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Most examinations of bone start with conventional radiographs obtained with at least two views exposed at a 90-degree angle to each other (called orthogonal views ) so as to localize abnormalities better and to visualize as much of the bone as possible ( Fig. 21.1 ).
Still, conventional radiographs cannot visualize the entire circumference of a tubular bone and they are not particularly sensitive for demonstrating musculoskeletal soft-tissue abnormalities other than significant soft-tissue swelling.
It is important to remember that, although the cortex completely surrounds the entire bone, on conventional radiographs it is best seen where it is viewed in profile (i.e., where the x-ray beam passes tangentially to the bone).
CT and MRI are able to demonstrate the entire circumference and internal matrix of bone including, especially with MRI, the surrounding soft tissues not visible on conventional radiographs. This is accomplished by computer -aided reformatting and a superior ability to display more subtle differences in tissue densities ( Fig. 21.2 ).
MRI is an excellent means of studying the components of marrow, a fact that makes it so useful in the study of marrow pathology. Whereas the cortex is the part of the bone most easily visualized on conventional radiographs, cortical bone has a very low signal intensity on conventional MRI sequences ( Fig. 21.3 ).
On conventional radiographs, visualized long bones exhibit a dense cortex of compact bone that completely envelopes a less-dense medullary cavity containing cancellous bone arranged as trabeculae , separated primarily by blood vessels, hematopoietic cells, and fat. The shaft of the bone is the diaphysis, capped on each end by the epiphyses. Where the diaphysis and epiphysis join (i.e., the metaphysis ) is the site of the epiphysial growth plate in children.
The proportions of cortical versus trabecular bone vary in different skeletal sites and even at different locations in the same bone (i.e., the cortex is naturally thicker in some places than in others) (see Fig. 21.2A ).
Fig. 21.4 contains a diagram of a typical synovial joint and compares the structures visualized on conventional radiographs and MRI.
Bones reflect the general metabolic status of the individual. Their composition requires a protein-containing, collagenous matrix (osteoid) upon which bone mineral , principally calcium phosphate , is transformed into cartilage and bone.
Bones are continuously undergoing remodeling processes that include resorption of old or diseased bone by osteoclasts and formation of new bone by osteoblasts. Osteoblasts are responsible for bone matrix production, whereas osteoclasts resorb both the matrix and mineral.
Both osteoclastic and osteoblastic activity depend on the presence of a viable blood supply to bring those cells to the bone.
Bones also respond to mechanical forces, for example, the contractions of muscles and tendons, the process of bearing weight, constant use, or prolonged disuse, which help to form and/or maintain the shape as well as the content of each bone.
In this section, we arbitrarily divide abnormalities of bone density into two major categories based primarily on their appearance on conventional radiographs: those that produce a pattern of either increased or decreased bone density ( Table 21.1 ).
Density | Extent | Examples Used in This Chapter |
---|---|---|
Increased density | Diffuse | Diffuse osteoblastic metastases |
Focal | Localized osteoblastic metastases | |
Avascular necrosis of bone | ||
Paget disease | ||
Decreased density | Diffuse | Osteoporosis |
Hyperparathyroidism | ||
Focal | Localized osteolytic metastases | |
Multiple myeloma | ||
Osteomyelitis |
On conventional radiographs and CT, an increase in bone density produces sclerosis (increased whiteness) to the affected part. If the entire bone is sclerotic, there is a loss of the demarcation of the normal cortico-medullary junction because of the abnormally increased density of the medullary cavity relative to the cortex ( Fig. 21.5 ).
Examples of diseases that cause increased bone density include osteoblastic metastatic disease, avascular necrosis of bone, and Paget disease.
Diffuse, blood-borne, metastatic disease from carcinoma of the prostate is the prototype for a generalized increase in bone density. Osteoblastic metastatic disease, like that from the prostate, can also produce focal areas of increased bone density as well. These osteoblastic lesions are most often seen in the vertebrae, ribs, pelvis, humeri, and femora ( Fig. 21.6 ). Osteoblastic activity occurs beyond the control of normal physiologic constraints.
Focal sclerotic lesions can affect either the cortex, the medullary cavity, or both. Those that affect the cortex will usually produce periosteal new bone formation (periosteal reaction), which leads to an appearance of thickening of the cortex. Those that affect the medullary cavity will result in punctate, amorphous, sclerotic lesions surrounded by the normal medullary cavity ( Fig. 21.7 ).
