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(Radiographics. 2000;20:S27-S42.)
© RSNA, 2000

Pelvis

Evaluation of the Marrow Space in the Adult Hip1

Carol L. Andrews, MD

1 From the Department of Radiological Sciences, University of California, Los Angeles, 200 UCLA Medical Plaza, Suite 165-59, Los Angeles, CA 90095. Presented as a refresher course at the 1999 RSNA scientific assembly. Received April 19, 2000; revision requested May 23 and received June 25; accepted June 29. Address correspondence to the author (e-mail: candrews@mednet.ucla.edu).


   Abstract
Top
 Abstract
Introduction
 Normal Anatomy
 Pathologic Processes
 Conclusions
 References
 
The adult pelvis and hip contain extensive marrow space in which a variety of processes may occur. Evaluation of this space requires an understanding of normal maturation and recognition that the marrow of the pelvis (axial skeleton) and that of the proximal femurs (appendicular skeleton) contain variable amounts of red and yellow marrow. At magnetic resonance (MR) imaging, this variability yields patterns in normal marrow ranging from very uniform and homogeneous signal intensity to patchy and heterogeneous signal intensity. The marrow space serves as a reflection of patient health and may herald developing anemia with reconversion of inactive to active marrow. Pathologic processes to be considered include marrow edema related to trauma, tumors, or infection; marrow ischemia and infarction; marrow infiltration from primary or secondary neoplasms or from infection; or complete loss of normal myeloid tissue in the marrow space. Each process can be effectively studied with MR imaging.

Index Terms: Bone marrow, 44.833 • Bones, necrosis, 44.44 • Hip, diseases, 44.21, 44.40, 44.833 • Magnetic resonance (MR), tissue characterization, 44.121411, 44.121412, 44.121413 • Osteoporosis, 44.569


   Introduction
Top
 Abstract
 Introduction
Normal Anatomy
 Pathologic Processes
 Conclusions
 References
 
Magnetic resonance (MR) imaging of the pelvis provides an exquisite window into the marrow spaces of the pelvic bones and the proximal femurs and the axial and appendicular structures of the skeleton, respectively. The patterns exhibited may be very difficult to interpret without a clear understanding of what is normal and what is likely to go wrong. In this article, normal anatomic findings are presented, as well abnormal findings in the pathologic processes of marrow conversion abnormalities, myeloid depletion, marrow edema, marrow ischemia or necrosis, and marrow infiltration.


   Normal Anatomy
Top
 Abstract
 Introduction
 Normal Anatomy
Pathologic Processes
 Conclusions
 References
 
Housed within a bony trabecular network, marrow is responsible for maintenance of hematopoietic elements including red and white blood cell lines and platelets. Marrow that is hematopoietically active is often referred to as red marrow because of its beefy red appearance on gross inspection. Red marrow is composed of approximately 40% water, 40% fat, and 20% protein. Yellow marrow is relatively inactive with regard to blood cell development. Yellow marrow is composed of 80% fat with only 15% water and 5% protein (Fig 1) (1,2). Fat is present throughout both active and inactive marrows. Theoretically, fat plays a role in hematopoiesis. Some researchers suggest fat provides structure and nutritional support to the developing cell lines, whereas others believe it provides necessary growth factors for proper development of hematopoietic cells (1).



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  		Figure 1. Normal bone marrow. Photomicrograph (original magnification, x10; hematoxylin-eosin stain) demonstrates the appearance of active hematopoietic marrow. The myeloid elements, including white and red blood cell lines and megakaryocytes (arrowhead), are supported by lipocytes (short arrows) and housed by mature trabeculae (long arrow).

 
The lipid component of marrow provides a useful marker for marrow evaluation with MR imaging. At spin-echo MR imaging, the predominance of fat content seen in yellow marrow results in high signal intensity on T1-weighted images and intermediate signal intensity on T2-weighted images. Hematopoietic marrow, with its lower fat content and higher water content, has intermediate signal intensity on both T1- and T2-weighted images (Fig 2) (1–4).



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  		Figure 2a. Normal adult hip marrow. Coronal MR images obtained in different patients: T1-weighted image (repetition time msec/echo time msec = 450/25) (a), T2-weighted fast spin-echo image (2,500/90) (b), STIR image (2,400/20/160 [inversion time msec]) (c), and proton-density-weighted image (2,400/20) (d). These images demonstrate the patchy, intermediate signal intensity of the hematopoietic (active) marrow (thick arrows in a-c) distributed around the acetabulum and in the femoral metaphysis. The fat-laden inactive marrow (thin arrow in a-c), found in the epiphyses and apophyses, shows high to intermediate signal intensity and changes little in a-c. In d, the inactive marrow has very low signal intensity. The cortical bone (white arrowheads in a, c, and d) and primary weight-bearing trabeculae (black arrowheads in d) have low signal intensity.

 


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  		Figure 2b. Normal adult hip marrow. Coronal MR images obtained in different patients: T1-weighted image (repetition time msec/echo time msec = 450/25) (a), T2-weighted fast spin-echo image (2,500/90) (b), STIR image (2,400/20/160 [inversion time msec]) (c), and proton-density-weighted image (2,400/20) (d). These images demonstrate the patchy, intermediate signal intensity of the hematopoietic (active) marrow (thick arrows in a-c) distributed around the acetabulum and in the femoral metaphysis. The fat-laden inactive marrow (thin arrow in a-c), found in the epiphyses and apophyses, shows high to intermediate signal intensity and changes little in a-c. In d, the inactive marrow has very low signal intensity. The cortical bone (white arrowheads in a, c, and d) and primary weight-bearing trabeculae (black arrowheads in d) have low signal intensity.

 


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  		Figure 2c. Normal adult hip marrow. Coronal MR images obtained in different patients: T1-weighted image (repetition time msec/echo time msec = 450/25) (a), T2-weighted fast spin-echo image (2,500/90) (b), STIR image (2,400/20/160 [inversion time msec]) (c), and proton-density-weighted image (2,400/20) (d). These images demonstrate the patchy, intermediate signal intensity of the hematopoietic (active) marrow (thick arrows in a-c) distributed around the acetabulum and in the femoral metaphysis. The fat-laden inactive marrow (thin arrow in a-c), found in the epiphyses and apophyses, shows high to intermediate signal intensity and changes little in a-c. In d, the inactive marrow has very low signal intensity. The cortical bone (white arrowheads in a, c, and d) and primary weight-bearing trabeculae (black arrowheads in d) have low signal intensity.

