Skeletal System

Chapter 4

Skeletal System


Radiographer Notes

Three factors are critical in radiography of the skeletal system: (1) proper patient positioning; (2) correct alignment of the radiographic tube, the body part being imaged, and the image receptor; and (3) choice of exposure factors that produce optimal contrast and visibility of detail. In patients with suspected fractures, two projections as close as possible to 90 degrees to each other must always be obtained to demonstrate fracture relationships. A variety of projections (e.g., oblique, tangential, and coned-down) may be required to identify obscure fractures.

At times, the poor condition of a patient may require ingenuity on the part of the radiographer to obtain diagnostic radiographs when routine positioning methods cannot be accomplished. Patients with bone tumors, arthritis, or recent trauma are frequently in severe pain and extremely frightened of further injury or of suffering more discomfort. The radiographer must reassure such patients that positioning will be carefully accomplished with as little pain or discomfort as possible. The radiographer must remember that further injury to the patient can easily occur if the proper moving techniques are not used.

At times, the radiographer may need to perform cross-table or tube-angulation projections to obtain the required images without moving the patient. In such cases, the radiographic tube must be perpendicular to the image receptor and the body part to prevent image distortion. Variations in this relationship can obscure pathologic bone conditions or lead to errors in interpretation of the alignment of fracture fragments.

Bone radiographs require a short scale of contrast to provide maximal visibility of detail. The periosteum, cortex, and internal bone structure (trabeculae) must be well demonstrated to detect the often subtle changes of fractures, demineralization, and bone destruction. For example, periosteal new bone formation may indicate underlying tumor, infection, or prior trauma, whereas minute juxtaarticular erosions are often seen in arthritis. The scale of contrast must also allow visualization of the soft tissues and muscles because soft tissue swelling, calcifications, opaque foreign bodies, muscle wasting, and the presence of gas are all important radiographic findings.

It is recommended that lower to middle kVp ranges be used in all skeletal radiography. To achieve the necessary scale of contrast, extremity radiographs should be exposed using an exposure in the 60 to 69 kVp range, whereas a range of 70 to 85 kVp is recommended for studies of the spine, pelvis, thoracic cavity, and shoulder. As radiographers change to digital images, the kVp should be increased slightly to compensate for a slower system with only minimal increase in patient dose. The scale of contrast will be controlled by selection of the correct algorithm during processing of the image. Appropriate ratio grids, or Bucky devices, should be used for all body parts 10 cm or larger to aid in producing images with a higher contrast (by reducing secondary and scatter radiation).

Special techniques, such as magnification or tomography, may be necessary to detect subtle fractures or other pathologic bone conditions. For example, the navicular bone of the wrist typically requires the use of the magnification technique. For 2x linear or 4x area magnification, the object must be an equal distance from the radiographic tube and the image receptor. For 3x linear or 9x area magnification, the body part must be twice as far from the image receptor as from the x-ray tube. Close collimation is extremely important to prevent undercutting the image. A radiographic tube with a fractional focal spot of 0.3 mm or less is mandatory for a magnification factor of 2× or more to compensate for the excessive penumbra (geometric blur) that results from the object image receptor distance. Larger focal spot sizes cause excessive geometric blurred images that appear to have motion and lack recorded detail as a result of excessive geometric blur (penumbra).

Tomography may be required to make a definitive diagnosis if the plain radiographic images are equivocal or to delineate precisely the extent of bone involvement. For example, tomography was frequently needed in the evaluation of fractures of the tibial plateau and spine. Currently, CT is the modality of choice for evaluation of the bones and spinal injuries. It is for spinal injury as it best demonstrates the vertebrae and fracture fragments that could impinge on the spinal cord or peripheral nerves. MRI better demonstrates nontraumatic disk herniation or tumor impingement. In trauma cases, if CT results are inconclusive, MRI may better delineate soft tissue injury.

In most cases, it is essential to prevent motion of the body part being radiographed. To accomplish this, the radiographer should make the patient as comfortable as possible, use immobilization devices when necessary, and use the shortest possible exposure times. However, a few portions of the skeletal system are better visualized using a motion technique. For three such areas (the sternum and the lateral thoracic spine, and to obtain a transthoracic lateral projection of the upper humerus), a shallow breathing technique is used while the patient remains immobilized. A minimum exposure time of about 5 seconds and a very low mA should be used. The patient is instructed to breathe rhythmically during the entire exposure to blur out overlying ribs and lung markings. An additional technique, the Ottonello (or “wagging jaw”) method, is used to obtain an AP projection of the cervical spine. Movement of the jaw is used to blur out the image of the mandible, which otherwise would superimpose the upper portion of the cervical spine.

