Rheumatic Disorders

10.1 Introduction

10.1.1 Common Pathogenic Features

Rheumatic disorders affect primarily the musculoskeletal system, although any organ may be involved.

A large number of disorders are subsumed under the term “rheumatism” but present quite different manifestations and pose different diagnostic and therapeutic challenges. The WHO defines the term “rheumatism” as diseases occurring in the locomotor system, almost always associated with pain and commonly also with restriction of movement.

The four main WHO groups comprise:

1. Inflammatory rheumatic disorders.

2. Degenerative articular and spinal disorders.

3. Soft tissue rheumatic disorders.

4. Metabolic disorders with rheumatic symptoms.

This broad classification of rheumatic diseases is based in part on the various disease causes and in part on organ systems.

We have arranged this chapter on rheumatological disorders according to this classification scheme and shall present the wide variety of associated clinical characteristics and imaging findings that occur with these disorders. This includes inflammatory and degenerative arthropathies, as well as those of the spine and crystal-induced alterations. Osteoporosis is often assigned to the topic of “rheumatism,” but for didactic reasons is dealt with in Chapter 8.1 under the general heading “Metabolic, Hormonal, and Toxic Bone Disorders.”

10.1.2 Radiographic Features of the Peripheral Joints and their Role in Differential Diagnosis

To minimize repetition in the following chapters, fundamental radiographic features will now be presented, together with a brief discussion of differential diagnostic considerations.

Soft Tissue Swelling

Soft tissue swelling is recognized by a change in contour and by displacement or loss of fat planes:

• The characteristic sign of active arthritis is the voluminous, fusiform soft tissue swelling ( Fig. 10.1), which becomes apparent a few days after onset of the arthritis and is therefore the only “early” radiographic sign, typically affecting the hands and, in some patients, also the forefeet.

• In osteoarthritis soft tissue swelling is less pronounced and is usually asymmetric, with a firm and nodular clinical appearance in the fingers and toes. During an acute inflammatory exacerbation (known as “erosive” osteoarthritis; cf. Chapter 10.2) the appearance is that of an “arthritic” soft tissue swelling.

• In periarticular soft tissue inflammation (bursitis, tenosynovitis, fasciitis, abscess, infection) soft tissue swelling is even more asymmetric.

Note

Synovitis: This is an inflammation of the synovial membrane of the joints and tendon sheaths. The finding is nonspecific and most commonly seen in cases of rheumatic diseases, osteoarthritis, and infection as well as after trauma.

Pannus: In rheumatic disorders this term is used synonymously for synovitis, although it truly refers to chronic fibrovascular tissue. Modern literature no longer uses the term.

Effusion: An effusion is a nonspecific phenomenon associated with synovitis.

Juxta-articular Loss of Bone Mineral Density

Juxta-articular, heterogeneous, patchy or even bandlike demineralization develops; the cancellous bone loses its “sharpness,” the number of trabeculae is reduced. Those isolated trabeculae that remain therefore appear accentuated ( Fig. 10.2).

• In the context of arthritis, this is referred to as a “collateral phenomenon.” It is the arthritis that triggers this process of bone resorption (via neurocirculatory reflexes, increased perfusion, and activated osteoclasts). Initially, this is not related to the direct bone destruction by joint inflammation, which does not become radiographically evident until some weeks after the onset of the arthritis. These collateral phenomena are only detectable during an acute inflammatory flare and are completely reversible.

• Morphologically, disuse osteoporosis is indistinguishable from demineralization related to long-standing arthritis (pain-related immobilization) or prior trauma.

• The osteoporosis of CRPS (complex regional pain syndrome; Sudeck’s dystrophy), like soft tissue swelling, is a diffuse phenomenon and is not confined to the joints. It usually involves several bones of one limb.

• In self-limiting transient osteoporosis only one bone (most commonly the proximal femur) and one joint are involved.

• Juxta-articular loss of bone mineral density is not seen in osteoarthritis. Yet osteoarthritis and diffuse senile or disuse osteoporosis may of course be associated with one another.

Loss of the Subchondral Bone Plate

Loss of the subchondral bone plate ( Figs. 10.3 and 10.4) precedes erosion and is regarded as the first direct sign of arthritis. The cause may be either disuse demineralization (as part of a collateral phenomenon) or secondary to pus or synovitis.

• Absence of the subchondral bone plate is a specific sign of arthritis; this is particularly the case when the other parts of the joint contour remain preserved (“partial” loss).

• Loss of the subchondral bone plate is seen in osteoarthritis only where there is more significant destruction.

Fig. 10.1 Rheumatoid arthritis with involvement of the proximal interphalangeal joint.

Fig. 10.2 Juvenile chronic polyarthritis. Juxta-articular, as well as less marked diffuse osteopenia; the patient is 30 years old.

Fig. 10.3 Partial loss of the subchondral bone plate at the site of a developing erosion in a patient with rheumatoid arthritis.

Fig. 10.4 Rheumatoid arthritis. (a) Partial loss of the cortical margin of the radial styloid process. (b) MRI reveals synovitis and associated erosion at the radial styloid process. MRI demonstrates that loss of the bone plate is often caused by an erosion that is not viewed tangentially on standard radiographs. RSP, radial styloid process.

• Systemic demineralization (e.g., in cases of hyperparathyroidism, rickets, osteomalacia) is associated with destruction of the entire subchondral bone plate.

• In transient osteoporosis (transient bone marrow edema), the bone plate is lost, as in arthritis. This finding is usually confined to one joint and the joint space is not narrowed.

Erosion

An erosion is a focal bone defect involving the articular portions of the bone. Seen in profile, it is a defect; looked at end on, it appears as a rounded lucency, simulating a cyst. Depending on the activity of the disease process, the erosion can display a blurred, distinct, or even sclerotic border ( Fig. 10.5). In arthritis, erosions begin at the “bare areas,” i.e., the portions of the bone within the joint capsule that are not covered with articular cartilage. Outside of a joint, inflammatory tenosynovitis may produce superficial defects in adjacent bones. This can be a relatively specific indication of a synovial origin of the disease.

