Fig. 1
Sequence of marrow transformation as seen on T1-weighted images, where hematopoietic marrow is depicted as dark gray, marrow undergoing transformation as light gray, and fatty marrow as white. PE: proximal epiphysis; PM: proximal metaphysis; D: diaphysis; DM: distal metaphysis; and DE: distal epiphysis. Marrow conversion begins in the epiphyses followed by diaphysis and metaphyses. Conversion also follow a distal to proximal sequence
In the axial skeleton, the marrow remains hematopoietic throughout life, but the fat component increases with age. In infants younger than 1 year of age, the SI of the marrow is lower than the adjacent disc on T1-weighted images. Between 1 and 5 years of age, the SI is isointense or hyperintense relative to the disc, and over 5 years of age the vertebral body is hyperintense relative to the disc [4].
Hematopoietic marrow is highly cellular and well perfused whereas fatty marrow is poorly perfused [5, 6]. Hence, blood-borne diseases such as infection or metastatic disease tend to affect hematopoietic marrow, whereas fatty marrow is more often affected by ischemia. After gadolinium administration, hematopoietic marrow shows marked enhancement, whereas fatty marrow enhances poorly. On diffusion weighted imaging, the high cellularity of hematopoietic marrow results in restricted diffusion [7]. On FDG PET/CT or PET/MRI, hematopoietic marrow has an uptake that is less than that of the liver [8].
Hyperactive Marrow
Hyperplasia of the hematopoietic marrow occurs in diseases that produce anemia such as Thalassemia or sickle cell disease (Fig. 2). Granulocytic-colony stimulating factor also results in very active marrow, as does hypoxia, polycythemia vera and smoking. Hyperactive marrow can simulate metastatic disease, particularly in patients with a malignancy who are receiving granulocytic colony stimulating factor. Out-of-phase MR imaging helps differentiate between the two, as the signal intensity drops considerably with hematopoietic marrow (due to its fatty component) whereas it does not with metastatic disease.
Fig. 2
12-year-old with sickle cell disease. There is increased hematopoietic marrow in the proximal femurs because of the anemia. The SI in the epiphyses, which should be high because of fat, is very low because of bilateral avascular necrosis
Ischemia
Avascular necrosis is most often seen in the epiphysis of the proximal femur. Legg-Calvé-Perthes disease is an idiopathic condition affecting mostly boys 4–8 years of age. Radiographically the head undergoes sclerosis, collapse, fragmentation and ultimately healing. In order to heal appropriately, the femoral epiphysis must be well contained by the acetabulum. Radiographically, the degree of collapse of the lateral pillar of the femoral head is an important prognostic sign. Reperfusion occurs around the physis (periphyseal), which is important so that the physis does not close prematurely. Lucencies developing in the juxtaphyseal metaphysis are of bad prognosis, and they are associated with transphyseal reperfusion (instead of periphyseal reperfusion) and premature closure of the physis. MR imaging shows decreased SI on the femoral epiphysis on T1-weighted images, increased SI on T2-weighted images, absent enhancement after gadolinium administration, and increased ADC on diffusion-weighted images.
There are other causes of epiphyseal ischemia in children including steroids, sickle cell disease (Fig. 2), and Gaucher disease. An important subpopulation is the group of patients who are treated for leukemia. These patients have multiple infarcts throughout the bones, but the degree of subchondral involvement in the epiphysis determines the degree of pain. Early marrow inhomogeneity with a linear pattern in these high-risk patients is associated with subsequent development of infarcts.
Infarcts can occur in the metaphysis and diaphysis. Stagnant blood can result in high signal intensity on fat-suppressed T1-weighted images. Acute infarcts are also associated with increased marrow signal on T2-weighted images, and with subperiosteal fluid and surrounding soft tissue edema. Thus, it is difficult to differentiate between infection and infarction in conditions such as sickle cell disease. The difficulty in differentiating between these two conditions is aggravated by the fact that infection can develop in areas of pre-existing infarction.