Certain pathologic conditions of the skeletal system require that the radiographer alter routine technical settings. Some disorders produce greater bone density (e.g., sclerosis and increased bone growth), which increases attenuation; others decrease the density of the bony structures (e.g., lytic bone destruction and loss of calcium from bone), and so they will attenuate x-rays less (see Box 1-1). It is important to remember that the necessary technical changes may vary according to the stage of the underlying condition. However, the technical factors should not be changed to obscure or change the interpretation of the pathophysiologic changes.

Physiology of the skeletal system

The skeletal system is composed primarily of two highly specialized connective tissues: bone and cartilage. Bone consists of an organic matrix in which inorganic salts (primarily calcium and phosphate) are deposited. A fibrous membrane termed the periosteum covers the outer surfaces of bone, except at joint surfaces, where articular cartilage covers the bone and acts as a protective cushion. The periosteum contains a network of blood vessels from which nutrient arteries penetrate into the underlying bone. The main shaftlike portion is termed the diaphysis, and the ends of the bone are called epiphyses. The hollow, tubelike structure within the diaphysis, known as the medullary cavity, or marrow, is lined by an inner membrane termed the endosteum (Figure 4-1A).

There are two major types of bone. The outer layer consists of compact bone, which to the naked eye appears dense and structureless. Under the microscope, the matrix of compact bone consists of complex structural units called “haversian systems.” Cancellous (spongy) bone is composed of a weblike arrangement of marrow-filled spaces separated by thin processes of bone, called trabeculae, that are visible to the naked eye (Figure 4-1B). The relative amount of each type of bone depends on the strength required and thus varies from bone to bone and in different portions of the same bone. For example, the shafts of long bones, such as the femur and tibia, have a thick outer layer of compact bone, whereas the layer of compact bone is relatively thin in irregular bones, such as vertebral bodies and facial bones, and in short bones, such as the carpal and tarsal bones.

Most bones form from models composed of hyaline cartilage (enchondral ossification). In a typical long bone, a primary ossification center appears in the center of the cartilage precursor in about the eighth week of intrauterine life, and bone formation extends so that the entire shaft is usually ossified before birth. Just before or after birth, secondary ossification centers appear in the epiphyses, the ends of developing long bones. Until the linear growth of bone is complete, the epiphysis remains separated from the diaphysis by a cartilaginous plate called the epiphyseal cartilage. The epiphyseal cartilage persists until the growth of the bone is complete. At that time, the epiphyseal plate ossifies, and the epiphysis and diaphysis fuse (at various ages depending on the specific bones). Where the diaphysis meets the epiphyseal growth plate is a slight flaring, known as the metaphysis.

The increase in length of a developing long bone occurs by growth of the epiphyseal cartilage followed by ossification. Bones grow in diameter by the combined action of two special types of cells called osteoblasts and osteoclasts. Osteoclasts enlarge the diameter of the medullary cavity by removing bone from the diaphysis walls. At the same time, osteoblasts from the periosteum produce new bone around the outer circumference. Osteoblasts and osteoclasts thus continuously resorb old bone and produce new bone. This constant process of remodeling occurs until the bone assumes its adult size and shape.

The radiographic determination of bone age is useful for evaluating physiologic age and growth potential, and for predicting adult stature. The best known and most widely accepted method of determining skeletal bone age (skeletal maturation) is that of Greulich and Pyle in their radiographic atlas compiled from thousands of examinations of American children at different ages. This atlas contains standard radiographs for age and sex that permit an assessment of bone age based on the presence or absence of ossification centers and their configuration, and the fusion of epiphyses in various portions of the hand and wrist.

Throughout life, bone formation (ossification) and bone destruction (resorption) continue to occur. They are in balance during the early and middle years of adulthood. After about age 40 years, however, bone loss at the inner or endosteal surface exceeds bone gain at the outer margins. Thus in long bones, the thickness of compact bone in the diaphyses decreases, and the diameter of the medullary cavity increases. The bone eventually resembles a hollow shell and is less able to resist compressive and bending forces. This process may lead to collapse and loss of height of vertebral bodies as well as to fractures of long bones after relatively mild injury.

