Osteomyelitis is caused by a broad spectrum of infectious organisms that reach bone by hematogenous spread, by extension from a contiguous site of infection, or by direct introduction of organisms (trauma or surgery). Acute hematogenous osteomyelitis tends to involve bones with rich red marrow. In infants and children, the metaphyses of long bones (especially the femur and tibia) are most often affected; staphylococci and streptococci are the most common organisms. After the age of 8 months, the epiphyseal cartilage plate acts as a barrier against the spread of infection. In adults, acute hematogenous osteomyelitis primarily occurs in the vertebrae and rarely involves the long bones. Although the incidence and severity of osteomyelitis have decreased since the advent of antibiotics, this disease has recently become more prevalent as a complication of intravenous drug abuse. In diabetic patients and those with other types of vascular insufficiency, a soft tissue infection may spread from a skin abscess or a decubitus ulcer, usually in the foot, to cause cellulitis and eventually osteomyelitis in contiguous bones.

Because the earliest changes of osteomyelitis are usually not evident on plain radiographs until about 10 days after the onset of symptoms, radionuclide bone scanning with 99mTc-pyrophosphate is the most valuable imaging modality for the early diagnosis of osteomyelitis. Increased isotope uptake, reflecting the inflammatory process and increased blood flow, is evident within hours of the onset of symptoms. Because osteomyelitis may initially result in decreased accumulation of isotope due to ischemia, and because overlying cellulitis may mimic a bone infection, sequential studies and scanning with two different radionuclides (technetium and gallium) may be required.

On plain radiographs, the earliest evidence of osteomyelitis in a long bone is a localized, deep soft tissue swelling adjacent to the metaphysis. The inflammation causes displacement or obliteration of the normal fat planes adjacent to and between the deep muscle bundles, unlike skin infections, in which the initial swelling is superficial. The initial osseous change appears as subtle areas of metaphyseal lucency reflecting resorption of necrotic bone. Soon bone destruction becomes more prominent, producing a ragged, moth-eaten appearance. The more virulent the organism, the larger the area of destruction. Subperiosteal spread of inflammation elevates the periosteum and stimulates the laying down of layers of new bone parallel to the shaft. This results in a lamilar periosteal reaction that is characteristic of benign diseases, especially infection. Eventually, a large amount of new bone surrounds the cortex in a thick, irregular bony sleeve (involucrum). Disruption of cortical blood supply leads to bone necrosis. Segments of avascular dead bone (sequestra) remain as dense as normal bone and are clearly differentiated from the demineralized bone, infected granulation tissue, and pus about them.

After the acute infection has subsided, a pattern of chronic osteomyelitis develops. The bone appears thickened and sclerotic with an irregular outer margin. The cortex may become so dense that the medullary cavity is difficult to demonstrate. Reactivation of infection may appear as the recurrence of deep soft tissue swelling, periosteal calciffcation, or the development of lytic abscess cavities within the bone. However, plain radiographs are often inadequate to determine whether an active infection is present. Radionuclide scanning is much more sensitive and accurate in establishing a recurrence.

On CT, an early sign of osteomyelitis is an increase in the intramedullary density of bone, which is probably due to the replacement of low-density fatty tissue by higher-density pus, blood, and detritus. Computed tomography is also of value to determine the location and extent of the infection, to differentiate cortical and/or periosteal involvement from intramedullary involvement, to detect the presence of abscess formation, and to identify a need for surgical debridement or drainage.

In most patients, the radiographic findings, clinical history, and symptoms are sufficient to make the diagnosis of osteomyelitis. At times, however, especially in children, aggressive bone destruction and bizarre periosteal reaction may suggest a malignant bone tumor. If there is any doubt about the correct diagnosis, biospy is required.

Vertebral Osteomyelitis

The earliest sign of pyogenic vertebral osteomyelitis is subtle erosion of the subchondral bone plate with loss of the sharp cortical outline. This may progress to total destruction of the vertebral body associated with a paravertebral soft tissue abscess. As with osteomyelitis of the appendicular skeleton, plain radiographic changes may not develop for several weeks following infection, while radionuclide scans are positive early. Unlike neoplastic processes, osteomyelitis usually affects the intervertebral disk space and often involves adjacent vertebrae. Depending on the site of disease, anterior extension of vertebral osteomyelitis may cause retropharyngeal abscess mediastinitis, empyema, pericarditis, subdiaphragmatic abscess, psoas muscle abscess, or peritonitis; posterior extension of inflammatory tissue can compress the spinal cord or produce meningitis if the infection penetrates the dura to enter the subarachnoid space.