• In osteoarthritis, “pressure erosions” may be seen at the site of maximum loading; the abnormal loading associated with articular destruction can induce bone resorption and subsequently “cyst formation.”

• Erosions and bone destruction associated with gout are very often located “para-articularly,” some distance away from the joint. They can become quite large. Usually—but not always—gouty erosions are demarcated by a fine sclerotic margin.

• Destruction caused by an adjacent tumor presents as a solitary, broad-based bone defect or erosion, without any other joint alterations.

Subchondral Osteolytic Lesions (Geodes, “Signal Cysts”)

These are round (partially confluent) defects in the subarticular regions at the end of a bone ( Fig. 10.6). In arthritic conditions, these are also referred to as “signal cysts.”

• In rheumatoid arthritis they are rarely larger than 1 cm. Marginal sclerosis only appears after treatment or spontaneous healing. The finding must be seen in context with other radiographic features in order for a subchondral cyst to be regarded as a direct sign of arthritis.

• Subchondral cysts in association with osteoarthritis (“detritic cysts”) are usually multiple, are found at the main load-bearing sites, may be larger than 1 cm, and usually display marginal sclerosis.

• Intraosseous gouty tophi are characterized by a variety of features: punched-out defects may be seen alone or together with longitudinal oval osteolytic areas and may appear septated or demonstrate a trabecular pattern.

• In pigmented villonodular synovitis (PVNS), the osteolytic areas develop at the margins of the joint. There is nearly always marginal sclerosis but joint space narrowing and juxta-articular osteoporosis are absent (Chapter 4.6.5).

• A connection with the joint space is proof of an intraosseous ganglion, although this may not always be observable (Chapter 4.6.3).

Joint Space Narrowing

Joint space narrowing ( Fig. 10.7) is an indication of cartilage destruction.

• In arthritis narrowing is usually harmonic and symmetrical and involves the entire joint space, or large portions of it.

• Asymmetrical joint space narrowing, in particular the main weight-bearing area, is characteristic of osteoarthritis.

• Joint space narrowing also occurs in CPPD (calcium pyrophosphate deposition disease). Associated cartilage calcification (chondrocalcinosis) may be seen and can assist in arriving at the correct diagnosis.

Subchondral Sclerosis

This is reactive osteosclerosis.

• Subchondral sclerosis is unusual in active arthritis; however, it is found after reparative intervals in chronic forms of arthritis and following drug therapy as well as in cases where secondary osteoarthritis has developed.

• Subchondral sclerosis is a characteristic sign of osteoarthritis (Chapter 10.2).

Periarticular Periosteal Reaction

This is found at an epimetaphyseal location, but can also extend to the diaphysis, especially in small tubular bones.

• Periosteal new bone formation is often associated with spondylarthritis (e.g., psoriatic arthritis).

• A lamellated periosteal reaction ( Fig. 10.8) occurs in active, acute inflammatory joint processes, but may persist after healing.

• Chronic inflammatory arthropathies tend to develop solid, sometimes undulating, periosteal reaction ( Figs. 10.9 and 10.10).

DD. The differential diagnosis includes osteoarthritis, posttraumatic alterations, tumors, hematologic disorders, forms of vasculitis, and chronic venous insufficiency.

Fig. 10.5 Radiographic morphology of erosions over time. (a) Fresh erosion in a patient with gouty arthropathy with preexisting osteoarthritis. (b) Erosion in the process of healing in a patient with rheumatoid arthritis. (c) Healed erosion in a patient with psoriatic arthropathy.

Fig. 10.6 Signal cyst in a patient with rheumatoid arthritis.

Fig. 10.7 Comparison of the characteristic radiographic features of degenerative and inflammatory arthropathies.

Fig. 10.8 Periosteal reaction in a patient with spondylarthritis. Although this is a lamella, its thickness is an indication of a chronic process.

Fig. 10.9 Periosteal reaction in a patient with psoriatic arthropathy.

Fig. 10.10 Reactive bone production and periosteal reaction in a patient with psoriasis.

Reactive Bone Formation

Reactive bone formation may produce osteophytes, bony protuberances, and ossification at tendon insertions. The shape and distribution of these often provide clues for differential diagnosis. Some types of arthritis, such as psoriatic arthritis, tend to develop osseous proliferation in the region of the capsule and at tendon insertions. Blurred, “cotton wool–like” margins and rather faint radiopacity are characteristic.

• Osteophytes are typical for osteoarthritis. They originate typically at the margin between cartilage and bone (Chapter 10.2) and have a narrow cortex.

• “Protuberances” are small bony proliferations at the jointcapsule insertion or in a nearby extra-articular location of fingers and toes ( Figs. 10.11 and 10.12a). They are typical for psoriatic arthritis and in rare cases are also found in Reiter’s syndrome.

• Irregularly formed insertional ossification of joint capsule, tendons, and ligaments during fibro-osteotic processes (see Figs. 10.10 and 10.12b) are commonly found in spondylarthritis, yet practically never in rheumatoid arthritis.

Mutilation (Severe Destruction and Disfiguration) and Ankylosis

Erosions may progress to mutilations or even end in ankylosis with fibrous or bony bridging.

• Some types of arthritis tend to develop mutilations very early (e.g., psoriatic arthritis; Fig. 10.13). Otherwise, mutilations and ankylosis are usually a sign of advanced stages of a disease ( Fig. 10.14).

• In osteoarthritis ankylosis is only seen after long-standing disease, and then predominantly in the sacroiliac joints. Ankylosis is also a feature of spondylarthritis and chronic juvenile arthritis.

10.1.3 Radiographic Features of the Spine and Sacroiliac Joints and Their Differential Diagnosis

Vertebral Osteophytes

Vertebral osteophytes are commonly found at the vertebral margins of a degenerating intervertebral disk ( Fig. 10.15).

• A distinction is made between a submarginal osteophyte, which arises, initially horizontally, at the insertion of the anterior longitudinal ligament a few millimeters from the intervertebral disk, to later curve in a superior or inferior direction, and a marginal osteophyte, which continues to grow horizontally into the superior or inferior end plate.

• Osteophytes of two adjacent vertebrae can fuse together to form a bony bridge within the motion segment.