Metastatic disease to bone is found in a significant percentage of autopsied patients with carcinoma of the prostate. Multiple bone metastases from carcinoma of the prostate occur much more frequently than do solitary bone lesions, which are discussed later in this chapter ( Box 21.1 ).
Metastases to bone are far more common than primary bone tumors.
Metastases to bone fall into two major categories: those that stimulate the production of new bone are called osteoblastic and those that destroy bone are called osteolytic ; some metastases include lesions in which both osteoblastic and osteolytic changes are present.
Metastatic bone lesions from any source are very uncommon distal to the elbow or the knee ; when present in these locations, they are usually widespread and caused by lung or breast cancer.
The radionuclide bone scan is currently the study of choice for detecting skeletal metastases , regardless of the suspected primary ( Box 21.2 ). With diffuse bone metastases, a so-called superscan may be seen on radionuclide bone scan. The superscan demonstrates high radiotracer uptake throughout the skeleton, with poor or absent renal excretion of the radiotracer ( Fig. 21.8 ).
A radionuclide bone scan requires the intravenous administration of a minute amount of technetium 99M MDP , a radioactively tagged tracer that affixes to the surface of bone.
Technetium 99M is the radionuclide used to tag methylene diphosphonate (MDP), the portion that directs the tracer to bone.
Uptake of the radionuclide in bone depends, in part, on the bone’s blood supply and rate of bone turnover: processes with extremely high or extremely low bone turnover may produce false-negative scans.
Osteoblastic lesions almost always show increased activity (uptake of radiotracer). Even osteolytic metastases usually show some increased uptake because of the repair that occurs in most, but not all, osteolytic processes.
A bone scan is much less sensitive in detecting multiple myeloma , so conventional radiographic surveys of the skeleton are the initial study of choice when searching for myeloma lesions.
Bone scans are highly sensitive, but not very specific; a positive scan almost always requires another imaging procedure (conventional radiographs, CT, or MRI) to rule out nonmalignant causes of a positive bone scan (e.g., fractures or osteomyelitis).
Avascular necrosis (AVN) of bone (also called ischemic necrosis, aseptic necrosis, osteonecrosis) results from cellular death and eventually leads to the collapse of the affected bone. It usually involves those bones that have a relatively poor collateral blood supply (e.g., scaphoid in the wrist, femoral head) and tends to affect the hematopoietic elements of marrow earliest so that MRI is the most sensitive modality for detecting AVN.
There are numerous causes of avascular necrosis. Some of the more common are shown in Table 21.2 .
Location | Example of Disease |
---|---|
Intravascular | Sickle cell disease |
Polycythemia vera | |
Vascular | Vasculitis (Lupus and radiation-induced) |
Extravascular | Trauma (fractures) |
Idiopathic | Exogenous steroids and Cushing disease |
Legg-Calvé-Perthes disease |
On conventional radiographs, the devascularized bone becomes denser and therefore appears more sclerotic than the remainder of the bone. This especially occurs in the femoral head ( Fig. 21.9 ) and humeral head ( Fig. 21.10 ).
On MRI, there is usually a decrease from the normal high signal produced by fatty marrow ( Fig. 21.11 ).
On conventional radiographs, old medullary bone infarcts are recognized as dense, amorphous deposits of bone within the medullary cavities of long bones, frequently marginated by a thin, sclerotic membrane ( Fig. 21.12 ).
Paget disease is a chronic disease of bone , most often occurring in older men, now believed to be caused by chronic paramyxoviral infection. It is characterized by varying degrees of increased bone resorption and increased bone formation with bone formation predominating in those cases seen in more progressive forms of the disease.
The end result is almost always a denser bone that, despite its density, is mechanically inferior to normal bone and thus susceptible to pathologic fractures or bone-softening deformities such as bowing. The pelvis is most frequently involved , followed by the lumbar spine, thoracic spine, proximal femur, and calvarium.
Paget disease is usually diagnosed with conventional radiography. The imaging hallmarks of Paget disease are:
Thickening of the cortex.
Coarsening and thickening of the trabecular pattern ( Fig. 21.13 ).
Increase in the size of the bone involved. The “classic” history for Paget disease, rendered less useful since fashions have changed, was a gradual increase in a person’s hat size as the calvarium increased in size from this disease.
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