Tuberculous osteomyelitis most commonly involves the thoracic and lumbar spine. The infection tends to begin in the anterior part of the vertebral body, adjacent to the intervertebral disk. Irregular, poorly marginated bone destruction within the vertebral body is often associated with a paravertebral abscess, an accumulation of purulent material that produces a fusiform soft tissue mass about the vertebrae. The shadow of a paravertebral abscess is best seen in the dorsal spine; in the lumbar region, the only evidence of abscess formation may be the outward bulging of the psoas muscle shadow. The spread of tuberculous osteomyelitis causes a narrowing of the adjacent intervertebral disk and the extension of infection and bone destruction across the disk to involve the contiguous vertebral body. Unlike pyogenic infection, tuberculous osteomyelitis is rarely associated with periosteal reaction or bone sclerosis. In the untreated patient, progressive vertebral collapse and anterior wedging lead to a characteristic sharp kyphotic angulation (gibbus deformity). Healed lesions may demonstrate mottled calcific deposits in a paravertebral abscess and moderate recalcification and sclerosis of the affected bones.

Computed tomography is of special value in the diagnosis of osteomyelitis of the spine. This modality can precisely define the size of the surrounding soft tissue mass, its relation to nearby vital structures (aorta, spinal cord), and the presence of abscess cavities requiring surgical drainage. Serial CT scans during therapy may be used to confirm the expected decrease in size of the soft tissue mass.

Multiple myeloma is a disseminated malignancy of plasma cells that may be associated with bone destruction, bone marrow failure, hypercalcemia, renal failure, and recurrent infections. The disease primarily affects persons between 40 and 70 years of age. Typical laboratory findings include an abnormal spike of monoclonal immunoglobulin and the presence of Bence )ones protein in the urine. Up to 20 percent of patients with multiple myeloma develop amyloidosis.

The classic radiographic appearance of multiple myeloma is multiple punched-out osteolytic lesions scattered throughout the skeletal system and best seen on lateral views of the skull. Because the bone destruction is due to proliferation of plasma cells distributed throughout the bone marrow, the flat bones containing red marrow (vertebrae, skull, ribs, pelvis) are primarily affected. The appearance may be indistinguishable from that of a metastatic carcinoma, though the lytic defects in multiple myeloma tend to be more discrete and uniform in size. The sharply circumscribed lytic lesions eventually tend to coalesce, destroying large segments of bone. The destructive lesion may break through the cortex and periosteum to form a soft tissue mass. This most commonly involves a rib and rarely occurs in metastatic disease. Pathologic fractures are common, especially in the ribs, vertebrae, and long bones. Solitary or diffuse areas of sclerosis, simulating osteoblastic metastases, are rarely seen.

Extensive plasma cell proliferation in the bone marrow with no tendency to form discrete tumor masses may produce generalized skeletal deossification simulating postmenopausal osteoporosis. In the spine, decreased bone density and destructive changes in multiple myeloma are usually limited to the vertebral bodies, sparing the pedicles (lacking red marrow) that are frequently destroyed by metastatic disease. The severe loss of bone substance in the spine often results in multiple vertebral compression fractures. Because multiple myeloma causes little or no stimulation of new bone formation, radionuclide bone scans may be normal even with extensive skeletal infiltration. In patients with myeloma who have bone pain but normal or nonspecific radiographs, computed tomography (CT) may demonstrate characteristic destructive lesions.

Mild or severe renal failure develops in about 20 percent of patients with multiple myeloma. This may be related to tubular damage from large quantities of filtered monoclonal proteins or from hypercalcemia, uric acid nephropathy, or amyloidosis. In the past, dehydration induced by the preparation for some radiographic procedures has been implicated in the precipitation of renal failure. However, many now feel that if dehydration is avoided, a contrast study such as excretory urography or CT is not contra indicated in the absence of renal failure.