• Exuberant osteophyte formation is found primarily in cases of DISH (diffuse idiopathic skeletal hyperostosis; Chapter 10.4) in the form of spondylosis hyperostotica.

Syndesmophytes

A syndesmophyte refers to ossification of the outer fibers of the anulus fibrosus, caused by a progressive inflammatory process associated with all forms of spondylarthritis (Chapter 10.6). Initially syndesmophytes are thin vertical outgrowths along the contour of the juvenile disk; at a later stage they take on a more concave course ( Fig. 10.16). Eventually they thicken and incorporate the anterior longitudinal ligament. The end result of this polysegmental process is the “bamboo spine” ( Fig. 10.17).

Caution

Sometimes syndesmophytes are asymmetric in their distribution; they are thicker and not exactly vertical but rather more curved or comma-shaped and are separated from the edge of the vertebral body. They are commonly called nonmarginal syndesmophytes ( Fig. 10.18). These forms are more often found with psoriasis or reactive arthritis.

Fig. 10.11 Bony protuberances in psoriatic arthritis.

Fig. 10.12 Psoriatic arthropathy. (a) Bony changes at the distal interphalangeal joint of the fourth toe. (b) Bone production at the base of the fifth metatarsal at the peroneus brevis tendon insertion.

Fig. 10.13 Mutilation of the metatarsophalangeal joints of the second to fourth rays in psoriatic arthropathy. The proximal interphalangeal joints and the interphalangeal joint of the big toe are ankylosed.

Fig. 10.14 Ankylosis of the carpus producing an os carpale, a late result of rheumatoid arthritis.

Fig. 10.15 Osteophytes.

Fig. 10.16 Syndesmophyte in a patient with ankylosing spondylitis. Additional finding of smaller osteophytes.

Fig. 10.17 Bamboo spine in ankylosing spondylitis.

Fig. 10.18 Singular, and thus actually nonspecific, clearly asymmetric nonmarginal syndesmophyte. The patient had a known history of psoriatic spondylarthropathy.

Schmorl’s Nodes

A “Schmorl’s node” is a herniation of disk tissue through the vertebral end plate and into the cancellous bone of the vertebral body. Older Schmorl’s nodes usually demonstrate prominent marginal sclerosis ( Figs. 10.19 and 10.20).

• In Scheuermann’s disease (Chapter 7.4.1) these herniations are commonly found in the thoracic spine, characteristically in the anterior third of the vertebral body. If this intratrabecular herniation occurs in a still-growing spine, compensatory hyperostosis of the opposing end plate may develop (Edgren–Vaino sign; Figs. 10.21 and 10.22).

• Schmorl’s nodes must be differentiated from normal variants of the vertebral end plates that are of no clinical significance and represent notochord remnants. These usually focal depressions are typically located in the posterior third, usually in two opposing end plates, and have a linear configuration over several segments of the thoracic spine or the thoracolumbar junction (see Fig. 10.21).

• Similarly, in the lower lumbar vertebrae, broad-based, paramedian depressions of the end plates are located more posteriorly, creating the Cupid’s bow sign on the AP view, but are of no clinical significance ( Fig. 10.23).

Vacuum Phenomenon

Sometimes negative pressure forces nitrogen gas bubbles to escape from the degenerative disk ( Fig. 10.24).

• Such a vacuum phenomenon can also develop in osteoporotic fractures, especially when bone healing is delayed. This finding argues against a pathologic fracture due to underlying tumor.

• Accumulation of gas in the facet joints is a sign of joint degeneration—as in the sacroiliac joints.

Baastrup’s Sign

This often painful condition results from contact between the spinous processes related to an excessive lordosis of the lumbar spine. It is further compounded by degenerative loss of disk height. Increased sclerosis and cysts as well as new bone formation may develop in the contact zone ( Fig. 10.25). Occasionally, interspinal synovial pseudoarticulations or bursae develop.

Romanus Lesion (Anterior Spondylitis)

This refers to focal inflammation of the anterior or posterior borders of the vertebral body and is predominantly found in the thoracic spine. It occurs in spondylarthritis, especially in ankylosing spondylitis. It may also be associated with small, focal areas of osseous destruction ( Fig. 10.26). Sclerosis appears later, producing the “shiny corner” sign ( Fig. 10.27) due to its typical triangular shape on radiographs and CT. It should be noted that the term “Romanus lesion” was coined at a time when only radiographs were available, for which reason a classic Romanus lesion is characterized by the presence of sclerosis. However, MRI has shown that anterior inflammation can also develop, as evidenced by focal edemalike signal intensity at these sites, even without any sign of destruction. With time, this inflammation heals and leads to fat conversion ( Fig. 10.28; see also Fig. 10.26). Evidence of more than five such fatty Romanus lesions is highly specific for ankylosing spondylitis.

Fig. 10.19 Multisegmental Schmorl’s nodes in the inferior end plates. The prominent marginal sclerosis is an indication of a chronic condition.

Fig. 10.20 Schmorl’s nodes in two vertebrae. There is also chronic depression of the superior end plate of the lower vertebral body (sclerotic end plate, no vertebral body edema).

Fig. 10.21 Notochordal remnants. Additional Schmorl’s node in the superior end plate of L4 with compensatory bony protrusion of the opposing inferior end plate (Edgren–Vaino sign).

Fig. 10.22 Multiple Schmorl’s nodes. The relatively anterior site of the lesions and the obvious Edgren–Vaino sign (arrow) argue against a notochordal remnant.

Fig. 10.23 Cupid’s bow sign. (a) Broad-based depressions (arrows) of the posterior end plates. (b) Cupid’s bow sign is evident on the coronal view.

Fig. 10.24 Vacuum phenomenon. Gas within multiple intervertebral disks. Note also the compression fracture with intravertebral gas; this is supportive of an osteoporotic fracture.

Fig. 10.26 Ankylosing spondylitis. (a) Multisegmental hyperintense changes along the end plates. (b) The T1W view allows for differentiation between fat and edemalike inflammatory bone marrow changes. (c) The acute inflammatory lesions enhance with contrast.

Fig. 10.25 Baastrup’s disease (arrows). Note also the vacuum phenomenon in two intervertebral disk spaces.