Bones can also develop within a connective tissue membrane (intramembranous ossification). The clavicles and flat bones of the skull have no cartilaginous stage and begin to take shape when groups of primitive cells differentiate into osteoblasts, which secrete matrix material and collagenous fibrils. Deposition of complex calcium salts in the organic bone matrix produces rodlike trabeculae that join in a network of interconnecting spicules to form spongy or cancellous bone. Eventually, plates of compact or dense bone cover the core layer of spongy bone. Flat bones grow in size by the addition of osseous tissue to their outer surfaces (appositional growth). They cannot grow by expansion, as enchondral bone does. Bones perform five basic functions (Box 4-1).

Congenital/hereditary diseases of bone

Vertebral Anomalies

A transitional vertebra is one that has characteristics of vertebrae on both sides of a major division of the spine.


Most vertebral anomalies remain unnoticed and are incidental findings on radiographs. A cervical rib may compress the brachial nerve plexus (causing pain or numbness in the upper extremity) or the subclavian artery (decreasing blood flow to the arm) and therefore require surgical removal.

Spina Bifida

Spina bifida refers to a posterior defect of the spinal canal, resulting from failure of the posterior elements to fuse properly. A mild, insignificant form is spina bifida occulta, in which there is a splitting of the bony neural canal at the L5 or S1 level (Figure 4-4). Large defects are associated with spinal cord abnormalities and may lead to a variety of muscular abnormalities and lack of bladder or bowel control. In many cases a slight dimpling of the skin or a tuft of hair over the vertebral defect indicates the site of the lesion.

Large defects in the lumbar or cervical spine may be accompanied by herniation of the meninges (meningocele), or of the meninges and a portion of the spinal cord or nerve roots (myelomeningocele). A patient with a meningocele may be asymptomatic. Other malformations associated with a meningocele are clubfoot, gait disturbances, and bladder incontinence. The myelomeningocele has associated neurologic deficits at and below the site of protrusion. Almost all patients with myelomeningocele have the Chiari II malformation, with caudal displacement of posterior fossa structures into the cervical canal. Hydrocephalus is a frequent complication.

Radiographic Appearance

Spina bifida lesions are associated with large bony defects, absence of the laminae, and increased interpedicular distance (Figure 4-5). The herniated spinal contents are seen as a soft tissue mass posterior to the spine. Myelography, computed tomography (CT), or magnetic resonance imaging (MRI) can demonstrate the presence of spinal cord or nerve roots within the herniated sac. Prenatal real-time ultrasound can now demonstrate this serious malformation in utero on sagittal spine fetal images that determine the location and severity of the deformity.


Osteopetrosis (marble bones) is a rare hereditary bone dysplasia in which failure of the resorptive mechanism of calcified cartilage interferes with the normal replacement by mature bone. It prevents the bone marrow from forming, so that the bones become very brittle and stress fractures occur often. The patient may also become anemic as a result of the lack of blood-producing bone marrow. Osteopetrosis varies in severity and age at clinical presentation, from a fulminant, often fatal condition involving the entire skeleton at birth or in utero to an essentially asymptomatic form that is an incidental radiographic finding.

Osteogenesis Imperfecta

Osteogenesis imperfecta (brittle bones) is an inherited generalized disorder of connective tissue characterized by multiple fractures and an unusual blue color of the normally white sclera of the eye. Due to imperfectly formed or inadequate bone collagen, the adult patient with osteogenesis imperfecta is generally wheelchair bound because the skeletal structure does not support the body weight (Figure 4-7).

Radiographic Appearance

Patients with this condition suffer repeated fractures caused by the severe osteoporosis and the thin, defective cortices (Figure 4-8A). The fractures often heal with exuberant callus formation (often so extensive as to simulate a malignant tumor), sometimes causing bizarre deformities. Because of the severe cortical bone loss in advanced stages of disease, producing a good radiographic image may require lowering the kilovoltage to compensate for the loss of bone quality. Ossification of the skull progresses slowly, leaving wide sutures and multiple juxtasutural accessory bones within a suture (wormian bones) that produce a mosaic appearance (Figure 4-8B). “Child abuse” may be confused with osteogenesis imperfecta because of the presentation of multiple fractures in different stages of the healing process.