 


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  		Figure 2d. Normal adult hip marrow. Coronal MR images obtained in different patients: T1-weighted image (repetition time msec/echo time msec = 450/25) (a), T2-weighted fast spin-echo image (2,500/90) (b), STIR image (2,400/20/160 [inversion time msec]) (c), and proton-density-weighted image (2,400/20) (d). These images demonstrate the patchy, intermediate signal intensity of the hematopoietic (active) marrow (thick arrows in a-c) distributed around the acetabulum and in the femoral metaphysis. The fat-laden inactive marrow (thin arrow in a-c), found in the epiphyses and apophyses, shows high to intermediate signal intensity and changes little in a-c. In d, the inactive marrow has very low signal intensity. The cortical bone (white arrowheads in a, c, and d) and primary weight-bearing trabeculae (black arrowheads in d) have low signal intensity.

 
With the advent of rapid-acquisition (fast or turbo) MR sequences, the signal intensity of predominantly fat-filled spaces is less muted on T2-weighted images, resulting in higher signal intensity of the fatty marrow spaces than is typically seen on standard T2-weighted spin-echo images (3). With all spin-echo sequences, whether standard or rapid acquisition, the perceived ratio of yellow to red marrow tends to be overestimated. Areas that appear to contain only fatty marrow normally also have active hematopoiesis, although in smaller quantities (1,2,4).

Since the high signal intensity of fat may mask underlying processes, techniques that negate the fat signal intensity can be useful in evaluating subtle abnormalities. This high signal intensity can be removed from the images by using a variety of techniques. The two most common methods are (a) chemical suppression, in which specific spectroscopic frequencies (such as fat) are selectively diminished by means of a spoiler sequence, without the loss of signal from nearby frequencies (such as gadolinium); and (b) short inversion time inversion-recovery (STIR) technique, in which a 180° inversion pulse used prior to standard spin-echo techniques nulls the fat signal and may also negate signal from nearby peaks such as gadolinium (1,3,5,6). With both techniques, the high fat signal intensity is removed and any processes with relatively high water content will appear hyperintense.

Gradient-echo imaging is particularly useful in imaging of the paramagnetic effects of blood products or in imaging with iron-oxidebased contrast agents, but it has limitations in the osseous structures. It may or may not be useful in marrow space evaluation. Gradient-echo imaging is particularly sensitive to inhomogeneities of the field being examined, and the multiple complex interfaces of the trabeculae, particularly in the metaphyses and the posterior elements of the spine, may result in signal loss (2,7). Areas where known marrow edema exists may appear normal with this technique. Gradient-echo imaging is described on the basis of vendor terminology and the number of pulse manipulations (5).

The trabecular and cortical bone yield very little signal and are hypointense on MR images obtained with all sequences (1,2). Thus, the major tensile and compressive trabecular bands in the proximal femurs and all cortical bone have low signal intensity on both T1- and T2-weighted images (3,6,8).

Marrow undergoes conversion from hematopoietically active red marrow to hematopoietically inactive yellow marrow in a very orderly and predictable fashion in a healthy person. At birth, all the marrow produces blood cells, but by age 1 year, marrow in the epiphyses and apophyses is changed to inactive (Figs 3, 4) (9,10). As aging continues, the marrow continues to convert to yellow marrow but at a slower rate. This conversion is from distal to proximal, from the appendicular to the axial skeleton and from the diaphyses of the long bones toward the metaphyses. Thus, in the lower extremity, the foot develops yellow marrow before the femur. Conversion of marrow in the femur begins in the diaphyses and progresses toward the metaphyses. Conversion of marrow in the flat bones of the pelvis lags behind that in the lower extremity. Marrow in the spine is typically the last to become inactive (Fig 5) (1,2,4).



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  		Figure 3a. Normal newborn hip marrow. Coronal T1-weighted (420/24) (a) and T2-weighted (2,420/20) (b) spin-echo MR images emphasize the lack of yellow marrow, with all marrow spaces exhibiting the intermediate signal intensity of active hematopoietic marrow (arrows) in all regions of the proximal femur (particularly in the epiphysis and apophysis) in a and with higher signal intensity in b.

 


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  		Figure 3b. Normal newborn hip marrow. Coronal T1-weighted (420/24) (a) and T2-weighted (2,420/20) (b) spin-echo MR images emphasize the lack of yellow marrow, with all marrow spaces exhibiting the intermediate signal intensity of active hematopoietic marrow (arrows) in all regions of the proximal femur (particularly in the epiphysis and apophysis) in a and with higher signal intensity in b.

 


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  		Figure 4a. Normal hip marrow in an 11-month-old male infant. Sagittal T1-weighted (400/20) (a) and T2-weighted (2,400/20) (b) spin-echo MR images show the high signal intensity in a of the capital femoral epiphyses (arrow), which have converted from red marrow to yellow marrow, leaving intermediate signal intensity in b.

 


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  		Figure 4b. Normal hip marrow in an 11-month-old male infant. Sagittal T1-weighted (400/20) (a) and T2-weighted (2,400/20) (b) spin-echo MR images show the high signal intensity in a of the capital femoral epiphyses (arrow), which have converted from red marrow to yellow marrow, leaving intermediate signal intensity in b.

 


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  		Figure 5. Normal hip marrow in a 14-year-old male adolescent. Coronal T1-weighted (350/15) MR image exhibits the high signal intensity of inactive marrow not only in the capital femoral epiphyses and the greater trochanter apophysis (arrowheads) but also in the distal diaphysis (arrow), as conversion to yellow marrow proceeds from distal to proximal in this long bone.

 
In the pelvis, hematopoietic marrow is diffusely distributed, with areas of focal fatty marrow found around the sacroiliac joints, acetabula, and symphysis pubis (9,11,12). This hematopoietic marrow may become more prominent or may be replaced by fatty marrow as the patient ages. These changes tend to be bilateral and symmetric (Fig 6) (13,14).



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  		Figure 6a. Normal hip marrow in a 70-year-old woman. Coronal T1-weighted (400/20) (a) and STIR (2,400/20/160) (b) MR images of the hip demonstrate the typical, patchy pattern of fatty marrow conversion in the supraacetabular ilium (arrowheads), with high signal intensity in a and very low signal intensity in b.

 


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  		Figure 6b. Normal hip marrow in a 70-year-old woman. Coronal T1-weighted (400/20) (a) and STIR (2,400/20/160) (b) MR images of the hip demonstrate the typical, patchy pattern of fatty marrow conversion in the supraacetabular ilium (arrowheads), with high signal intensity in a and very low signal intensity in b.

