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).

Box 4-1 5 Basic Functions of Bones

1. Bones serve as the supporting framework of the body.

2. Bones protect the vital organs (e.g., the skull protects the brain, and the rib cage protects the heart and lungs).

3. Bones serve as levers on which muscles can contract and shorten and thus produce movement at a joint.

4. Red bone marrow within certain bones (spinal column, upper humerus, and upper femur in the adult) is the major site of production of blood cells.

5. Bone serves as the major storehouse for calcium salts. The maintenance of a normal level of calcium, which is essential for survival, depends on a balance in the rates of calcium movement between the blood and bones.

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.

Radiographic Appearance

Transitional vertebrae most frequently occur at the lumbosacral junction and contain expanded transverse processes, which may form actual unilateral or bilateral joints with the sacrum (Figure 4-2). When unilateral, this process often leads to degenerative change involving the opposite hip and the intervertebral disk space above it. At the thoracolumbar junction, the first lumbar vertebra may have rudimentary ribs articulating with the transverse processes. The seventh cervical vertebra may also have a rudimentary rib (Figure 4-3).

Figure 4-2 Transitional vertebrae. Expanded transverse process at the lumbosacral junction.

Figure 4-3 Bilateral cervical ribs (arrowheads).

Treatment

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.

Figure 4-4 Spina bifida occulta (arrows).

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.

Figure 4-5 Meningomyelocele. A, Frontal projection of the abdomen shows greatly increased interpedicular distance of the lumbar vertebrae. B, In another patient, lateral projection demonstrates a large soft tissue mass (arrows) situated posterior to the spine. Notice the absence of the posterior elements in the lower lumbar and sacral regions.

Treatment

Prenatal intervention involves the daily supplement of folic acid, which has reduced the number of incidences of spina bifida. The ability to diagnose the fetus allows for fetal intervention, experimental surgery that helps minimize nerve deficits. Spina bifida occulta and meningoceles usually require no treatment. Sometimes a meningocele requires surgical repair, depending on the size and location of the protrusion. A myelomeningocele generally requires surgical repair. When this repair is being completed, a shunt is placed to prevent hydrocephalus.

Osteopetrosis

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.

Radiographic Appearance

Osteopetrosis results in a symmetric, generalized increase in bone density (Figure 4-6). To produce a diagnostic image, the radiographer must increase the exposure factors (milliampere seconds [mAs] and kilovolts peak [kVp]) to compensate for the increase in bone formation (increased attenuation factor). The image may appear blurred because of the structural changes; in some cases, a good image may be difficult to produce.

Figure 4-6 Osteopetrosis. A, Striking sclerosis of the bones of the hand and wrist. B, Generalized increased bone density of the lower spine, pelvis, and hips.

Treatment

Currently, no effective treatment exists for osteopetrosis. Medications designed to increase bone resorption and blood cell production may help control the disease. For the most severe cases bone marrow transplantation is the only way to improve the prognosis of this pathologic disorder. For less severe cases, bone marrow transplants increase the production of blood cells to manage the anemia. Transplantation of osteoclastic precursors may help control the balance of bone formation and resorption.

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).

Figure 4-7 Osteogenesis imperfecta of the adult foot. Demineralization and the lack of bony cortices are demonstrated on anteroposterior and lateral projections.

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.

Figure 4-8 Osteogenesis imperfecta. A, Generalized flattening of vertebral bodies associated with fractures of multiple ribs and long bones in an infant. B, Multiple wormian bones.

Treatment

The aim of treatment is to reduce fractures by using proper safety measures. Because of defective cortices in severe cases, the long bones become less supportive. Therefore in some instances, extendable rods are surgically placed to provide more support, help prevent new fractures from occurring, and prevent long bone bowing (Figure 4-9). Currently, drugs are prescribed to regulate the osteoclastic formation, thus keeping the bone density more normal. As research continues, stem cell transplants may become a viable cure.

Figure 4-9 Osteogenesis imperfecta. Anteroposterior (A) and lateral (B) projections of the lower leg show extension rod placement to strengthen bone and decrease fracture possibility.

Achondroplasia

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.

Radiographic Appearance

Typical radiographic findings include progressive narrowing of the interpedicular distances from above downward, which is the opposite of normal, and scalloping of the posterior margins of the lumbar vertebral bodies (Figure 4-10). The decreased enchondral bone formation may make the long bones appear short and thick with a widened metaphysis (Erlenmeyer flask deformity) (Figure 4-11). CT is beneficial in demonstrating the degree of spinal narrowing caused by spondylosis and the changes in the vertebral column.