SOLITARY MYELOMA (PLASMACYTOMA)

Infrequently, a single plasma cell tumor presents as an apparent solitary destructive bone lesion with no evidence of the major disease complications usually associated with multiple myeloma. A solitary myeloma causes a central area of destruction, usually in the shaft of a long bone. The tumor may be highly destructive, expanding or ballooning the bone before it breaks through the cortex. Residual streaks of bone can produce a tra-beculated or soap-bubble radiographic appearance, especially in the pelvis. In the spine, an affected vertebral body can collapse or be completely destroyed; a surrounding soft tissue mass is often present. Although plasmacytomas may remain solitary for long periods, widespread destructive lesions usually-appear within 1 or 2 years as the condition develops into typical multiple myeloma.
Computed tomography is superior to plain radiographs in the evaluation of extraosseus plasmacytomas, demonstrating both the extent of the soft tissue mass and the underlying bony involvement. This modality is also helpful in demonstrating disseminated disease in a patient who has an apparent solitary plasmacytoma.

Radiographically detectable skeletal involvement occurs in up to 70 percent of cases of childhood leukemia as a result of the infiltration of leukemic cells into the marrow. The earliest radiograpic sign of disease is usually a transverse radiolucent band at the metaphyseal ends of the long bones, most commonly about the knees, ankles, and wrists. Although in infancy this appearance is nonspecific and also occurs with malnutrition or systemic disease, the presence of these transverse lucent metaphyseal bands after the age of 2 years strongly suggests acute leukemia.

As the proliferation of neoplastic cells in the marrow becomes more extensive, actual destruction of bone may occur. This may cause patchy lytic lesions, a permeative moth-eaten appearance, or diffuse destruction with cortical erosion. A reactive response to proliferating leukemic cells can cause patchy or uniform osteosclerosis; subperiosteal proliferation incites periosteal new bone formation. Diffuse skeletal demineralization, resulting from both leukemic infiltration of the bone marrow and alteration of protein and mineral metabolism, can result in vertebral compression fractures.
Skeletal changes are much less common in chronic leukemia and are usually limited to generalized demineralization in the flat bones, where active marrow persists in adulthood. The demonstration of focal areas of destruction, or periosteal new bone formation, suggests transformation into an acute phase of the disease.

Paget’s disease (osteitis deformans) is one of the most common chronic diseases of the skeleton. Destruction of hone followed by a reparative process results in weakened, deformed, and thickened bony structures. The disease is seen most commonly during middle life, affects men twice as often as women, and has been reported to occur in about 3 percent of all persons over 40 years of age. Although the destructive phase often predominates initially, there is most frequently a combination of destruction and repair; in the pelvis and the weight-bearing bones of the lower extremities, the reparative process may begin early and be the prominent feature. Often affecting multiple bones, Paget’s disease particularly involves the pelvis, femurs, skull, tibias, vertebrae, clavicles, and ribs.

In the skull, Paget’s disease begins as an area of sharply demarcated radiolucency (osteoporosis circumscripta) that represents the destructive phase of the disease and primarily involves the outer table, sparing the inner table. Deossification begins in the frontal or occipital area and spreads slowly to encompass the major portion of the calvarium. During the reparative process, the development of irregular islands of sclerosis in the inner table is followed by thickening of the diploe and later of the outer table, resulting in a mottled, cotton-wool appearance.

In the spine, Paget’s disease characteristically causes enlargement of the vertebral body. Increased trabecu-lation, which is most prominent at the periphery of the bone, produces a rim of thickened cortex and a picture-frame appearance. Dense sclerosis of one or more vertebral bodies (ivory vertebrae) may present a pattern simulating osteoblastic metastases or Hodgkin’s disease, though in Paget’s disease the vertebrae are also expanded in size.

The pelvis is the most common and often the initial site of Paget’s disease. A distinctive early sign is coarsening of the trabeculae along the iliac margins that produces thickening of the pelvic brim. A combination of destructive and reparative changes is usually seen. Although diffuse sclerosis may simulate osteoblastic metastases, the characteristic cortical thickening and coarse trabeculation should suggest Paget’s disease.
In the long bones, the destructive phase almost invariably begins at one end of the bone and extends along the shaft for a variable distance before typically ending in a sharply demarcated, V-shaped configuration (blade-of-grass appearance). In the reparative stage the bone is enlarged, with an irregularly widened cortex and coarse, thickened trabeculae. Although dense, the bones are soft and deformities are common, especially the shepherd’s crook deformity of the upper femur and anterior bowing of the tibia. Transverse fractures may also occur, especially on the convex side of bowed long bones.