 

   Pathologic Processes
Top
 Abstract
 Introduction
 Normal Anatomy
 Pathologic Processes
Conclusions
 References
 
Although many different abnormalities can occur in the marrow space, the processes may be summarized as (a) marrow conversion abnormalities, (b) myeloid depletion, (c) marrow edema, (d) marrow ischemia or necrosis, and (e) marrow infiltration (1,15).

Conversion Abnormalities
Abnormalities in the conversion of red to yellow marrow occur where there is an increased demand for hematopoietic marrow. This may be seen as a failure of the marrow to proceed through the normal conversion pattern described previously and is typical in children and young adults with chronic illnesses (such as cyanotic heart disease or kidney or liver failure) or congenital anemias including thalassemia major or sickle cell disease (1,15).

The conversion to yellow marrow may be delayed by continued high demand for red cell production. Often described as hyperplastic marrow, this patchy red marrow predominates in the metaphyses of the long bones and in the flat bones of the pelvis. Hyperplastic marrow is typical in aerobically fit adults (Fig 7), menstruating women, smokers, and obese patients (3,15–17).



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  		Figure 7. Normal hip marrow in a 22-year-old male distance runner. Coronal T1-weighted (400/24) MR image exhibits persistent hematopoietic marrow (arrows) in the femoral neck and adjacent acetabulum, where conversion to yellow marrow would typically have occurred in a less active but otherwise healthy individual.

 
Marrow may proceed through normal conversion to yellow marrow but undergo reconversion to red marrow when high demands are placed on it. This is seen in previously healthy adults who become ill, with resultant anemia placing increased demands on the marrow space (Fig 8).



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  		Figure 8a. Marrow abnormality in a 32-year-old woman with severe ulcerative colitis. Coronal T1-weighted (400/20) (a) and STIR (2,400/20/160) (b) MR images show extensive reconversion of marrow space to hematopoietic marrow. All marrow of the pelvis, lower lumbar spine, and proximal femoral metadiaphyses (arrows) has been recruited and has intermediate signal intensity. Despite the extensive reconversion elsewhere, the epiphyses and apophyses retain yellow marrow (arrowheads) and have not undergone reconversion.

 


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  		Figure 8b. Marrow abnormality in a 32-year-old woman with severe ulcerative colitis. Coronal T1-weighted (400/20) (a) and STIR (2,400/20/160) (b) MR images show extensive reconversion of marrow space to hematopoietic marrow. All marrow of the pelvis, lower lumbar spine, and proximal femoral metadiaphyses (arrows) has been recruited and has intermediate signal intensity. Despite the extensive reconversion elsewhere, the epiphyses and apophyses retain yellow marrow (arrowheads) and have not undergone reconversion.

 
When a higher demand for production of myeloid elements is placed on marrow, it recruits the marrow space back in an orderly sequence, the reverse of normal fatty marrow conversion. Thus, the axial skeleton increases production, followed by the metaphyses of the long bones from proximal to distal and from metaphysis to diaphysis. This recruitment of marrow space generally spares the epiphyses unless the need for hematopoietic marrow is severe.

This reconverted marrow is typically patchy rather than confluent, but it has the signal intensity expected for normal red marrow, that is, intermediate on T1- and T2-weighted spin-echo images and STIR images. Reconverted marrow generally extends to but does not cross the physeal scar region, and the signal intensity of epiphyses and apophyses remains high on T1-weighted images, intermediate to low on T2-weighted images, and very low on fat-suppressed images (1,15).

Myeloid Depletion
Myeloid depletion occurs when the marrow space is completely devoid of hematopoietic elements. Chemotherapy, aplastic anemia, and radiation therapy are typical clinical settings in which myeloid depletion is seen (18,19). Myeloid depletion is the one setting in which the markedly high T1-weighted signal intensity of the marrow space corresponds to a true lack of myeloid elements within the marrow space. Thus, the involved marrow space has uniformly high signal intensity on T1-weighted images and uniformly low signal intensity on fat-suppressed T2-weighted images (15).

Irradiated marrow tends to demonstrate a sharply defined linear border with the adjacent normal marrow, corresponding to the margins of the radiation port (19). This change to yellow marrow occurs very quickly. If the patient undergoes imaging in the acute phase of radiation therapy, the marrow space will appear with intermediate signal intensity on T1-weighted images and high signal intensity (within the defined port) on T2-weighted, STIR, and gradient-echo images (Fig 9). In the subacute phase (2–6 weeks), the marrow rapidly undergoes fatty replacement and is typically replaced completely by 6–8 weeks (Fig 10) (19,20).



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  		Figure 9. Myeloid depletion in a 16-year-old female adolescent, 9 days after completion of radiation therapy for soft-tissue sarcoma of the right thigh. Coronal gradient-echo (8/2.3) MR image highlights the marrow edema (arrow) in the right femur and hip. Radiation port edges (arrowheads) are evident as very abrupt demarcations between the signal intensities of abnormal and normal marrow.

 


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  		Figure 10. Myeloid depletion in a 50-year-old man, 6 months after radiation therapy for lung carcinoma metastatic to the sacrum. Coronal T1-weighted (400/24) MR image through the middle of the pelvis shows the uniform high signal intensity of a marrow space completely depleted of myeloid elements. The radiation port (arrows) is well demarcated, involving the ischium, lower lumbar spine, and left greater trochanter. The previously irradiated tumor (arrowhead) has recurred.

 
Marrow Edema
Edema may be seen in the marrow space in a variety of settings including trauma; adjacent to tumors, infection, and arthritis; and in transient osteoporosis (1,3,21–23). The origin of edema is debated. Some authors suggest the source of the signal is hypervascularity (as seen around tumors and infection), hyperperfusion (transient osteoporosis), or increased permeability (disrupted vessels in trauma, abnormal vessels in and around tumors) (21,22).

Edematous marrow has low signal intensity on T1-weighted images and markedly high signal intensity on T2-weighted fat-suppressed and STIR images. But unlike reconversion marrow, it is much more intense on STIR images and does not respect boundaries such as the physeal scar (8).

In the setting of trauma, the edema surrounds the primary area of fracture. The fracture is typically seen clearly on T1-weighted images as a discrete, low-signal-intensity line with a surrounding halo of edema with intermediate signal intensity. On T2-weighted and STIR images, the actual fracture line may become obscured in the surrounding high signal intensity of the edema (Fig 11) (8).