Fig. 10.27 Romanus lesion. Typical postinflammatory triangular regions of sclerosis (shiny corner sign) with multilevel syndesmophytes.

Fig. 10.28 Multiple fatty Romanus lesions, related to multilevel anterior spondylitis.

Andersson Lesion (Inflammatory Type)

Inflammatory lesions can occur with spondylarthritis that destroy the osteochondral junction between vertebral body and intervertebral disk (see Fig. 10.26). A characteristic feature is circumscribed central or paracentral destruction, which is later usually surrounded by an extensive perilesional sclerotic zone.

• Degenerative types of osteochondrosis look similar. Bandlike subchondral sclerosis is more suggestive of osteochondrosis.

• An irregular pattern of bone destruction without sclerosis is found in acute bacterial spondylodiskitis.

Andersson Lesion (Noninflammatory, Pseudarthrosis Type)

This is a pseudarthrosis secondary to a transdiskal or transvertebral fatigue fracture with involvement of the posterior vertebral elements in a largely stiff spine (as found in the late stages of ankylosing spondylitis; Fig. 10.29).

Much more common, however, is an acute fracture of a spinal column that has developed in a rigid spine secondarily to ankylosing spondylitis, even in the absence of a significant injury. It is usually found at the cervicothoracic or thoracolumbar junction, is almost always unstable, and involves all three columns. This is not an Andersson lesion, however.

Vertebral Body Enlargement and Deformity

Vertebral body deformity and enlargement are typically seen in Paget’s disease and vertebral hemangioma ( Fig. 10.30; also Chapter 4.3.7). It must be differentiated from the pure deformity of vertebral body squaring and barrel-shaped vertebrae ( Fig. W10.1), which develop secondary to inflammatory destruction of the vertebral margins and bone apposition found in advanced spondylarthritis. Compression fractures can increase the sagittal or transversal diameter of a vertebra, but usually result in a significant loss of height as well.

Block Vertebrae

The expression “block vertebrae” refers to osseous fusion of two or more adjacent vertebrae. Partial block vertebra formation occurs when the vertebrae are fused across a portion of the disk or, for example, only via the facet joints.

• Acquired postinflammatory or degenerative block vertebrae characteristically display bone apposition (bridging osteophytes) at the site of fusion ( Fig. 10.31).

• Congenital block vertebrae often demonstrate a tapered appearance at the level of the fusion and are not associated with bridging osteophytes ( Figs. 10.32 and 10.33).

Sacroiliitis

Sacroiliitis (bi- or unilateral; Figs. 10.34 and 10.35) is the key symptom of spondylarthritis. A bacterial origin should also be included in the differential diagnosis when there is evidence of unilateral sacroiliitis with significant marginal destruction (initially without sclerosis).

The radiographic appearance of sacroiliitis includes the following signs:

• Thinning of the subchondral cortex.

• Erosions (more severe on the iliac than on the sacral side).

• Irregular pseudo-widening of the joint space secondary to confluent erosions, preceded by joint-space narrowing.

• Irregular subchondral sclerosis.

• Osseous bridging and later bony ankylosis.

• Capsular and ligamentous ossification later in the course.

Fig. 10.29 Andersson lesion (pseudarthrosis type) in ankylosing spondylitis.

Fig. 10.30 Vertebral enlargement in a patient with “vertebral hemangioma.” Note the loss of concavity of its anterior margin.

Fig. 10.31 Acquired, degenerative blockvertebra formation. This finding is indistinguishable from a postinflammatory ankylosis, but the patient was never known to have suffered from a local or systemic inflammatory disease.

Fig. 10.32 Congenital block vertebrae covering three vertebrae and two disk spaces. Note the degeneration of the adjacent segments superior and inferior to the block vertebrae as a result of the increased movement and stresses in these segments.

Fig. 10.33 Congenital, partial block vertebrae formation with fusion of the facet joints. Thick-slice MPR obtained from one CT dataset.

Fig. 10.34 Sacroiliitis. Multiple abnormalities of the sacroiliac joints including irregular subchondral sclerosis, destruction, and areas of bridging ossification, especially in the right lower third of the joint.

Fig. 10.35 Bilateral sacroiliitis on MRI. Increased intra- and periarticular contrast enhancement, as well as irregularity of the joint spaces.

10.2 Osteoarthritis of the Peripheral Joints

10.2.1 Basic Principles of Imaging Techniques

The term “osteoarthritis” refers to various “degenerative” joint diseases that are characterized by progressive articular dysfunction. A distinction is made between primary (idiopathic) and secondary osteoarthritis. Although osteoarthritis has so far been classified as a noninflammatory arthropathy, many authors are now asserting that intermittent episodes of inflammation strongly affect the disease course and clinical presentation. For this reason osteoarthritis, as a slowly progressive chronic arthropathy, will be included in the rheumatological section.

Pathology. For purposes of clinical classification, idiopathic and secondary types of osteoarthritis should be distinguished. From a pathophysiological view, however, this concept must be called into question. Today it is assumed that a trigger causes early changes to the joint and subsequently initiates catabolic as well as reparative mechanisms. Such triggers include, for example, direct or indirect injury to the joint, joint inflammation, chronic overuse, and other systemic factors.

The concept of a primary cartilage disease has been abandoned, given that multiple structures within a joint are involved in the disease process. In particular, a close link between articular cartilage and subchondral bone has been recognized. The term “osteoarthritis” therefore appears appropriate. Nevertheless, osteoarthritis is phenotypically characterized by a progressive loss of cartilage.

Multiple risk factors have been defined over the years that would suggest progressive articular damage. Joint-related factors include joint malalignment (knee, hip), impingement, congenital or hereditary malformations (e.g., dysplasia of the hip), intrinsic degeneration, such as meniscal and labral damage, focal cartilage defects, ligamentous laxity, and subchondral bone marrow lesions (as detected by MRI). Systemic factors include obesity, genetic predisposition, nutrition (e.g., vitamin D deficiency), metabolic diseases (e.g., gout), age, and sex. A diagnosis of osteoarthritis is based on both radiographic and clinical features. The radiographic diagnosis of osteoarthritis is based on the presence of osteophytes (see also Kellgren–Lawrence classification); the clinical diagnosis rests on a combination of symptoms listed below under “Clinical presentation.” There is currently no universally accepted MRI-based definition of osteoarthritis.

