be helpful to distinguish the abnormality . Distinguishing whether a compression fracture is an insufficiency or pathologic fracture may pose a dilemma [19, 40]. Often, specific MRI characteristics can help differentiate benign from malignant fractures. Findings of a convex posterior vertebral body border, abnormal SI involving one or both pedicles, epidural or focal paraspinal mass, or additional spinal metastases are suggestive of a pathologic fracture . Findings of a low T1-weighted SI band with other areas of normal marrow, retropulsion, or multiple compression fractures are indicative of a benign fracture . In- and out-of-phase imaging and diffusion-weighted imaging may also be helpful in problematic cases [42–44], although the usefulness of diffusion-weighted imaging remains controversial .
Malignancy—Focal areas of abnormal signal may represent neoplasm. The most common neoplastic processes that involve the spine are metastatic disease, lymphoma, and plasma cell dyscrasia, either solitary plasmacytoma or multiple myeloma . Neoplastic foci within the spine produce signal changes on T1-weighted images reflecting increased cellularity of the neoplastic lesions with infiltration or replacement of fat . The majority of neoplastic cases can be differentiated from red and yellow marrow by signal that is lower than the adjacent disk or muscle [3, 5]. Difficulty may be encountered with intermediate T1-weighted vertebral body hemangiomas, which have little intralesional fat and may be distinguished from metastatic disease by CT . In addition to the most common lesions discussed previously, primary tumors of the spine can produce low T1-weighted signal within the vertebral body. More often than not, primary bone tumors of the vertebral body present with paravertebral or epidural extension (Figs. 5A and 5B). Exceptions to this do occur, and biopsy of a bone marrow lesion or imaging follow-up may be warranted.
Fibrous dysplasia—Fibrous dysplasia is a rare benign fibroosseous lesion of bone that can manifest in multiple locations in bone (polyostotic) or a single location (monostotic) . Fibrous dysplasia is extremely uncommon in the spine; most cases have been associated with polyostotic fibrous dysplasia, but it can manifest as the monostotic form  (Figs. 6A and 6B). Typically, fibrous dysplasia has low T1-weighted SI and variable T2-weighted SI [47, 49]. Enhancement varies depending on the histologic composition of any given lesion . Despite its rarity, fibrous dysplasia should be included on the list of bone marrow abnormalities that cause decreased T1-weighted signal.
Centered in the Posterior Elements
T1-weighted signal abnormality within the posterior elements can be the result of metastasis, myeloma, lymphoma, fracture, or primary bone tumor. In our experience at a center for multiple myeloma treatment, we frequently see myeloma lesions in the posterior elements. Without any other bone marrow involvement, a solitary T1-weighted signal abnormality in the posterior elements is more likely caused by a primary bone tumor. If a primary tumor is suspected, a lesion appears aggressive, or extensive signal abnormality is present, CT can be helpful in further characterizing a lesion, especially for detection of internal matrix .
Diffuse or Multifocal Decrease in T1-Weighted Signal
Diffuse or multifocal decreased T1-weighted signal is caused by replacement of fatty marrow, which can be due to cellular tissue or edema. Diffuse benign processes include hematopoietic marrow hyperplasia and hemosiderin deposition. Systemic inflammatory processes, such as sarcoidosis, gout, or spondyloarthropathy, can also have extensive osseous involvement. Neoplastic cell infiltration resulting in diffuse spinal T1-weighted hypointensity can be seen with hematologic malignancies.
When the hematopoietic capacity of the existing red marrow is exceeded, fatty marrow reconverts to red marrow. The pattern of reconversion is the reverse of that of physiologic marrow conversion, from axial to appendicular. Hematopoietic hyperplasia can result in diffusely T1-weighted hypointense signal in the axial skeleton (Figs. 7A and 7B), but the SI is usually slightly hyperintense relative to muscle on STIR and fat-suppressed T2-weighted images. It is often seen with chronic anemia, such as sickle cell disease, thalassemia, and hereditary spherocytosis  (Figs. 8A and 8B). These diseases result in the expansion of red marrow leading to the widening of medullary spaces and thinning of cortical bone. The vertebral bodies can develop a biconcave deformity due to the cortical thinning and softening of bone, producing the characteristic fish vertebrae or in the case of infarction in sickle cell disease, H-shaped vertebrae [51, 52]. Similarly, red marrow conversion may occur in circumstances in which there is an increased oxygen requirement, such as in endurance athletes .
Chronic illnesses, heavy smoking, and obesity tax hematopoietic reserves and are associated with marrow hyperplasia . In anemia of chronic illness, the release of iron from macrophages is impaired such that there is abnormally increased bone marrow iron , which manifests as decreased T1-weighted SI. HIV-positive patients may also show similar MR findings . In addition, many cancer patients may be treated with agents to stimulate hematopoietic elements, such as granulocyte-colony-stimulating factor and erythropoietin, as an adjunct to chemotherapy and radiation, which can result in hyperplasia of red marrow .