Paget’s disease may lead to severe clinical complications. The downward thrust of the heavy head upon the softened bone of the spine may cause basilar invagination of the skull, compression of the brainstem, and numerous cranial nerve defects. Expansion and distortion of softened vertebral bodies, sometimes with pathologic fractures, may compress the spinal cord and produce nerve root deficits. Multiple microscopic arteriovenous malformations in pagetoid bone may result in high-output cardiac failure. The most serious complication of Paget’s disease is sarcomatous degeneration, which fortunately occurs in fewer than 1 percent of patients with this condition. Most of the lesions are osteosarcomas, though fibrosarcomas and chondrosarcomas may occur.

Osteoporosis is a generalized or localized deficiency of bone matrix in which the mass of bone per unit volume is decreased in amount but normal in composition. Bone is a living, constantly changing tissue, and normally there is a balance between the amount of old bone being removed and the amount of new bone replacing it. Osteoporosis is usually due to accelerated resorption of bone, though decreased bone formation may lead to osteoporosis in such entities as Cushing’s syndrome, prolonged steroid administration, and disuse or immobilization osteoporosis. Loss of mineral salts causes osteoporotic bone to become more lucent than normal. This may be difficult to detect, since about 30 percent of the bone density must be lost before the loss can be demonstrated on routine radiographs.

The major causes of generalized osteoporosis are senility and postmenopausal hormonal changes. As a person ages, the bones lose density and become more brittle, fracturing more easily and healing more slowly. Many elderly persons are also less active and have poor diets that are deficient in protein. In postmenopausal osteoporosis there is a deficiency in the gonadal hormonal levels and decreased osteoblast activity. Other causes of generalized osteoporosis include endocrine dysfunctions, malnutrition, deficiency diseases, neoplastic disorders (multiple myeloma, metastases), and hemoglobinopathies.

Regardless of the cause, the radiographic appearance is similar in all conditions producing osteoporosis. The most striking change is cortical thinning with irregularity and resorption of the endosteal surfaces. In the long bones or the midshafts of the metacarpals and metatarsals, osteoporosis is evident if the sum of the thickness of the two cortices is less than one-half the diameter of the bone. There is a decrease in the number and thickness of trabeculae in spongy bone. However, the remaining trabeculae lying along lines of stress (weight bearing, muscle contraction) are accentuated and have an increased density and width. Although the bone density is generally decreased, the normal mineralized but thin cortex appears to be relatively dense, in contrast to the deossified spongy bone.

The radiographic changes of osteoporosis primarily involve the spine and pelvis. As the bone density of a vertebral body decreases, the cortex appears as a thin line that is relatively dense and prominent, producing the typical picture-frame pattern. Because of the severe loss of bone density, anterior wedging or compression fractures of one or more vertebral bodies may result, most commonly in the middle and lower thoracic and upper lumbar areas.The intervertebral disks may expand into the weakened vertebral bodies and produce characteristic concave contours of the superior and inferior disk surfaces (“fish” contour). In the skull, the calvarium may show spotty loss of density, and there is commonly deossification of the floor of the sella turcica and dorsum sellae.

LOCALIZED OSTEOPOROSIS

Localized osteoporosis may result from disuse, neurovascular disturbances (Sudeck’s atrophy), local joint disease, or inflammation. To maintain osteoblastic activity at normal levels, bones must be subjected to a normal amount of stress and muscular activity. Within a few weeks after the fracture of a bone, localized osteoporosis becomes detectable, especially distal to the site of injury. The loss of bone matrix is primarily due to inactivity, though hyperemia, impaired venous flow, and neural changes may also play some role. The cortical margin of an involved bone becomes thin but, unlike the bone destruction due to disease, never completely disappears. Sudeck’s atrophy (reflex sympathetic dystrophy) is the rapid development of painful osteoporosis following rather trivial injury. Probably of neurovascular origin, Sudeck’s atrophy most often involves the hands and feet with a mottled, irregular osteoporosis that primarily affects the periarticular region. The juxta-articular cortex may become extremely thin but remains intact, unlike in an arthritic process. Unusual types of localized osteoporosis include regional migratory osteoporosis (transitory osteoporosis), in which osteoporosis follows the development of severe pain about a major joint such as the hip, knee, or ankle in middle-aged or elderly persons, and transitory demineralization of the femoral head, a disorder characterized by a painful hip and progressive osteoporosis of the femoral head.