Clinical presentation. Pain with weight bearing, limitation of motion, crepitation, and morning stiffness are primary symptoms. Osteoarthritis is characterized by intermittent episodes of increased pain (“flares”) that are associated with acute “inflammatory” changes, such as joint effusion and synovitis. The appearance, or increase in size, of bone marrow lesions as seen in MRI correlates with the degree of pain. Other typical clinical symptoms of osteoarthritis include joint malalignment, deformity, instability, and muscular weakness.

A discrepancy between the degree of radiographic abnormalities within the joint and clinical symptoms has long been recognized.

Commonly used (but not exactly defined) clinical terms

• “Activated” osteoarthritis, known osteoarthritis with acute, renewed pain. Synovitis, joint effusion, and bone marrow edema usually develop. The cause of the synovitis and pain is usually related to acutely sloughed fragments of articular cartilage and bone, known as detritus.

• Erosive osteoarthritis is characterized by an acute episode of inflammation and radiographic evidence of progressive central erosions, especially in the hands.

Radiography. Technique. Standing (weight-bearing) views of the joints of the lower limbs should be obtained. This is particularly important to assess for associated limb malalignment (“long-leg view”).

Conventional radiography remains the diagnostic standard for osteoarthritis. It serves to establish the diagnosis, to narrow the differential diagnosis, and for follow-up studies to assess the progression of disease. A radiograph is not capable of demonstrating directly the articular cartilage, unless chondrocalcinosis (CPPD) with (secondary) calcification of the hyaline cartilage matrix is present. However, it does allow indirect conclusions to be drawn about cartilage integrity. It should be borne in mind that only more advanced cartilage loss is demonstrated radiographically when there is evidence of joint-space narrowing.

Radiographic signs of osteoarthritis ( Figs. 10.36 and 10.37)

• Osteophytes.

• Joint space narrowing.

• Subchondral sclerosis.

• Subchondral cysts.

• Loose joint bodies.

• Soft tissue swelling and/or effusion.

• Chondrocalcinosis and meniscal calcifications.

• Joint deformity and attrition (increased concavity or flattening of the joint surfaces).

Atlases with illustrative examples can be of great assistance for reporting purposes (e.g., the atlas by Altman and coworkers from 1995 or the revised version from 2007 see References for Chapter 10.2 under “Grading Osteoarthritic Changes”).

The Kellgren–Lawrence classification is used to grade the severity of osteoarthritis; it is assessed from a plain AP radiograph:

• Grade 0: No osteophytes, no joint space narrowing.

• Grade 1: Possible small, marginal osteophyte.

• Grade 2: Definite osteophyte formation.

• Grade 3: Joint-space narrowing.

• Grade 4: Complete loss of the joint space (bone-to-bone contact).

CT. CT is also not capable of displaying cartilage directly but it can reveal radiographic abnormalities at an earlier time. CT can depict subchondral cysts and osteophytes unobscured by overlying structures ( Fig. 10.38) and assist in locating loose joint bodies. CT arthrography is an excellent modality for demonstrating surface alterations involving the articular cartilage surfaces. CT is of particular value for differentiating between changes of osteoarthritis and classical rheumatological disorders (Chapter 10.2.2). This applies in particular to the axial skeleton and to joints with complex anatomy, such as the wrist and tarsus (see also the corresponding text sections in Chapter 10.2.2).

Fig. 10.36 Classic appearance of primarily medial (“varus”) osteoarthritis of the knee.

Fig. 10.37 Markedly advanced osteoarthritis of the shoulder.

Fig. 10.38 Medial tibiofemoral osteoarthritis. Since the CT view is obtained with the patient supine, the actual degree of cartilage loss can only be partially assessed. Additionally, there is a fracture of the tibial plateau.

MRI. Technique. With regard to sequence selection, PDW (echo time 15–25 ms) and intermediate FSE sequences (echo time 35–40 ms) are the clinical standard. These are usually acquired with fat suppression to obtain better contrast between subchondral bone and hyaline cartilage. Without fat suppression, it is not possible to sufficiently capture bone marrow alterations. The earliest alterations to cartilage are recognizable on PDW, intermediate, and T2W FSE sequences as increased intrachondral signal intensity (corresponding to edematous changes) ( Fig. W10.2).

High-resolution 3D-GRE sequences (e.g., FLASH, SPGR, DESS, MEDIC [Multi-Echo Data Image Combination], etc.) may be helpful supplements but have not yet become established in clinical routine. The disadvantages of these gradient sequences are the relatively long acquisition times, susceptibility artifacts, lack of sensitivity for displaying subchondral lesions, and poorer demonstration of focal cartilage defects ( Fig. W10.3). These sequences are primarily used for cartilage segmentation and for 3D-volumetric analysis during research projects.

Contrast-enhanced sequences are sometimes useful for assessing the degree of synovitis, which can be quite pronounced in clinically acute episodes of osteoarthritis ( Fig. W10.4). Subchondral bone marrow lesions may display strong contrast enhancement and cysts (“geodes”) are readily apparent.

The role of MRI in clinical practice is less for arriving at a specific diagnosis than for excluding associated complications such as osteonecrosis or insufficiency fractures; it may be used in some cases for assessing the degree of joint abnormality during preoperative planning (cartilage transplantation).

Findings. Subchondral bone marrow signal. Common findings on MRI of osteoarthritis are subchondral areas of focal increased signal intensity, evident on water-sensitive fat-suppressed sequences (as well as on T1W fat-suppressed sequences after contrast agent application), which are associated with overlying cartilage lesions. The term “bone marrow lesion” has become established for these subchondral areas of high signal.

Cartilage. Many MRI classification systems of cartilage damage use a scale ranging from 0 to 4 in accordance with a classification system used for arthroscopy that is based on the suggestions proposed by Outerbridge (1961) (see References for Chapter 10.2 under “Reviews on Osteoarthritis and Imaging of the Cartilage”). However, these classifications have only limited application to daily clinical practice. Close communication with the referring clinician is imperative. Ideally, the report should describe any cartilage pathology and include at least the following points:

• Anatomical site (e.g., medial trochlea, medial patellar facet, central weight-bearing part of the medial tibia, etc.).

