In the clinic

Determination of skeletal age

Throughout life the bones develop in a predictable way to form the skeletally mature adult at the end of puberty. In western countries skeletal maturity tends to occur between the ages of 20 and 25 years. However, this may well vary according to geography and socioeconomic conditions. Skeletal maturity will also be determined by genetic factors and disease states.

Up until the age of skeletal maturity, bony growth and development follows a typically predictable ordered state, which can be measured through either ultrasound, plain radiographs, or MRI scanning. Typically, the nondominant (left hand) is radiographed and is compared to a series of standard radiographs. From these images the bone age can be determined (Fig. 1.13).

In certain disease states, such as malnutrition and hypothyroidism, bony maturity may be slow. If the skeletal bone age is significantly reduced from the patient's true age, treatment may be required.

In the healthy individual the bone age accurately represents the true age of the patient. This is important in determining the true age of the subject. This may also have medicolegal importance.

Figure 1.13 A developmental series of radiographs showing the progressive ossification of carpal (wrist) bones from 3(A) to 10(E) years of age.

Bone marrow transplants

The bone marrow serves an important function. There are two types of bone marrow, the red marrow (otherwise known as myeloid tissue) and the yellow marrow. Red blood cells, platelets, and most white blood cells arise from within the red marrow. In the yellow marrow a few white cells are made; however this marrow is dominated by large fat globules (producing its yellow appearance) (Fig. 1.14).

From birth most of the body's marrow is red; however, as the subject ages, more red marrow is converted into yellow marrow within the medulla of the long and flat bones.

Bone marrow contains two types of stem cells. Hemopoietic stem cell grafts give rise to the white blood cells, red blood cells, and platelets. Mesenchymal stem cells differentiate into structures that form bone, cartilage, and muscle.

There are a number of diseases that may involve the bone marrow, including infection and malignancy. In patients who develop a bone marrow malignancy (e.g., leukemia) it may be possible to harvest nonmalignant cells from the patient's bone marrow or cells from another person's bone marrow. The patient's own marrow can be destroyed with chemotherapy or radiation and the new cells infused. This treatment is bone marrow transplantation.

 Figure 1.14 T1-weighted image in the coronal plane, demonstrating the relatively high signal intensity returned from the femoral heads and proximal femoral necks, consistent with yellow marrow. In this young patient, the vertebral bodies return an intermediate darker signal that represents red marrow. There is relatively little fat in these vertebrae, hence the lower signal return.

In the clinic

Bone fractures

Fractures occur in normal bone because of abnormal load or stress, in which the bone gives way. Fractures may also occur in bone that is of poor quality (osteoporosis); in such cases a normal stress is placed upon a bone that is not of sufficient quality to withstand this force and subsequently fractures.

In children whose bones are still developing, fractures may occur across the growth plate or across the shaft. These shaft fractures typically involve partial cortical disruption, similar to breaking a branch of a young tree; hence they are termed "greenstick" fractures (Fig. 1.15).

After a fracture has occurred, the natural response is to heal the fracture. Between the fracture margins a blood clot is formed into which new vessels grow. A jelly-like matrix is formed, and further migration of collagen-producing cells occurs. On this soft tissue framework, calcium hydroxyapatite is produced by osteoblasts and forms insoluble crystals, and then bone matrix is laid down. As more bone is produced, a callus can be demonstrated forming across the fracture site.Treatment of fractures requires a fracture line reduction. If this cannot be maintained in plaster of Paris cast, it may require internal or external fixation with screws and metal rods.

 Figure 1.15 Radiograph, lateral view, showing greenstick fractures of the distal radius and distal ulna.

Avascular necrosis

Avascular necrosis is cellular death of bone resulting from a temporary or permanent loss of blood supply to that bone. Avascular necrosis may occur in a variety of medical conditions, some of which have an etiology that is less than clear. A typical site for avascular necrosis is a fracture across the femoral neck in an elderly patient. In these patients there is loss of continuity of the cortical medullary blood flow with loss of blood flow deep to the retinacular fibers. This essentially renders the femoral head bloodless; it subsequently undergoes sclerosis and collapse. In these patients it is necessary to replace the femoral head with a prosthesis (Fig. 1.16).

 Figure 1.16 Image of the hip joints demonstrating loss of height of the right femoral head with juxta-articular bony sclerosis and subchondral cyst formation secondary to avascular necrosis. There is also significant wasting of the muscles supporting the hip, which is secondary to disuse and pain.

In the clinic
Osteoporosis

 Figure 1.17 Radiograph of the lumbar region of the vertebral column demonstrating a wedge fracture of the L1 vertebra. This condition is typically seen in patients with osteoporosis.

Osteoporosis is a disease in which the bone mineral density is significantly reduced. This renders the bone significantly more at risk of fracture. Typically, osteoporotic fractures occur in the femoral necks, the vertebra, and the wrist. Although osteoporosis may occur in men, especially elderly men, the typical patients are postmenopausal women. There are a number of risk factors that predispose bones to develop osteoporosis. These factors include poor diet, steroid usage, smoking, and premature ovarian failure. Treatment involves removing underlying potentiating factors, such as improving diet and preventing further bone loss with drug treatment, (e.g., vitamin D and calcium supplements; newer treatments include drugs that increase bone mineral density) (Figs. 1.17 and 1.18).

Figure 1.18 Radiograph of the lumbar region of the vertebral column demonstrating three intra-pedicular needles, all of which have been placed into the middle of the vertebral bodies. The high-density material is radiopaque bone cement, which has been injected as a liquid to set solid. 

Epiphyseal fractures

As the skeleton develops, there are stages of intense growth typically around the ages of 7 to 10 years and later in puberty. These growth spurts are associated with increased cellular activity around the growth plate and the metaphyseal region. This increase in activity renders the growth plates and metaphyseal regions more vulnerable to injuries, which may occur from dislocation across a growth plate or fracture through a growth plate. Occasionally an injury may result in growth plate compression, destroying that region of the growth plate, which may result in asymmetric growth across that joint region. All fractures across the growth plate must be treated with care and expediency, requiring fracture reduction.