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  		Figure 11a. Stress fracture in a 55-year-old male runner. (a) Initial frontal radiograph, obtained at the time of symptom onset, shows no abnormality. (b, c) Coronal T1-weighted (420/24) (b) and STIR (2,400/20/160) (c) MR images, obtained 1 week after a, help confirm the presence of an incomplete stress fracture (arrow in b) with low signal intensity in the medial femoral neck, which has a bright halo (arrow in c) of marrow edema. (d) Frontal radiograph, obtained 6 weeks after a, shows the stress fracture (arrow) in the healing phase.

 


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  		Figure 11b. Stress fracture in a 55-year-old male runner. (a) Initial frontal radiograph, obtained at the time of symptom onset, shows no abnormality. (b, c) Coronal T1-weighted (420/24) (b) and STIR (2,400/20/160) (c) MR images, obtained 1 week after a, help confirm the presence of an incomplete stress fracture (arrow in b) with low signal intensity in the medial femoral neck, which has a bright halo (arrow in c) of marrow edema. (d) Frontal radiograph, obtained 6 weeks after a, shows the stress fracture (arrow) in the healing phase.

 


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  		Figure 11c. Stress fracture in a 55-year-old male runner. (a) Initial frontal radiograph, obtained at the time of symptom onset, shows no abnormality. (b, c) Coronal T1-weighted (420/24) (b) and STIR (2,400/20/160) (c) MR images, obtained 1 week after a, help confirm the presence of an incomplete stress fracture (arrow in b) with low signal intensity in the medial femoral neck, which has a bright halo (arrow in c) of marrow edema. (d) Frontal radiograph, obtained 6 weeks after a, shows the stress fracture (arrow) in the healing phase.

 


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  		Figure 11d. Stress fracture in a 55-year-old male runner. (a) Initial frontal radiograph, obtained at the time of symptom onset, shows no abnormality. (b, c) Coronal T1-weighted (420/24) (b) and STIR (2,400/20/160) (c) MR images, obtained 1 week after a, help confirm the presence of an incomplete stress fracture (arrow in b) with low signal intensity in the medial femoral neck, which has a bright halo (arrow in c) of marrow edema. (d) Frontal radiograph, obtained 6 weeks after a, shows the stress fracture (arrow) in the healing phase.

 
Although MR imaging is not typically used in the setting of acute trauma, it has a role in occult trauma. When a radiograph is normal or equivocal but the clinical question of a fracture remains, MR imaging may be key in the diagnosis. In the past, continued evaluation would be accomplished with bone scanning, requiring hospital admission and a potential delay in diagnosis and treatment. However, MR imaging is far more sensitive in this setting and is now the recommended method of evaluation (8). The diagnosis can be made with a single T1-weighted coronal study. There may be accompanying injuries or abnormalities (such as muscle tears), however, and a STIR study may add useful information (Fig 12) (3,24).



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  		Figure 12a. Intertrochanteric fracture in a 72-year-old woman. (a) Frontal radiograph fails to demonstrate a discrete fracture line. (b, c) Coronal T1-weighted (480/40) (b) and STIR (2,500/50/160) (c) MR images obtained the same day show extensive fractures not only in the subcapital region but also in the intertrochanteric region. The fracture lines are depicted with discrete low signal intensity (arrowheads in b) but are masked by the surrounding edema (arrowheads in c). Adjacent soft-tissue edema (arrow in c) is also depicted.

 


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  		Figure 12b. Intertrochanteric fracture in a 72-year-old woman. (a) Frontal radiograph fails to demonstrate a discrete fracture line. (b, c) Coronal T1-weighted (480/40) (b) and STIR (2,500/50/160) (c) MR images obtained the same day show extensive fractures not only in the subcapital region but also in the intertrochanteric region. The fracture lines are depicted with discrete low signal intensity (arrowheads in b) but are masked by the surrounding edema (arrowheads in c). Adjacent soft-tissue edema (arrow in c) is also depicted.

 


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  		Figure 12c. Intertrochanteric fracture in a 72-year-old woman. (a) Frontal radiograph fails to demonstrate a discrete fracture line. (b, c) Coronal T1-weighted (480/40) (b) and STIR (2,500/50/160) (c) MR images obtained the same day show extensive fractures not only in the subcapital region but also in the intertrochanteric region. The fracture lines are depicted with discrete low signal intensity (arrowheads in b) but are masked by the surrounding edema (arrowheads in c). Adjacent soft-tissue edema (arrow in c) is also depicted.

 
Marrow edema may also be seen in the setting of transient osteoporosis. Marrow edema was described in 1959 in two women in their 3rd trimesters of pregnancy (25), but it is more typical in middle-aged men. Although the origin of transient osteoporosis is uncertain, it may be the forme fruste of osteonecrosis (22). However, recent histopathologic studies failed to demonstrate osteonecrosis in the bone biopsy specimens of patients with transient osteopenia (26). Other proposed mechanisms include synovitis, occult trauma, and reflex sympathetic dystrophy (26).

These patients present with a typical history of abrupt-onset hip pain without prior trauma. Septic arthritis may have a similar clinical appearance and must be specifically excluded. The symptoms are self-limited, and typical treatment is with non-steroidal antiinflammatory drugs and protected weight bearing.

Radiographic evaluation may reveal marked osteoporosis surrounding the painful hip. The joint space is normal and there may or may not be evidence of a joint effusion. MR imaging highlights the diffuse but nonspecific pattern of edema in the femoral head and neck (27), which has low signal intensity on T1-weighted images and high signal intensity on T2-weighted and STIR images. A small joint effusion is often present, but the surrounding soft tissues are normal (Fig 13).



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  		Figure 13a. Transient osteoporosis in a 45-year-old man. (a) Initial frontal pelvic radiograph exhibits subtle osteopenia (arrows) in the right hip. (b) Computed tomographic scan obtained 1 week later helps confirm the asymmetric osteopenia (arrow). (c, d) Coronal T1-weighted (350/40) (c) and fat-suppressed T2-weighted (2,540/90) (d) MR images obtained 2 weeks later reveal the low signal intensity (arrow in c) and high signal intensity (arrow in d) of extensive marrow edema in the right femoral head and neck.

 


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  		Figure 13b. Transient osteoporosis in a 45-year-old man. (a) Initial frontal pelvic radiograph exhibits subtle osteopenia (arrows) in the right hip. (b) Computed tomographic scan obtained 1 week later helps confirm the asymmetric osteopenia (arrow). (c, d) Coronal T1-weighted (350/40) (c) and fat-suppressed T2-weighted (2,540/90) (d) MR images obtained 2 weeks later reveal the low signal intensity (arrow in c) and high signal intensity (arrow in d) of extensive marrow edema in the right femoral head and neck.