• Surface involvement in two dimensions (in millimeters or centimeters).

• Maximal depth (superficial or full thickness, extending to bone).

Any associated pathologic features relevant for prognosis should also be included ( Figs. 10.39 and 10.40):

• Osteophytes.

• Joint effusion.

• Synovitis (best recognized as an increase in synovial thickness and signal intensity after IV contrast administration).

• Bone marrow lesion (definition above).

• Meniscal pathology, including meniscal extrusion.

• Plicae.

• Patellar malalignment.

• Subchondral cysts.

• Ligament pathology.

NUC. Technetium 99 m multiphase bone scan demonstrates areas of focally increased perfusion (blood pool phase; Fig. 10.41) and increased bone turnover (osseous late phase). Bone marrow lesions detected on MRI display increased uptake on bone scans and a significantly increased carbohydrate turnover on PET scanning.

DD. The large group of arthritic conditions—especially psoriatic arthritis, infectious arthritis, and crystal arthropathies—should be considered in the differential diagnosis, which may be particularly difficult in the presence of erosive osteoarthritis.

• Osteophytes in osteoarthritis are “marginal” in location, in the direct vicinity of the joint space, whereas the new bone production such as is seen in psoriatic arthritis is found in the region of the capsule and tendon insertions.

• Subchondral sclerosis is a characteristic sign of osteoarthritis, and is an unusual finding in other types of arthritis and, if present, is then the result of a reparative process of a chronic disease course.

• Marginal erosions in the immediate vicinity of capsular insertions, as are seen in rheumatoid arthritis, are not found in osteoarthritis.

• Joint-space narrowing is usually located in the region of a loaded part of the joint and is therefore often asymmetric. In the inflammatory arthritides, on the other hand, the narrowing tends to be symmetrical and involves all parts of the joint space.

Chapter 10.1.2 provides a schematic comparison of the most important signs of osteoarthritis in comparison with an inflammatory arthritis.

Significant increased signal intensity or enhancement of the joint capsule and reinforcing ligaments on water-sensitive or postcontrast images can pose differential diagnostic problems. These changes may occur in osteoarthritis as a result of synovial irritation by cartilage and bone detritus and can sometimes mimic the appearance of an inflammatory arthritis. This applies particularly to minor joints (fingers, small vertebral joints) and joints with complex anatomy (wrist, tarsus). Correlation with radiographs or, if need be, CT allows for a confident diagnosis of osteoarthritis by demonstrating subchondral sclerosis, osteophytes, and, in some cases, a vacuum phenomenon.

Fig. 10.39 Advanced tibiofemoral osteoarthritis.

Fig. 10.40 Medial tibiofemoral osteoarthritis.

Fig. 10.41 Bone scan. Abnormal, increased tracer uptake in the medial right knee during the blood pool phase.

Imaging Procedures after Surgical Cartilage Replacement

Several surgical procedures have been developed to address cartilage repair, including microfracture surgery, osteochondral transplantation, and matrix-associated chondrocyte transplantation. Microfracturing of the subchondral bone using fine drilling promotes the formation of fibrous repair cartilage at that site. With osteochondral transplantation, a cylinder of bone and its overlying articular cartilage is harvested from a non–weight-bearing portion of the articular surface and then fitted into the area of cartilage defect. The aim of the procedure is the complete integration of the cylinder to achieve a smooth surface (also referred to as “mosaicplasty”). Chondrocyte transplantation is a two-stage procedure that involves the harvest of cartilage cells that are then cultured in vitro where they multiply. The artificially generated chondrocytes are then introduced into the cartilage defect in a second arthroscopic procedure.

All repair procedures are particularly successful for circumscribed defects and in younger patients (under 50 years of age). Imaging evidence of success is defined as the complete filling of the defect with complete marginal integration and without signs of cartilage hypertrophy ( Fig. 10.42). Although clinical improvement is often achieved, long-term results are still lacking as to whether osteoarthritis can be prevented or delayed by these procedures.

10.2.2 Individual Joints

Hip Joint

Osteoarthritis of the hip is common ( Figs. 10.43–10.45 and Fig. W10.5). Surgical treatment of early and precursor forms of osteoarthritis of the hip is increasingly being advocated, on the basis of the concept of femoroacetabular impingement (FAI) (Chapters 2.11.3 and 2.11.4). Another recognized risk factor for osteoarthritis of the hip is developmental hip dysplasia, which today usually receives early treatment as a result of ultrasound screening in the neonatal period.

The joint space narrowing is primarily of a superolateral location, and less commonly mediocaudal. Periosteal thickening at the femoral neck is referred to as Wiberg’s sign. If the femoral head migrates into the acetabulum with increasing depth of the joint socket, this is referred to as “protrusio acetabuli,” whereas migration of the femoral head in a lateral direction is known as “decentralizing osteoarthritis of the hip.”

DD. The diagnosis of an infectious arthritis is suggested by the presence of a joint effusion, characteristic marked osteopenia, and the rapid progression of osteolytic areas. In bacterial arthritis, the pattern of bone destruction is clearly more irregular than in rheumatic arthritic conditions. The diagnosis can be confirmed with joint aspiration.

Knee Joint

A distinction is made between tibiofemoral and patellofemoral osteoarthritis, with the latter being promoted by anatomical variations of the patellofemoral joint (patellar and trochlear dysplasia, patella alta, lateralization of the patellar tendon insertion at the tibial tubercle).

Characteristic features of osteoarthritis of the knee include the following:

• The patellofemoral and the medial femorotibial joint compartments are most commonly affected ( Figs. 10.46–10.48, Figs. W10.6–W10.8).

• Meniscal injury and extrusion as well as joint malalignment are important risk factors.

• Loose joint bodies are common sequelae of osteoarthritis.