Figure 4-10 Achondroplasia. Posterior scalloping of multiple vertebral bodies (arrowheads).

Figure 4-11 Achondroplasia. View of the pelvis demonstrates femoral head deformity caused by decreased endochondral bone formation.

Treatment

Achondroplasia has no cure, and treatments address complications or deformities associated with the disease process. Patients afflicted with it live normal independent and productive lives. With today’s technology, the long bones can be surgically lengthened. Growth hormone treatment for achondroplasia is still considered experimental; however, preliminary reports indicate positive results in increasing bone growth.

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.

Figure 4-12 Hip dysplasia of the right hip in a 2-year-old child. Cleaves (frog-leg) view of the pelvis demonstrates superior and posterior displacement.

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.

Treatment

Treatment depends on the type of femoral head movement: subluxation or dislocation. Children not diagnosed and treated before walking may appear to “waddle like a duck.” Immobilization of the femoral head is the most common treatment. To accomplish this, a harness or pelvic cast is used. Such immobilization allows the acetabulum to continue to form correctly before the infant begins to walk.

Summary of Findings for Congenital/Hereditary Bone Diseases

US, ultrasound.

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).

Figure 4-13 Mutilating rheumatoid arthritis. Severe, bilaterally symmetric destructive changes of the hands and wrists with striking subluxations.

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).

Figure 4-14 Rheumatoid arthritis. Striking periarticular osteoporosis.

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).

Figure 4-15 Subluxation of the atlantoaxial joint in rheumatoid arthritis. A, Routine lateral image of the cervical spine shows a normal relationship between the anterior border of the odontoid process and the superior portion of the anterior arch of the atlas (arrowhead). B, With flexion, there is wide separation between the anterior arch of atlas (solid arrow) and the odontoid (open arrow).

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.

Figure 4-16 Ankylosing spondylitis. Bilateral, symmetric obliteration of the sacroiliac joints and “bamboo spine.”

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.

Figure 4-17 Lumbar spine. Severe vertebral fusion illustrates “bamboo spine.”

Figure 4-18 Ankylosing spondylitis. Oblique fracture of the midcervical spine with anterior dislocation of the superior segment is seen in a patient who fell while dancing and struck his head. Fracture extends through the lateral mass and lamina.

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.

Figure 4-19 Reiter’s syndrome. Striking bony erosion (arrows) at insertion of the Achilles tendon on the posterosuperior margin of calcaneus.

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).

Figure 4-20 Reiter’s syndrome. Erosive changes about the metatarsophalangeal joint of the fifth digit. Erosions involve juxtaarticular region, leaving articular cortex intact.

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.

Figure 4-21 Psoriatic arthritis. Bizarre pattern of asymmetric bone destruction, subluxation, and ankylosis. Notice the particularly severe pencil-in-cup deformity of the third proximal interphalangeal joint, and the bony ankylosis involving the wrist and the phalanges of the second and fifth digits.

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.

Figure 4-22 Psoriatic arthritis. Severe mutilating arthritis of the foot and ankle. There is extreme pencil-like destruction of the metatarsals and phalanges, with ankylosis of almost all tarsal joints.

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).

Figure 4-23 Osteoarthritis of fingers. Note narrowing of the interphalangeal joints with spurring and erosions.

Figure 4-24 Osteoarthritis of the hip.

Figure 4-25 Osteoarthritis of the knee.

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.

Figure 4-26 Acute staphylococcal arthritis. A, Several days after instrumentation of the shoulder for joint pain, there is separation of the humeral head from the glenoid fossa caused by fluid in the joint space. B, Six weeks later, pronounced cartilage and bone destruction are evident, with sclerosis on both sides of the glenohumeral joint. C, Septic arthritis. On a radionuclide bone scan, a focal area of increased activity in the right shoulder correlates with the clinical history of septic arthritis.

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.

Figure 4-27 Tuberculous arthritis of the elbow with complete destruction of the joint space. A large chronic granulomatous mass can be seen in the antecubital region.

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.

Figure 4-28 Rheumatoid arthritis. A, This posteroanterior image of the hand demonstrates dislocation and joint destruction of the second through fifth metacarpophalangeal joints. B, Postoperative image, with digits fully extended, illustrates 2-5th metacarpalphalangeal joint implants.

Bursitis

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.

Figure 4-29 Bursitis. Transverse scan of the posterior aspect of the elbow shows the thick-walled, fluid-containing olecranon bursa. Power color Doppler imaging shows the bursa’s activity.

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.

Figure 4-30 Calcific tendinitis. Frontal projection of the shoulder demonstrates amorphous calcium deposits (arrows) in the supraspinatus tendon.

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.

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).