 


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  		Figure 13c. Transient osteoporosis in a 45-year-old man. (a) Initial frontal pelvic radiograph exhibits subtle osteopenia (arrows) in the right hip. (b) Computed tomographic scan obtained 1 week later helps confirm the asymmetric osteopenia (arrow). (c, d) Coronal T1-weighted (350/40) (c) and fat-suppressed T2-weighted (2,540/90) (d) MR images obtained 2 weeks later reveal the low signal intensity (arrow in c) and high signal intensity (arrow in d) of extensive marrow edema in the right femoral head and neck.

 


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  		Figure 13d. Transient osteoporosis in a 45-year-old man. (a) Initial frontal pelvic radiograph exhibits subtle osteopenia (arrows) in the right hip. (b) Computed tomographic scan obtained 1 week later helps confirm the asymmetric osteopenia (arrow). (c, d) Coronal T1-weighted (350/40) (c) and fat-suppressed T2-weighted (2,540/90) (d) MR images obtained 2 weeks later reveal the low signal intensity (arrow in c) and high signal intensity (arrow in d) of extensive marrow edema in the right femoral head and neck.

 
Osteonecrosis
Osteonecrosis occurs in many locations in the appendicular skeleton, but the femoral head is particularly susceptible to this process, which is also referred to as avascular necrosis. The anatomy of the femoral head results in a relative paucity of blood flow to the mature femoral head. The predominant blood supply comes through the medial femoral circumflex artery (28). In addition, regions composed of yellow marrow have a stronger predilection for infarction than do areas of hematopoietic marrow. The femoral head, one of the first places to convert to yellow marrow, is at risk for osteonecrosis (29).

Causes of osteonecrosis include trauma, medication (steroids), sickle cell anemia, alcoholism, barotrauma (Caisson disease), Gaucher disease, radiation therapy, and idiopathic causes (1,22,30,31). Although the causes are varied, the pattern of injury and osseous response is predictable. After initial ischemic insult, myeloid cell death is evident within 6–12 hours. The osteocytes die in 48 hours, and the lipocytes die within 2–6 days (1). The bone responds with increased blood flow typical of healing in inflammation. Granulation tissue forms and fibrosis develops in the area of injury. Bone resorption is followed by osteoblastic reinforcement.

Attempts at staging the presence and severity of femoral head osteonecrosis were originally based on the evaluation of a combination of bone scans and radiographs (Table 1). This staging system was proposed to determine the severity of osteonecrosis and to allow intervention in earlier stages to avoid advanced degenerative joint disease (Fig 14) (30).


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  		TABLE 1. Stages of Osteonecrosis of the Femoral Head
 


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  		Figure 14a. Osteonecrosis in different patients, with Ficat stage (30). In stage 0 disease (not shown), radiographs and bone scans are normal. In stage I disease, the frontal radiograph (not shown) is normal, and the technetium 99m bone scan (a) shows decreased uptake in the femoral head (arrow). In stage II disease, the frontal radiograph (b) shows increasing sclerosis of the femoral head (arrowheads), and the bone scan (c) shows increased activity (arrow). (Disease of stage II or greater demonstrates increased uptake on a bone scan.) In stage III disease, the frontal radiograph depicts not only the increased sclerosis of the femoral head but also the subchondral lucency or crescent sign of a developing subchondral fracture. In stage IIIa disease, the fracture (arrowheads in d) is present without subchondral collapse. In stage IIIb disease, there is evidence of fracture and collapse across the articular surface (arrows in e). In stage IV disease, the frontal radiograph shows the increased sclerosis of osteonecrosis, with the narrowing joint space and developing osteophytes that characterize secondary osteoarthritis (arrows in f).

 


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  		Figure 14b. Osteonecrosis in different patients, with Ficat stage (30). In stage 0 disease (not shown), radiographs and bone scans are normal. In stage I disease, the frontal radiograph (not shown) is normal, and the technetium 99m bone scan (a) shows decreased uptake in the femoral head (arrow). In stage II disease, the frontal radiograph (b) shows increasing sclerosis of the femoral head (arrowheads), and the bone scan (c) shows increased activity (arrow). (Disease of stage II or greater demonstrates increased uptake on a bone scan.) In stage III disease, the frontal radiograph depicts not only the increased sclerosis of the femoral head but also the subchondral lucency or crescent sign of a developing subchondral fracture. In stage IIIa disease, the fracture (arrowheads in d) is present without subchondral collapse. In stage IIIb disease, there is evidence of fracture and collapse across the articular surface (arrows in e). In stage IV disease, the frontal radiograph shows the increased sclerosis of osteonecrosis, with the narrowing joint space and developing osteophytes that characterize secondary osteoarthritis (arrows in f).

 


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  		Figure 14c. Osteonecrosis in different patients, with Ficat stage (30). In stage 0 disease (not shown), radiographs and bone scans are normal. In stage I disease, the frontal radiograph (not shown) is normal, and the technetium 99m bone scan (a) shows decreased uptake in the femoral head (arrow). In stage II disease, the frontal radiograph (b) shows increasing sclerosis of the femoral head (arrowheads), and the bone scan (c) shows increased activity (arrow). (Disease of stage II or greater demonstrates increased uptake on a bone scan.) In stage III disease, the frontal radiograph depicts not only the increased sclerosis of the femoral head but also the subchondral lucency or crescent sign of a developing subchondral fracture. In stage IIIa disease, the fracture (arrowheads in d) is present without subchondral collapse. In stage IIIb disease, there is evidence of fracture and collapse across the articular surface (arrows in e). In stage IV disease, the frontal radiograph shows the increased sclerosis of osteonecrosis, with the narrowing joint space and developing osteophytes that characterize secondary osteoarthritis (arrows in f).

 


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  		Figure 14d. Osteonecrosis in different patients, with Ficat stage (30). In stage 0 disease (not shown), radiographs and bone scans are normal. In stage I disease, the frontal radiograph (not shown) is normal, and the technetium 99m bone scan (a) shows decreased uptake in the femoral head (arrow). In stage II disease, the frontal radiograph (b) shows increasing sclerosis of the femoral head (arrowheads), and the bone scan (c) shows increased activity (arrow). (Disease of stage II or greater demonstrates increased uptake on a bone scan.) In stage III disease, the frontal radiograph depicts not only the increased sclerosis of the femoral head but also the subchondral lucency or crescent sign of a developing subchondral fracture. In stage IIIa disease, the fracture (arrowheads in d) is present without subchondral collapse. In stage IIIb disease, there is evidence of fracture and collapse across the articular surface (arrows in e). In stage IV disease, the frontal radiograph shows the increased sclerosis of osteonecrosis, with the narrowing joint space and developing osteophytes that characterize secondary osteoarthritis (arrows in f).