Fig. 10.42 Cartilage repair procedures. (a) and (b) are from follow-up studies after microfracture surgery, and (c) after autologous chondrocyte transplantation. (Courtesy of Dr. W. Fischer, Augsburg, Germany). (a) Six weeks after drilling of the femoral condyle, subchondral bone marrow alterations are clearly visible with regenerative tissue already starting to form. (b) After 12 weeks an almost complete filling of the defect with fibrocartilage regenerate tissue is evident. (c) Complete filling in of an extensive defect in the talar dome.

Fig. 10.43 Signs of osteoarthritis of the hip.

Fig. 10.44 Predominantly medial osteoarthritis of the hip with mild acetabular protrusion.

Fig. 10.45 Osteoarthritis of the hip.

Fig. 10.46 Tibiofemoral and patellofemoral osteoarthritis.

Fig. 10.47 Tibiofemoral osteoarthritis and meniscal calcification.

Fig. 10.48 Subchondral bone marrow alteration in osteoarthritis of the knee. These lesions are often a combination of diffuse “edemalike” changes and cystic components. A concomitant effusion is present.

Ankle Joint and Foot

Osteoarthritis of the ankle is comparatively rare. It is usually related to an earlier injury or other predisposing factors (osteonecrosis, osteochondrosis dissecans, malalignment, extensive sporting activities with recurrent microtrauma, etc.; Figs. 10.49 and W10.9). The talar head often displays a dorsal hooked or beaklike osteophyte in the region of the talonavicular joint or at the junction of the talar body and the talar neck ( Fig. 10.50). The body may be deformed and demonstrate numerous cysts and subchondral sclerosis. A posttraumatic etiology is often recognizable by additional well-corticated ossific fragments at the sites of ligament insertions.

The most common cause of degenerative arthritis in the region of the metatarsal phalangeal and interphalangeal joints is malalignment of the toes. Hallux valgus produces a rotation of the base of the proximal phalanx around its longitudinal axis with an associated lateral shift in the position of the hallux and the sesamoid bones ( Fig. 10.51). Subsequently, osteoarthritis develops between the metatarsal head and the sesamoids, which is not necessarily visible on the dorsoplantar view. Often extreme hyperostoses of the metatarsal heads and “cystoid” bone remodeling are noticeable in later stages. Additional associated soft tissue swelling (bursitis) is not uncommon.

Wrist and Fingers

The distal (Heberden’s osteoarthritis; Figs. 10.52 and 10.53) and proximal interphalangeal joints (Bouchard’s osteoarthritis) are the most common sites of involvement of osteoarthritis; women are significantly more often affected than men.

A genetic component appears to play a larger role in its development in the interphalangeal joints of the fingers than is the case in the lower limbs and the other joints of the upper limbs. The clinically noticeable Heberden and Bouchard nodes are caused by osteophytes covered by a thickened layer of soft tissue and by mucoid soft tissue nodules or cysts. A characteristic feature is also the “gullwing” appearance, mostly seen in erosive osteoarthritis (see Fig. 10.53). This includes osteoarthritis of the carpus, which is usually most prominent along its radial aspect and most commonly involves STT osteoarthritis between scaphoid, trapezium, and trapezoideum ( Fig. 10.54) and basal thumb osteoarthritis of the first carpometacarpal joint ( Fig. 10.55).

Erosive osteoarthritis is of particular significance in the hand. The distribution is irregular and moves from interphalangeal joint to interphalangeal joint in phases, often with a break of several months. The clinical picture resembles that of an inflammatory arthritis with swelling, erythema and severe pain. Women between the ages of 40 and 60 years are affected. Typical radiographic features include marked erosions and cysts in the interphalangeal joints ( Fig. 10.56). The erosions of erosive osteoarthritis have a more central location and combine with marginal osteophytes to produce a characteristic “gullwing” appearance. They may transform into (sometimes large) cysts or become sclerotic. Another rare type of osteoarthritis of the hand is the osteoclastic subtype. Subchondral areas of lucent remodeling of the medullary cavity are characteristic, extending over at least one-third of the length of the affected small tubular bones. Primary locations are the proximal and distal interphalangeal joints. These alterations cannot be regarded as detritic cysts, but are probably the result of an imbalance of local bone metabolism ( Figs. 10.57 and W10.10). This type of osteoarthritis often poses differential diagnostic difficulties. Chronic tophaceous gout, superimposed inflammatory arthritis (secondary rheumatoid arthritis with preexistent osteoarthritis), and osteoarthritis of the hand combined with an additional process such as fibrous dysplasia, intraosseous ganglion, or benign tumor should all be considered.

Risk factors for osteoarthritis of the wrist include positive ulnar variance (congenital or posttraumatically acquired) with subsequent overloading of the triangular fibrocartilage and the lunate (ulnolunate impaction syndrome) and ligamentous lesions (most commonly scapholunate and lunotriquetral). Scaphoid fractures and tears of the scapholunate ligament also often result in subsequent osteoarthritis, the end stages of which are referred to as SNAC and SLAC wrist, respectively (Chapter 2.9.3).

DD. Gouty arthropathy, psoriatic arthritis, superimposed arthritis (secondary rheumatoid arthritis with preexistent osteoarthritis), and infectious arthritis should be excluded. Ankylosis can also develop in the fingers, which is not typical for osteoarthritis.

Fig. 10.49 Posttraumatic osteoarthritis of the ankle. Almost complete loss of the tibiotalar joint space and significant anterior as well as posterior osteophyte formation is evident ( see also Fig. W10.9).

Fig. 10.50 Osteoarthritis of the ankle joint. Lateral radiograph.

Fig. 10.51 Early osteoarthritis of the first metatarsophalangeal joint in the presence of mild hallux valgus.

Fig. 10.52 Heberden’s osteoarthritis of the fingers. Evidence of an osteophyte of the terminal phalanx and asymmetric joint space narrowing.

Fig. 10.53 Heberden’s osteoarthritis of the little finger with deformity of the joint surface.

Fig. 10.54 STT osteoarthritis.

Fig. 10.55 Basal thumb osteoarthritis.

Fig. 10.56 Osteoarthritis of several finger joints with erosive components.

Fig. 10.57 Cystic (“osteoclastic”) osteoarthritis of the hand. See also Fig. W10.10.