Diffuse T1 hypointensity of spinal marrow may be the result of neoplastic cell infiltration. Typically, neoplastic processes have lower T1-weighted signal and have hyperintense STIR and fat-suppressed T2-weighted signal relative to the adjacent disk and paravertebral muscles (Fig. 9). Pathologic processes show avid enhancement, but this may be difficult to appreciate when it is a diffuse process. In these cases, comparison of unenhanced and gadolinium-enhanced bone marrow SI may be helpful. Most patients over 40 years old with diffuse marrow infiltration show a greater than 35% SI increase, whereas normal marrow shows a 35% or lower SI increase .
Spinal involvement and appearance vary with malignancies. In leukemia, bone marrow infiltration is often a component of systemic disease (Figs. 10A and 10B). Low T1-weighted leukemic infiltrates are particularly apparent in yellow marrow but can be difficult to differentiate in patients with predominantly red marrow . With lymphoma, 30% of patients have skeletal involvement, with the long bones being affected more than the spine . Lymphoma may manifest with extension into the epidural space from the vertebral body. Metastases can present with diffuse or multifocal T1-weighted hypointensities. Metastases show cortical destruction more often than hematopoietic malignancies .
Renal osteodystrophy broadly applies to all pathologic features of bone in patients with renal failure. Abnormal retention of phosphate by the kidneys results in hyperphosphatemia, which in turn causes hypocalcemia and consequently hyperparathyroidism . Therefore, any one of these disorders may produce renal osteodystrophy, in which the spine is osteopenic and exhibits heterogeneous T1-weighted signal. There is central demineralization with sclerosis of the margins. Low T1-weighted and T2-weighted signal along the endplates may give the characteristic rugger jersey appearance .
Sarcoidosis is a multisystem disorder characterized by noncaseating epithelial granulomas, with osseous involvement seen in 1–13% of patients  (Figs. 11A, 11B, and 11C). Sclerotic lesions of the spine are uncommon but can mimic blastic metastatic disease  (Fig. 11D). Osseous involvement usually occurs at the initial manifestation but has been reported to appear many years after resolution of thoracic sarcoidosis . MRI usually shows multifocal enhancing vertebral body lesions that are hypointense on T1-weighted images and hyperintense on T2-weighted images.
Inflammatory lesions of spondyloarthropathy may present with focal areas of low T1-weighted signal in the acute stage. These acute lesions are low on T1-weighted images and high on T2-weighted and STIR images and have corresponding bone erosions on CT . These are not pathognomonic for ankylosing spondylitis because the inflammatory lesions can also be seen with other spondyloarthropathies and the rare SAPHO syndrome (synovitis, acne, pustulosis, hyperostosis, and osteitis) .
Myelofibrosis is characterized by the replacement of normal marrow by fibrotic tissue, which can result in anemia and extramedullary hematopoiesis. It is associated with chemotherapy or radiation therapy for lymphoma, leukemia, multiple myeloma, and metastatic disease. Occasionally, it is a primary disorder. The characteristic findings on MRI are very low T1-weighted and T2-weighted signal in the marrow and slightly hyperintense signal relative to muscle on fat-suppressed images.
In systemic mastocytosis, there is an abnormal proliferation of mast cells in the skin, bone marrow, spleen, liver, and lymph nodes. Other hematologic disorders, such as myeloproliferative and myelodysplastic syndromes, or lymphoreticular malignancies can coexist . Mast cells can synthesize a variety of cytokines that may affect the skeletal system, increasing bone resorption and leading to osteoporosis . Spinal marrow involvement may be homogeneous or heterogeneous and appear as T1-weighted hypointensity .
Hemosiderosis can result in hypointense marrow signal on all MR sequences because of the magnetic susceptibility of hemosiderin. Breakdown of RBCs in hemolytic anemias can lead to hemosiderin accumulation, as can chronic blood transfusions . A clue to the diagnosis will be hypointensity of the liver and spleen.
Congenital diseases, such as Gaucher disease, may present with hypointense T1-weighted marrow signal (Fig. 12). This autosomal recessive disorder results in the accumulation of glucocerebrosides within histiocytes because of decreased levels of the enzyme glucocerebrosidase. The marrow disease begins in the axial skeleton after the distribution of reconverted marrow . The marrow fat is replaced by infiltration of Gaucher cells, which manifests as T1-weighted and T2-weighted hypointensity. In some cases, the STIR sequences reveal hyperintense inclusions, which may indicate acute bone crisis, occult fracture, infection, or bone infarction .
Spinal involvement by gout is rare, with relatively few reports in the literature. Nevertheless, it should be kept in the differential diagnosis for areas of low T1-weighted signal. Gout has a variable MRI appearance but most often manifests as areas of low T1-weighted and variable T2-weighted signal intensity, with homogeneous or peripheral gadolinium enhancement [73–76]. Gout can occur in the vertebral bodies, which sometimes mimics discitis-osteomyelitis. It can also involve the facet joints or odontoid process or occur within paraspinal soft tissues [73–75, 77–81]. Fortunately, most spinal gout cases occur in patients with known gouty arthropathy, which has a male predominance [73, 82]. In rare cases, gout can coexist with discitis-osteomyelitis . CT may be helpful in identifying calcifications [74, 83], but biopsy may be necessary to establish the diagnosis.
The authors thank B. J. Manaster and Kent Sanders for helpful reviews of the manuscript.
CME SAM Musculoskeletal Imaging
Presented at the 2010 annual meeting of the American Roentgen Ray Society, San Diego, CA.
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