 


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  		Figure 14e. Osteonecrosis in different patients, with Ficat stage (30). In stage 0 disease (not shown), radiographs and bone scans are normal. In stage I disease, the frontal radiograph (not shown) is normal, and the technetium 99m bone scan (a) shows decreased uptake in the femoral head (arrow). In stage II disease, the frontal radiograph (b) shows increasing sclerosis of the femoral head (arrowheads), and the bone scan (c) shows increased activity (arrow). (Disease of stage II or greater demonstrates increased uptake on a bone scan.) In stage III disease, the frontal radiograph depicts not only the increased sclerosis of the femoral head but also the subchondral lucency or crescent sign of a developing subchondral fracture. In stage IIIa disease, the fracture (arrowheads in d) is present without subchondral collapse. In stage IIIb disease, there is evidence of fracture and collapse across the articular surface (arrows in e). In stage IV disease, the frontal radiograph shows the increased sclerosis of osteonecrosis, with the narrowing joint space and developing osteophytes that characterize secondary osteoarthritis (arrows in f).

 


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  		Figure 14f. Osteonecrosis in different patients, with Ficat stage (30). In stage 0 disease (not shown), radiographs and bone scans are normal. In stage I disease, the frontal radiograph (not shown) is normal, and the technetium 99m bone scan (a) shows decreased uptake in the femoral head (arrow). In stage II disease, the frontal radiograph (b) shows increasing sclerosis of the femoral head (arrowheads), and the bone scan (c) shows increased activity (arrow). (Disease of stage II or greater demonstrates increased uptake on a bone scan.) In stage III disease, the frontal radiograph depicts not only the increased sclerosis of the femoral head but also the subchondral lucency or crescent sign of a developing subchondral fracture. In stage IIIa disease, the fracture (arrowheads in d) is present without subchondral collapse. In stage IIIb disease, there is evidence of fracture and collapse across the articular surface (arrows in e). In stage IV disease, the frontal radiograph shows the increased sclerosis of osteonecrosis, with the narrowing joint space and developing osteophytes that characterize secondary osteoarthritis (arrows in f).

 
In 1987, Mitchell et al (32) classified the common patterns of signal intensity seen at MR imaging in osteonecrosis and correlated them with the various tissues identified at histopathologic examination (Table 2) (Fig 15). This original description was directed toward refining the staging of osteonecrosis, but it has primarily served as a classification scheme based on radiologic-pathologic correlation (32).


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  		TABLE 2. Lesion Classification with Histopathologic–MR Imaging Correlation
 


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  		Figure 15a. Osteonecrosis in different patients, with Mitchell classification (32). (a, b) Coronal T1-weighted (400/20) (a) and STIR (2,200/50/160) (b) MR images demonstrate increased signal intensity in the superolateral head in a that is decreased in b, representing fatty tissue (class A) (white arrow). A region of low signal intensity in the femoral neck in a becomes much brighter in b, representing fluid (class C) (black arrow). (c, d) Coronal T1-weighted (400/40) (c) and STIR (2,200/40/160) (d) MR images demonstrate a region of high signal intensity in c that is also depicted in d and represents hemorrhage (class B) (arrow). (e, f) Coronal T1-weighted (350/30) (e) and STIR (2,200/50/160) (f) MR images show low signal intensity within the femoral head in both e and f, representing fibrosis (class D) (arrow).

 


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  		Figure 15b. Osteonecrosis in different patients, with Mitchell classification (32). (a, b) Coronal T1-weighted (400/20) (a) and STIR (2,200/50/160) (b) MR images demonstrate increased signal intensity in the superolateral head in a that is decreased in b, representing fatty tissue (class A) (white arrow). A region of low signal intensity in the femoral neck in a becomes much brighter in b, representing fluid (class C) (black arrow). (c, d) Coronal T1-weighted (400/40) (c) and STIR (2,200/40/160) (d) MR images demonstrate a region of high signal intensity in c that is also depicted in d and represents hemorrhage (class B) (arrow). (e, f) Coronal T1-weighted (350/30) (e) and STIR (2,200/50/160) (f) MR images show low signal intensity within the femoral head in both e and f, representing fibrosis (class D) (arrow).

 


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  		Figure 15c. Osteonecrosis in different patients, with Mitchell classification (32). (a, b) Coronal T1-weighted (400/20) (a) and STIR (2,200/50/160) (b) MR images demonstrate increased signal intensity in the superolateral head in a that is decreased in b, representing fatty tissue (class A) (white arrow). A region of low signal intensity in the femoral neck in a becomes much brighter in b, representing fluid (class C) (black arrow). (c, d) Coronal T1-weighted (400/40) (c) and STIR (2,200/40/160) (d) MR images demonstrate a region of high signal intensity in c that is also depicted in d and represents hemorrhage (class B) (arrow). (e, f) Coronal T1-weighted (350/30) (e) and STIR (2,200/50/160) (f) MR images show low signal intensity within the femoral head in both e and f, representing fibrosis (class D) (arrow).

 


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  		Figure 15d. Osteonecrosis in different patients, with Mitchell classification (32). (a, b) Coronal T1-weighted (400/20) (a) and STIR (2,200/50/160) (b) MR images demonstrate increased signal intensity in the superolateral head in a that is decreased in b, representing fatty tissue (class A) (white arrow). A region of low signal intensity in the femoral neck in a becomes much brighter in b, representing fluid (class C) (black arrow). (c, d) Coronal T1-weighted (400/40) (c) and STIR (2,200/40/160) (d) MR images demonstrate a region of high signal intensity in c that is also depicted in d and represents hemorrhage (class B) (arrow). (e, f) Coronal T1-weighted (350/30) (e) and STIR (2,200/50/160) (f) MR images show low signal intensity within the femoral head in both e and f, representing fibrosis (class D) (arrow).