Achondroplasia is the most common form of dwarfism; it results from diminished proliferation of cartilage in the growth plate (decreased enchondral bone formation). This autosomal dominant condition does not affect membranous bone formation. Therefore the individual has short limbs, which contrast with the nearly normal length of the trunk (axial skeleton). Other characteristic physical features are a large head with frontal bulging, saddle nose, a prognathous (jutting) jaw, and prominent buttocks that give the false impression of lumbar lordosis.

Congenital Hip Dysplasia (Dislocation)

Congenital hip dysplasia, also known as developmental hip dysplasia, results from incomplete acetabulum formation caused by physiologic and mechanical factors. Physiologically, the fetus is exposed to increased hormone levels during delivery. Mechanically, as the fetus grows and occupies more space, the amount of amniotic fluid decreases, placing gentle pressure on the infant. Hip dysplasia is more common in females. During pediatric assessment of the hip, when the leg is flexed and abducted, the hip may “pop” out of joint and a “click” is felt or heard. The tendons and ligaments responsible for proper femoral head alignment are affected.

Radiographic Appearance

Anteroposterior (AP) pelvis and bilateral frog-leg (Cleaves) views are required to make a diagnosis (Figure 4-12). In many cases the AP image appears almost normal with only a slightly larger joint space. On the bilateral frog-leg view, the hip is usually dislocated superiorly and posteriorly. Because children with this disorder will undergo a multitude of follow-up images to recheck development, it is very important to shield the gonadal anatomy.

Ultrasound imaging (ultrasonography) now provides an alternative imaging method. The sonolucent femoral head can be viewed in relationship to the acetabulum to demonstrate the femoral angles. If sonography is available, its use allows the ionizing radiation dose to the child to be reduced, because previously, clinicians relied on two different x-ray projections for each assessment.

Inflammatory and infectious disorders

Rheumatoid Arthritis

Rheumatoid arthritis is a chronic systemic disease of unknown cause that appears primarily as a nonsuppurative (noninfectious) inflammatory arthritis of the small joints of the hands and feet. Women are affected about three times more frequently than men, and the average age at onset in adults is 40 years. Rheumatoid arthritis usually has an insidious origin and may either run a protracted and progressive course, leading to a crippling deformity of affected joints, or undergo spontaneous remissions of variable length. There is usually symmetric involvement of multiple joints, and the disease often progresses proximally toward the trunk until practically every joint in the body is involved.

Rheumatoid arthritis begins as an inflammation of the synovial membrane (synovitis) that lines the joints. The excessive exudate, a result of the inflammation, causes proliferation of the synovium. The resulting mass of thickened granulation tissue (pannus, meaning “covers like a sheet”) causes erosion of the articular cartilage and underlying bony cortex, fibrous scarring, and even the development of ankylosis (bony fusion across a joint). The erosion occurs because the inflammatory cells produce lytic enzymes. A combination of the fusion of joint surfaces and an inflammatory laxity of ligaments leads to the development of crippling deformities in the end stage of the disease (Figure 4-13).

Radiographic Appearance

The earliest radiographic evidence of rheumatoid arthritis is fusiform periarticular soft tissue swelling caused by joint effusion and hyperplastic synovial inflammation. Disuse and local hyperemia (increased blood flow) lead to periarticular osteoporosis that initially is confined to the portion of bone adjacent to the joint but may extend to involve the entire bone (Figure 4-14). Extension of the pannus from the synovial reflections onto the bone causes characteristic small foci of destruction at the edges of the joint, where articular cartilage is absent. These typical marginal erosions have poorly defined edges without a sclerotic rim and sometimes may be seen only on oblique or magnification projections. Destruction of articular cartilage causes narrowing of the joint space. The laying down of bony trabeculae across a narrow joint space may completely obliterate the joint cavity and produce solid bony ankylosis, which most frequently involves the bones of the wrist (see Figure 4-13).

Ligamentous involvement produces a variety of contractures and subluxations causing the common ulnar deviation of the hands (see Figure 4-13). In the cervical spine, rheumatoid arthritis characteristically produces atlantoaxial subluxation (Figure 4-15), an increased distance between the anterior border of the odontoid and the superior border of the anterior arch of the atlas (normally less than 2.5 mm), which results from weakening of the transverse ligaments from synovial inflammation. The synovial inflammation appears as a soft tissue mass that causes a narrowing of the atlantoaxial articulation on CT images. CT also demonstrates associated erosion of the odontoid (in about two thirds of patients).

