Bone marrow

Normal bone marrow is divided into red and yellow marrow, a distinction made on the grounds of how much fat it contains.

Red marrow is composed of:

  • hematopoietic cells
  • supporting stroma
  • reticulum (phagocytes and undifferentiated progenitor cells)
  • scattered fat cells
  • a rich vascular supply

Conversely, yellow marrow has all the same constituents as red, except that fat cells make up the vast majority, with resulting poor vascularity. Distribution varies with age and from one individual to another but should be symmetric.

During infancy red marrow occupies the entire ossified skeleton except for epiphyses and apophyses. Gradually red marrow 'retreats' centrally, such that by 25 years of age it is essentially confined to the axial skeleton (pelvis, spine, shoulder girdle, skull). The conversion of red to yellow marrow begins peripherally (phalanges) before occurring in the femora/humeri. Within the long bones, the epiphysis is the first undergo conversion followed by the diaphysis before extending to the metadiaphysis 5,6

Also, islands of red marrow may be seen anywhere in the skeleton, typically in a subcortical distribution, often with central yellow marrow giving it a bull's eye appearance on axial imaging. Additionally, red marrow is found in subchondral crescents again of the proximal humerus and femur 2.

Yellow marrow can also be seen focally in vertebra around the basivertebral vein, adjacent to degenerative disc disease and Schmörl nodes, and within hemangiomas.

  • T1: always slightly hyperintense to muscle and disc (due to scattered fat cells)
  • T2: can be difficult to distinguish from yellow marrow as both are somewhat hyperintense
  • STIR: red marrow remains hyperintense, cf. yellow marrow which is saturated out
  • follows subcutaneous fat on all sequences

Broadly marrow pathology can be divided into:

  1. proliferation
  2. depletion
  3. replacement
  4. vascular abnormalities
  5. miscellaneous

Most of the above conditions (covered individually in the encyclopedic section) affect the marrow diffusely. The exception is multiple myeloma which has a predilection for focal deposits, and Waldenstrom macroglobulinemia which causes infarcts.

The MRI appearance is variable:

  • normal red marrow appearance (10-25% of all leukemic patients will have normal appearing marrow)
  • abnormal distribution of what appears to be normal red marrow
  • abnormal signal from red marrow in a normal distribution
  • abnormal signal and distribution

The abnormal signal is due to replacement of the small amounts of fat cells normally found in red marrow, such that T1 signal will decrease to or below the signal from disc or muscle. T2 signal is more variable, but will in general increase when compared to muscle.

Myelofibrosis and mastocytosis incite such prominent sclerosis that the marrow is very dark on both T1 and T2; a similar appearance to marrow in hemosiderosis in patients with hemolysis from sickle cell disease and thalassemia.

The leukaemias typically affect the metaphyses > diaphyses > epiphyses. Changes in the latter indicate a large tumor load, and therefore has prognostic implications.

Yellow-to-red reconversion generates red marrow in abnormal distribution. Signal is, therefore, a very important aspect of correct image interpretation. It occurs in the reverse order to that of red to yellow conversion, and is seen in:

Red marrow reconversion can be difficult to differentiate from metastases in the spine. A useful pair of sequences is T1 in- and out-of-phase. If there is low focal signal on T1 in-phase, this may be due to either pathology. However, the scattered fat cells in red marrow cause marked signal loss on out-of-phase images. There is no such signal loss in metastases.

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Cases and figures

  • Figure 1: diagram - marrow conversion
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  • Case 1: CLL
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  • Case 2: myelofibrosis
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