 


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  		Figure 15e. Osteonecrosis in different patients, with Mitchell classification (32). (a, b) Coronal T1-weighted (400/20) (a) and STIR (2,200/50/160) (b) MR images demonstrate increased signal intensity in the superolateral head in a that is decreased in b, representing fatty tissue (class A) (white arrow). A region of low signal intensity in the femoral neck in a becomes much brighter in b, representing fluid (class C) (black arrow). (c, d) Coronal T1-weighted (400/40) (c) and STIR (2,200/40/160) (d) MR images demonstrate a region of high signal intensity in c that is also depicted in d and represents hemorrhage (class B) (arrow). (e, f) Coronal T1-weighted (350/30) (e) and STIR (2,200/50/160) (f) MR images show low signal intensity within the femoral head in both e and f, representing fibrosis (class D) (arrow).

 


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  		Figure 15f. Osteonecrosis in different patients, with Mitchell classification (32). (a, b) Coronal T1-weighted (400/20) (a) and STIR (2,200/50/160) (b) MR images demonstrate increased signal intensity in the superolateral head in a that is decreased in b, representing fatty tissue (class A) (white arrow). A region of low signal intensity in the femoral neck in a becomes much brighter in b, representing fluid (class C) (black arrow). (c, d) Coronal T1-weighted (400/40) (c) and STIR (2,200/40/160) (d) MR images demonstrate a region of high signal intensity in c that is also depicted in d and represents hemorrhage (class B) (arrow). (e, f) Coronal T1-weighted (350/30) (e) and STIR (2,200/50/160) (f) MR images show low signal intensity within the femoral head in both e and f, representing fibrosis (class D) (arrow).

 
An interface between areas of osseous resorption and healing is often present at MR imaging and is referred to as the double-line sign (33). The sign is created by a high-signal-intensity line, representing hyperemic tissue, immediately apposed to a low-signal-intensity line, representing sclerotic (reinforced) bone (Fig 15e, 15f). MR imaging tends to underestimate the presence and/or amount of collapse of the articular surface unless a focused, small field of view is used to acquire images.

Infiltration
Marrow spaces may be filled as a result of acute inflammatory cells, neoplastic processes, or marrow-packing disorders as with the glucocerebrosides of Gaucher disease or the fibrosis of myeloproliferative disease. These processes may infiltrate through the existing trabecular meshwork or may destroy that bone as it replaces the marrow (1,15).

The appearance of the marrow-packing disorders is often a reflection of the amount of fibrosis involved in various disease processes. Myelodysplasia, with a high fibrous content, is relatively uniform, with intermediate signal intensity on T1- and T2-weighted images (34,35). The marrow appearance in Gaucher disease is similar, but the involved bones (especially the long bones) are undertubulated, resulting in flared metaphyses (Erlenmeyer flask deformity) (Fig 16). This deformity and associated organomegaly may serve as clues to the diagnosis (36).



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  		Figure 16a. Gaucher disease in a 22-year-old man. Coronal T1-weighted (400/30) (a) and fat-suppressed T2-weighted (2,400/80) (b) MR images demonstrate the patchy, intermediate signal intensity (arrow) of a marrow space that has been replaced by deposits of glucocerebrosides. Note the flaring of the distal femoral metaphyses (arrowheads in b).

 


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  		Figure 16b. Gaucher disease in a 22-year-old man. Coronal T1-weighted (400/30) (a) and fat-suppressed T2-weighted (2,400/80) (b) MR images demonstrate the patchy, intermediate signal intensity (arrow) of a marrow space that has been replaced by deposits of glucocerebrosides. Note the flaring of the distal femoral metaphyses (arrowheads in b).

 
In infection, the signal intensity is nonspecific low signal intensity on T1-weighted images and high signal intensity on T2-weighted images. The process is typically poorly contained. Cortical disruption and adjacent soft-tissue involvement is well delineated with MR imaging. Gadolinium enhancement may increase the conspicuity of the process, although the presence of enhancement is also nonspecific (Fig 17).



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  		Figure 17a. Abscess in a 52-year-old man. Coronal T1-weighted (380/20) (a) and STIR (220/50/160) (b) MR images demonstrate marked deformity of the proximal femoral diaphyses (white arrows in a) related to prior trauma. A region of low signal intensity in the femoral head in a corresponds to osteomyelitis related to prior hardware and has high signal intensity in b (black arrows).

 


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  		Figure 17b. Abscess in a 52-year-old man. Coronal T1-weighted (380/20) (a) and STIR (220/50/160) (b) MR images demonstrate marked deformity of the proximal femoral diaphyses (white arrows in a) related to prior trauma. A region of low signal intensity in the femoral head in a corresponds to osteomyelitis related to prior hardware and has high signal intensity in b (black arrows).

 
With neoplastic infiltration of bone, the common characteristics of high signal intensity on T2-weighted and STIR images and low signal intensity on T1-weighted images are similar to those of infection. MR imaging is very limited in evaluation of the lesional matrix, which is often key in determination of tumor type. However, MR imaging provides exquisite information regarding involvement of the surrounding compartments such as the soft tissues, adjacent joints, and neurovascular bundle (Fig 18). Neoplastic processes may be depicted as diffuse, patchy recruitment of the marrow spaces, discrete focal involvement, or diffuse and uniform (9,15).



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  		Figure 18a. Ewing sarcoma in a 14-year-old male adolescent. (a) Coronal T1-weighted (400/15) MR image shows low signal intensity of tumor (arrows) in the affected left proximal femur. (b) Axial T2-weighted (2,200/80) MR image at the level of the greater trochanter shows the nonspecific increased signal intensity of the tumor (arrow) but also the extension of this tumor into the surrounding soft tissues (arrowheads).

 


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  		Figure 18b. Ewing sarcoma in a 14-year-old male adolescent. (a) Coronal T1-weighted (400/15) MR image shows low signal intensity of tumor (arrows) in the affected left proximal femur. (b) Axial T2-weighted (2,200/80) MR image at the level of the greater trochanter shows the nonspecific increased signal intensity of the tumor (arrow) but also the extension of this tumor into the surrounding soft tissues (arrowheads).

 
The diffuse pattern of marrow involvement may be very difficult to see because of its uniformity. In hip imaging, the adjacent spine may hold the clue to the process. On T1-weighted images, the signal intensity of the marrow space should always be higher than that of the adjacent intervertebral disks. In widely infiltrative processes and in severe anemia, the reverse may be true (eg, the signal intensity of the marrow space is lower than that of the adjacent disk) (Fig 19) (37).