Rheumatoid nodules are soft tissue masses that usually appear over the extensor surfaces on the ulnar aspect of the wrist or the olecranon but occasionally are seen over other body prominences, tendons, or pressure points. These characteristic nodules, which develop in about 20% of patients with rheumatoid arthritis and do not occur in other diseases, aid in making the diagnosis.

Rheumatoid Variants: Ankylosing Spondylitis, Reiter’s Syndrome, and Psoriatic Arthritis

Radiographic Appearance of Ankylosing Spondylitis

Ankylosing spondylitis almost always begins in the sacroiliac joints, causing bilateral and usually symmetric involvement. Blurring of the articular margins and patchy sclerosis generally progress to narrowing of the joint space and may lead to complete fibrous and bony ankylosis (Figure 4-16). The disease typically progresses from the lumbar spine upward.

Ossification in the paravertebral tissues and longitudinal spinal ligaments (poker spine) combines with extensive lateral bony bridges (syndesmophytes) between vertebral bodies to produce the characteristic “bamboo spine” of advanced disease (Figure 4-17; see Figure 4-16). Limitation of activity leads to generalized skeletal osteoporosis and a tendency to fracture in response to the stress of minor trauma (Figure 4-18). CT demonstrates both the fusion due to intraarticular and ligamentous ossification and any spinal stenosis caused by the displacement of the fractures.

Radiographic Appearance of Reiter’s Syndrome

Reiter’s syndrome (reactive arthritis) is characterized by arthritis, urethritis, and conjunctivitis. It primarily affects young adult men and appears to occur after certain types of venereal or gastrointestinal infections. Reiter’s syndrome most frequently involves the sacroiliac joints, heel, and toes (Figure 4-19). Unlike in ankylosing spondylitis, the sacroiliac involvement here is usually bilateral but asymmetric, and Reiter’s syndrome tends to cause only minimal changes in the spine.

Although the radiographic changes in peripheral joints often mimic rheumatoid arthritis, Reiter’s syndrome tends to be asymmetric and primarily involves the feet rather than the hands (Figure 4-20).

Radiographic Appearance of Psoriatic Arthritis

Psoriatic arthritis refers to a rheumatoid arthritis–like destructive process involving peripheral joints that develops in patients with typical skin changes of psoriasis (Figure 4-21). Unlike rheumatoid arthritis, psoriatic arthritis predominantly involves the distal rather than the proximal interphalangeal joints of the hands and feet, produces asymmetric rather than symmetric destruction, and causes little or no periarticular osteoporosis.

Characteristic findings include bony ankylosis of the interphalangeal joints of the hands and feet and resorption of the terminal tufts of the distal phalanges (Figure 4-22). Characteristics common to both Reiter’s syndrome and psoriatic arthritis include erosions and hypertrophic changes occurring in the origin and insertion of the tendons and ligaments.

Osteoarthritis (Degenerative Joint Disease)

Osteoarthritis is an extremely common generalized disorder characterized pathologically by loss of joint cartilage and reactive new bone formation. Part of the wear and tear of the aging process, degenerative joint disease tends to affect predominantly the weight-bearing joints (spine, hip, knee, ankle) and the interphalangeal joints of the fingers. A secondary form of degenerative joint disease may develop in a joint that has been repeatedly traumatized or subjected to abnormal stresses because of orthopedic deformities, or it may be a result of a septic or inflammatory arthritis that destroys cartilage.

Radiographic Appearance

The earliest radiographic findings in degenerative joint disease are narrowing of the joint space, caused by thinning of the articular cartilage, and development of small bony spurs (osteophytes) along the margins of the articular edges of the bones. In contrast to the smooth, even narrowing of the joint space in rheumatoid arthritis, the joint space narrowing in degenerative joint disease is irregular and more pronounced in that part of the joint where weight-bearing stress is greatest and where degeneration of the articular cartilage is most noticeable. The articular ends of the bones become increasingly dense (periarticular sclerosis). Erosion of the articular cortex may produce typical irregular, cystlike lesions with sclerotic margins in the subchondral bone near the joint. Calcific or ossified loose bodies may develop, especially at the knee. With advanced disease, relaxation of the joint capsule and other ligamentous structures may lead to subluxation. Local osteoporosis does not occur unless pain causes prolonged disuse of the joint.

