Age-related evolution and reconversion
In late intrauterine life and infancy, the entire volume of bone marrow actively participates in red blood cell production, supplemented by extramedullary hematopoiesis in the liver and spleen. As a person matures and the lifespan of erythrocytes increases, the need for such massive hematopoiesis disappears. Erythropoiesis in the liver and spleen ceases, and red bone marrow gradually withdraws from the diaphyses of long tubular bones. By the age of twenty-five, active hematopoietic tissue remains predominantly in the axial skeleton, flat bones, and the proximal metaphyses of the humerus and femur.
However, under chronic stress and increased demand for erythropoiesis (e.g., intensive smoking, obstructive sleep apnea, high-altitude sports, or obesity), this process reverses. Physiological bone marrow reconversion develops.
MRI semiotics of reconversion and nodular hyperplasia
On MRI, areas of reconversion are most commonly detected in the distal femur, proximal tibia, and humerus. They have distinct "geographic" margins bordering the normal yellow marrow.
- On T1-weighted images (T1WI) without contrast, the signal is diffusely or focally decreased: it takes an intermediate value between the bright signal of fatty bone marrow and the dark signal of skeletal muscles.
- In STIR and proton density-weighted fat-suppressed (PDW fat-suppressed) sequences, a mild increase in signal intensity is observed.
- On gradient echo (gradient echo) sequences, the signal becomes hypointense.
Focal nodular hyperplasia of the vertebrae and metaphyses presents a particular diagnostic challenge. It exhibits an MRI signal typical of red bone marrow, but can avidly take up the radiotracer on 18F-FDG PET/CT. This makes it extremely difficult to distinguish from bone metastases; a biopsy may be required to definitively rule out malignancy.
Myelodysplastic syndromes (MDS)
MDS is a progressive group of clonal stem cell disorders. According to the 2016 World Health Organization classification (which replaced the FAB system), the incidence increases sharply with age: from 3.3 cases per 100,000 in the general population to 15–50 cases in individuals over 70. Defective blood cell production leads to chronic anemia, bleeding, and infections.
On MRI, involvement (e.g., of the glenoid cavity of the scapula or the humeral metaphysis) manifests as decreased signal on T1WI and corresponding hyperintensity on STIR/PDW. The pattern of involvement is critical: a diffuse or focal anomaly pattern is associated with a poorer prognosis and rapid progression to leukemia. A known complication of MDS is presacral extramedullary hematopoiesis.
Hemoglobinopathies
Normally, a hemoglobin molecule consists of a globin protein (574 amino acids forming four helical chains: two $\alpha$ and two $\beta$) and four heme groups with an iron atom. Hereditary defects in chain synthesis lead to hemoglobinopathies:
- Thalassemias are autosomal recessive disorders with reduced production of $\alpha$- or $\beta$-chains. Homozygous $\alpha$-thalassemia is fatal and causes hydrops fetalis, while homozygous $\beta$-thalassemia causes severe childhood anemia and skeletal abnormalities. Complex (compound) forms can cause bone damage due to marked bone marrow hyperplasia even without blood transfusion dependence.
- Hemoglobin variants — abnormal chains are produced due to a single amino acid substitution. For example, in sickle cell anemia (HbS), valine replaces glutamine at the sixth position of the $\beta$-chain.
Briefly: answers to topical questions
In which bones do bone infarcts most commonly occur in sickle cell anemia?
In sickle cell anemia, bone infarcts occur in various parts of the skeleton, causing specific clinical and radiographic manifestations.
- Ribs and sternum — lesions can clinically mimic heart or lung diseases.
- Small bones of the hands and feet (metacarpals, metatarsals, and phalanges) — lead to the development of dactylitis (dactylitis).
- Vertebral endplates — lead to the formation of "fish vertebrae" or H-shaped vertebrae.
- Epiphyses (especially the femoral head) — lead to avascular necrosis and joint effusion.
How does the normal MRI signal intensity of red and yellow bone marrow differ?
Normally, on MRI, red bone marrow is characterized by lower signal intensity compared to yellow bone marrow.
| Bone marrow type | MRI signal intensity |
|---|---|
| Red bone marrow | Low MR signal (intermediate between bone marrow fat and skeletal muscle on T1WI) |
| Yellow (fatty) bone marrow | High MR signal |
These differences must be taken into account when interpreting tomograms to avoid diagnostic errors associated with physiological bone marrow conversion.
For the differential diagnosis of MDS and tumor infiltration on T1-weighted images, remember a simple rule: in MDS, the bone marrow signal intensity decreases, but always remains higher than that of surrounding skeletal muscles.
Class and exam questions
Does the radiographic appearance of bones change in anemias?
On radiographs, bone tissue changes are visible only in chronic anemias. Anemias that do not cause reactive erythropoiesis (e.g., aplastic anemia) do not alter the radiograph, but on MRI they manifest as a generalized increase in signal from fatty bone marrow.
What is focal nodular bone marrow hyperplasia and why is it dangerous?
This is a variant of hyperplastic red bone marrow that on MRI and PET/CT can visually mimic bone metastases or primary medullary bone tumors.
What complications are characteristic of homozygous $\alpha$-thalassemia?
Homozygous $\alpha$-thalassemia is one of the most common causes of hydrops fetalis. This condition typically results in intrauterine or perinatal death.
What else to study on this topic
- Mechanisms of presacral extramedullary hematopoiesis in MDS
- Specific skeletal changes in homozygous $\beta$-thalassemia in childhood
- MRI findings of granulocyte colony-stimulating factor therapy on bone marrow
- Compound forms of hemoglobinopathies: hemoglobin H disease and $\beta$-thalassemia intermedia
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