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  		Figure 19. Leukemia in a 35-year-old woman. Coronal T1-weighted (300/30) MR image exhibits the extensive low-to-intermediate signal intensity related to widespread involvement of marrow, which results in reversal of the normal pattern. The marrow space (arrows) has signal intensity slightly lower than that of the adjacent intervertebral disk.

 
An increasingly common scenario that requires evaluation has to do with the aggressive treatment of metastatic disease of the bone with marrow irradiation and high-dose chemotherapy followed by bone marrow or stem cell transplantation. Distinguishing recurrent metastatic disease from repopulating (rebound) hematopoietic marrow may be very difficult, because both tend to have intermediate signal intensity on T1-weighted images and a higher signal intensity on T2-weighted images. Additionally, both may occur in the same anatomic regions.

Opposed-phase gradient-echo imaging may be useful in the evaluation of this treated marrow. Most neoplastic processes, such as metastatic disease, replace the typical marrow elements such as fat, osseous trabeculae, and hematopoietic elements, but marrow edema and hyperplastic red marrow do not (2,38,39). Opposed-phase imaging allows detection of fat within a lesion, thus distinguishing metastatic disease (with no fat in the tissue) from hyperplastic marrow (in which fat is present) (2,3,39). The echo times are selected to evaluate the spins of water and fat when they are in phase with each other and when they are out of phase. The typical echo time (at 1.5 T) is 4.2 msec for in-phase imaging and 2.25 or 6.5 msec for out-of-phase imaging (3). In-phase imaging depicts lesions in the marrow space with intermediate signal intensity. With out-of-phase imaging, however, areas containing fat (eg, hyperplastic marrow) will become much lower in signal intensity, but areas containing metastatic disease remain intermediate in signal intensity (Fig 20).



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  		Figure 20a. Recurrent breast cancer metastases in a 48-year-old woman after stem cell transplantation. Coronal in-phase (160/4.2 with 75° flip angle) (a, c) and out-of-phase (160/2.7 with 75° flip angle) (b, d) MR images demonstrate the presence of intermediate signal intensity in a and c that becomes low signal intensity in b and d (arrows). The distribution is similar to that expected for normal hematopoietic marrow in the metaphysis of the long bones and surrounding the acetabulum. In c, magnification of the left hip demonstrates two areas of intermediate signal intensity (arrow, arrowhead). In d, the signal intensity of the intertrochanteric region becomes much lower (arrow), representing repopulating hematopoietic marrow. A focus at the base of the greater trochanter (arrowhead in c and d), however, remains intermediate in signal intensity and was confirmed to represent recurrent breast cancer metastasis.

 


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  		Figure 20b. Recurrent breast cancer metastases in a 48-year-old woman after stem cell transplantation. Coronal in-phase (160/4.2 with 75° flip angle) (a, c) and out-of-phase (160/2.7 with 75° flip angle) (b, d) MR images demonstrate the presence of intermediate signal intensity in a and c that becomes low signal intensity in b and d (arrows). The distribution is similar to that expected for normal hematopoietic marrow in the metaphysis of the long bones and surrounding the acetabulum. In c, magnification of the left hip demonstrates two areas of intermediate signal intensity (arrow, arrowhead). In d, the signal intensity of the intertrochanteric region becomes much lower (arrow), representing repopulating hematopoietic marrow. A focus at the base of the greater trochanter (arrowhead in c and d), however, remains intermediate in signal intensity and was confirmed to represent recurrent breast cancer metastasis.

 


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  		Figure 20c. Recurrent breast cancer metastases in a 48-year-old woman after stem cell transplantation. Coronal in-phase (160/4.2 with 75° flip angle) (a, c) and out-of-phase (160/2.7 with 75° flip angle) (b, d) MR images demonstrate the presence of intermediate signal intensity in a and c that becomes low signal intensity in b and d (arrows). The distribution is similar to that expected for normal hematopoietic marrow in the metaphysis of the long bones and surrounding the acetabulum. In c, magnification of the left hip demonstrates two areas of intermediate signal intensity (arrow, arrowhead). In d, the signal intensity of the intertrochanteric region becomes much lower (arrow), representing repopulating hematopoietic marrow. A focus at the base of the greater trochanter (arrowhead in c and d), however, remains intermediate in signal intensity and was confirmed to represent recurrent breast cancer metastasis.

 


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  		Figure 20d. Recurrent breast cancer metastases in a 48-year-old woman after stem cell transplantation. Coronal in-phase (160/4.2 with 75° flip angle) (a, c) and out-of-phase (160/2.7 with 75° flip angle) (b, d) MR images demonstrate the presence of intermediate signal intensity in a and c that becomes low signal intensity in b and d (arrows). The distribution is similar to that expected for normal hematopoietic marrow in the metaphysis of the long bones and surrounding the acetabulum. In c, magnification of the left hip demonstrates two areas of intermediate signal intensity (arrow, arrowhead). In d, the signal intensity of the intertrochanteric region becomes much lower (arrow), representing repopulating hematopoietic marrow. A focus at the base of the greater trochanter (arrowhead in c and d), however, remains intermediate in signal intensity and was confirmed to represent recurrent breast cancer metastasis.

 
Other techniques have also been proposed to emphasize the differences in water content of metastatic disease and rebound red marrow by varying the echo time in a particular pulse sequence. With the signal intensity of muscle as an internal control, metastatic foci are more intense on STIR images. Hyperplastic (rebound) marrow, however, may be difficult to distinguish with a standard echo time but may become readily evident with a lengthened echo time. For example, a routine echo time is 34 msec for a 1.5-T MR imager (GE Medical Systems, Milwaukee, Wis). With a lengthened echo time of 48–60 msec, the signal decay of rebound red marrow is more pronounced, and the water-laden metastatic foci become more conspicuous (Buckwalter K, oral communication, February 2000).


   Conclusions
Top
 Abstract
 Introduction
 Normal Anatomy
 Pathologic Processes
 Conclusions
References
 
The marrow space of the adult hip includes both the flat bones of the pelvis and the appendicular femur. MR imaging of the hip provides an excellent method of evaluating not only normal marrow patterns but also pathologic processes. MR imaging is very sensitive to the processes in which there is an increase in water but may be limited in helping define the exact abnormality. Consideration of the common pathologic conditions including reconversion of fatty marrow, trauma, osteonecrosis, and infiltration will assist the imager in determining the significance of variations in the signal intensity of marrow.


   Footnotes
 
Abbreviation: STIR = short inversion time inversion-recovery


   References
Top
 Abstract
 Introduction
 Normal Anatomy
 Pathologic Processes
 Conclusions
 References
 

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