In the fingers, degenerative joint disease involves primarily the distal interphalangeal joints (Figure 4-23). Marginal spurs produce well-defined bony protuberances that appear clinically as the palpable and visible knobby thickening of Heberden’s nodes. In the hip, the most prominent finding is asymmetric narrowing of the joint space that involves predominantly the superior and lateral aspects of the joint, where the greatest stress of weight bearing exists (Figure 4-24). Joint space narrowing is also asymmetric in the knee, where it predominantly involves the medial femorotibial compartment (Figure 4-25).

Infectious Arthritis

Pyogenic (pus-forming) organisms may gain entry into a joint by the hematogenous route, by direct extension from an adjacent focus of osteomyelitis, or from trauma to the joint (e.g., after surgery). The onset of bacterial arthritis usually occurs abruptly with a high fever, shaking chills, and one or a few severely tender and swollen joints. The most common type today is a migratory arthritis from Lyme disease.

Radiographic Appearance

Soft tissue swelling is the first radiographic sign of acute bacterial arthritis. In children, fluid distention of the joint capsule may cause widening of the joint space and actual subluxation, especially about the hip and shoulder. Periarticular edema displaces or obliterates adjacent tissue fat planes (Figure 4-26A). Rapid destruction of articular cartilage causes joint space narrowing early in the course of the disease. The earliest bone changes, which tend to appear 8 to 10 days after the onset of symptoms, are small focal erosions in the articular cortex. Because of the delay in bone changes, detection of the characteristic soft tissue abnormalities is essential for early diagnosis. Severe, untreated infections cause extensive destruction and a loss of the entire cortical outline (see Figure 4-26). With healing, sclerotic bone reaction results in an irregular articular surface. If the articular cartilage has been completely destroyed, bony ankylosis usually follows.

Radiographic Appearance of Tuberculous Arthritis

Tuberculous arthritis is a chronic, indolent (organic) infection that has an insidious (gradual) onset and a slowly progressive course (Figure 4-27). It usually involves only one joint, and it affects primarily the spine, hips, and knees. Most patients have a focus of tuberculosis elsewhere in the body, most commonly in the lungs.

A distinctive early radiographic feature of tuberculous arthritis is the extensive juxtaarticular (near a joint) osteoporosis that precedes bone destruction—in contrast to bacterial arthritis, in which osteoporosis is a relatively late finding. Joint effusion leads to a nonspecific periarticular soft tissue swelling. Cartilage and bone destruction occur relatively late in the course of tuberculous arthritis and tend to initially involve the periphery of the joint, sparing the maximal weight-bearing surfaces that are destroyed in pyogenic arthritis. Therefore, joint space narrowing occurs late in tuberculous arthritis, in contrast to the early narrowing seen with bacterial infections. As in pyogenic arthritis, the earliest evidence of bone destruction is usually erosion at the margins of the articular ends of bone. With progressive disease, there is ragged destruction of the articular cartilage and subchondral cortex and disorganization of the joint, often with preservation of necrotic fragments of bone (sequestra) that may involve opposing surfaces (“kissing sequestra”).

Treatment of Arthritis

Arthritis therapy should protect affected joints, maintain mobility, and strengthen muscles. For this to occur, lifestyle changes, use of support devices, drugs, and surgery may be necessary. For those with rheumatoid arthritis and osteoarthritis, which make up 90% of all cases diagnosed, rest and exercise are recommended to minimize inflammation and preserve the range of motion. The first-line medications are nonsteroidal antiinflammatory drugs (NSAIDs), which decrease the inflammatory response but do not affect the disease process. Prostaglandin inhibitors, such as aspirin and ibuprofen (salicylates), fall into this category of drugs that reduce the triggering of inflammation. A more aggressive group of drugs, disease-modifying antirheumatic drugs, are used in advanced stages to reduce symptoms. The antimetabolite methotrexate, a cytotoxic drug, tempers cell division in the synovial joint. Invasive surgery involves replacing joints with new artificial joints (Figure 4-28) to increase joint mobility. For infectious arthritis, antibiotics usually eradicate the infection and cure the arthritis. Aspiration may be needed if fluid accumulates in the bursa.


Bursitis refers to an inflammation of the bursae, small fluid-filled sacs located near the joints that reduce the friction caused by movement. Repeated physical activity commonly causes bursitis, but trauma, rheumatoid arthritis, gout, or infection also can cause this inflammation. Bursitis or tenosynovitis is usually not visualized on plain radiographs, but disorders of the bursa and synovium can be seen on ultrasound images (Figure 4-29). Plain radiographic images may exclude other disorders that cause similar symptoms.

Radiographic Appearance

The major radiographic manifestation of bursitis is the deposition of calcification in adjacent tendons, which is a common cause of pain, limitation of motion (frozen joints), and disability about a joint. Calcific tendinitis most commonly involves the shoulder, and calcification may be demonstrated radiographically in about half the patients with persistent pain and disability in the shoulder region (Figure 4-30). However, calcification may also be detected in asymptomatic persons, and severe clinical symptoms may occur without evidence of calcification. Calcific tendinitis appears as amorphous calcium deposits that most frequently occur about the shoulder in the supraspinatus tendon, where they are seen directly above the greater tuberosity of the humerus. The deposits vary greatly in size and shape, from thin curvilinear densities to large calcific masses.

In the acute early stages of bursitis, ultrasonography demonstrates the bursa filled with synovial fluid and having ill-defined margins. During the acute phase of true tendinitis, the thickened tendon has ill-defined margins. Both bursitis and tendinitis may demonstrate increased vascularity on Doppler ultrasound.

Rotator Cuff Tears

The rotator cuff of the shoulder is a musculotendinous structure composed of the teres minor, infraspinatus, supraspinatus, and subscapularis muscles. Rupture of the rotator cuff produces a communication between the shoulder joint and the subacromial bursa that can be demonstrated by arthrography (the injection of contrast material directly into the shoulder joint) (Figure 4-31). Currently, MRI is considered the modality of choice for demonstrating a rotator cuff disorder. The normal rotator cuff appears as a black structure, but tears cause it to have high signal intensity (Figure 4-32). However, ultrasound may be the preferred initial modality to demonstrate the tear of the tendon (Figure 4-33) because of its wider availability and lower cost.

Tears of the Menisci of the Knee

Meniscal tears are a common cause of knee pain. Although occasionally the result of acute trauma, meniscal tears more frequently reflect a degenerative process caused by the chronic trauma inherent in human knee function. In the past, meniscal tears were best demonstrated by arthrography, which is invasive; now, MRI is clearly the imaging modality of choice, as it is noninvasive and has an accuracy of 90% to 98%.

MRI demonstrates a tear as a sharply marginated line of high signal intensity (Figure 4-34) that crosses the normally dark, triangular meniscus. In addition, this modality can show the often-associated tears of the anterior and posterior cruciate ligaments and changes in the underlying bone. Ultrasound may demonstrate tenosynovitis of related tendons, which appears as a thickened synovial sheath (Figure 4-35).

Bacterial Osteomyelitis

Bacterial osteomyelitis is an inflammation of the bone (osteitis) and bone marrow (myelitis) caused by a broad spectrum of infectious (most often gram-positive) organisms that reach bone by hematogenous spread, by extension from an adjacent site of infection, or by direct introduction of organisms (after 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. Patients with acute osteomyelitis experience fever and localized warmth, swelling, and tenderness. In adults, acute hematogenous osteomyelitis primarily occurs in the vertebrae, causing localized back pain and muscle spasm, and it rarely involves the long bones. Although the incidence and severity of osteomyelitis have decreased since the advent of antibiotics, this disease has now become more prevalent as a complication of intravenous drug abuse (in which case, gram-negative organisms are found). In diabetic patients and patients 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 adjacent bones.

Osteomyelitis begins as an abscess of the bone. Pus produced by the acute inflammation spreads down the medullary cavity and outward to the surface. Once the infectious process has reached the outer margin of the bone, it raises the periosteum from the bone and may spread along the surface for a considerable distance.

Because the earliest changes of osteomyelitis are usually not evident on plain radiographic images until about 10 days after the onset of symptoms, radionuclide (technetium Tc-99m) bone scanning is the most valuable imaging modality for the early diagnosis of osteomyelitis. Increased nuclide uptake, reflecting the inflammatory process and increased blood flow, is evident within hours of the onset of symptoms (Figure 4-36).

Radiographic Appearance

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 in skin infections, in which the initial swelling is superficial. The initial bony 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 (Figures 4-37 and 4-38). The more virulent the organism, the larger the area of destruction. Subperiosteal spread of inflammation elevates the periosteum and stimulates the deposition of layers of new bone parallel to the shaft. This results in a layered 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 around them (Figure 4-39). Power Doppler ultrasound demonstrates increased vascularity in the inflammation elevating the periosteum.

Apr 10, 2017 | Posted by in PATHOLOGY & LABORATORY MEDICINE | Comments Off on Skeletal System

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