Shoulder and Elbow

Osteoarthritis of the acromioclavicular joint is common, albeit usually clinically asymptomatic ( Fig. 10.58). Hypertrophy of the capsule and osteophytes with caudad projection can result in narrowing of the subacromial space and in development of subacromial impingement syndrome.

Osteoarthritis of the glenohumeral joint is less common and is often associated with advanced chronic pathology of the rotator cuff. Osteophytes are commonly located at the inferior humeral head ( Fig. 10.59).

Rapid destructive arthritis of the shoulder (Milwaukee shoulder) is the result of an idiopathic destructive inflammatory process. This disabling disease develops secondarily after phagocytosis of hydroxyapatite crystals. It usually presents bilaterally and primarily affects older women.

Osteoarthritis of the elbow joint is rare. It usually develops as a result of mechanical occupational overuse (mining industry, pneumatic drills) or secondary to injury. Associated loose bodies are commonly found within the joint ( Fig. 10.60).

10.2.3 Treatment of Osteoarthritis

There is still no drug capable of healing osteoarthritis. For this reason, all therapeutic approaches are “symptomatic.” Treatment of osteoarthritis follows a graduated approach, starting with counseling for the patient, physiotherapy, weight reduction, and increased muscle tone, backed up by nonsteroidal analgesics as required (see also OARSI [Osteoarthritis Research Society International] and EULAR [European League Against Rheumatism] guidelines in the References for Chapter 10.2 under “Clinical Diagnosis of Osteoarthritis”). Intra-articular injection of corticosteroids may be beneficial in advanced stages. The topical application of analgesics (e.g., capsaicin) may also be indicated. Intra-articular viscosupplementation is controversial. Nutritional supplementation with chondroitin and glucosamine has no positive effect on cartilage loss. Likewise, arthroscopic “lavage” does not demonstrate a significant advantage compared with placebo. Arthroscopic repair of an unstable meniscal tear or removal of a loose joint body may be beneficial, however. Surgical joint replacement has become an established procedure for treatment of osteoarthritis of the hip and knee joints in particular. There are no hard and fast criteria for surgical intervention, so it becomes an individual decision as to when a potential replacement should be considered.

Fig. 10.58 Early stage of acromioclavicular osteoarthritis.

Fig. 10.59 Advanced osteoarthritis of the shoulder. Large osteophytes at the medial humeral head and in the region of the greater tubercle, diffuse thinning of the glenohumeral cartilage and massive subdeltoid bursitis.

Fig. 10.60 Osteoarthritis of the elbow. In addition to joint space narrowing and osteophyte formation, multiple loose bodies are also evident.

10.3 Degeneration of the Spine

Degenerative disease of the spine is extremely common. Vertebral bodies and intervertebral disks, the facet joints, and the surrounding true synovial joints demonstrate the same degenerative alterations as other joints of the human body. The lower cervical and lumbar spines are subjected to the most weight bearing and motion and are therefore primarily affected. Isolated osteoarthritis of the facet joints (synonym: intervertebral joints) can occur, but is usually related to degenerative disk disease, which also has an effect on the integrity and mechanical properties of the surrounding musculoligamentous structures.

According to Kirkaldy-Willis, a “degenerative cascade” develops in the “three-joint complex” (comprised of the discovertebral complex and the two facet joints), which is associated with three successive stages of dysfunction, instability, and stabilization. This process of degeneration is the result of a complex interaction between an intervertebral disk and the facet joints at that level, whereby the initial event can begin at any of the three sites.

Four basic components are involved in spinal degeneration and they both influence and also augment each other:

• Degenerative disk disease.

• Osteophytes.

• Facet joint osteoarthritis and uncovertebral osteoarthritis.

• Ligamentous and soft tissue changes (ligamentous hypertrophy, ligamentous calcification and ossification; epidural lipomatosis).

10.3.1 Anatomy, Variants, and Information on Imaging and Technique

Anatomy. The spine is embryonically established as a system of multiple motion segments. Each motion segment has a three-joint complex comprising the intervertebral disk between two adjacent vertebral end plates anteriorly and the two facet joints in the posterior column.

The facet joints adopt a sagittal direction at the upper lumbar spine. These change in orientation both cranially and caudally so that in the upper thoracic spine they are oriented in a coronal plane and in the lower lumbar spine the joints are obliquely oriented. On an AP view, therefore, only the intervertebral joints of the upper lumbar spine are viewed in profile, and on a lateral view only those of the upper thoracic spine.

The arrangement of articular processes, neural arches, and spinal processes produces dorsal overlapping of the vertebral bodies, resembling the tiles of a roof and producing an “interlaminar window” and a route of access to the spinal canal that is not covered by bone.

The motion segment is surrounded and supported by ligaments and muscles. Facet joints (and the atlanto-axial joint) are true synovial joints. The intervertebral disk is a cartilaginous joint and consists of the nucleus pulposus, the anulus fibrosus, and the cartilaginous plates ( Fig. 10.61).

Structures sensitive to pain within the motion segment include (apart from the spinal nerve itself), the vertebral body periosteum, the peripheral portion of the anulus fibrosus, the posterior longitudinal ligament, the facet joint capsule, and the surrounding musculoligamentous structures.

Fig. 10.61 Schematic architecture of the intervertebral disk and the intervertebral foramen.

Normal Variants

Congenital variations are common in the spine. The exact labeling of a transitional vertebra at the lumbosacral junction (lumbarized sacral or sacralized lumbar) may only be possible if all vertebrae are counted, starting from C1 downward. If this is not possible, then it is referred to as a “lumbosacral transitional vertebra.”

• Cranial variations: cervical rib, sacralization of the fifth lumbar vertebra.

• Caudal variations: shortened first rib, lumbarization of the first sacral vertebra, rudimentary ribs at L1.

Note

Given that there are seven cervical vertebrae but eight cervical nerve roots, the following applies to the correct anatomical delineation of nerve roots in relation to their neural foramina:

• Cervical: exit of the nerve root above the corresponding vertebra (e.g., C6 nerve root exits in the C5–C6 neuroforamen.

• Thoracic and lumbar: exit of the nerve root below the corresponding vertebra (e.g., L4 nerve root exits in the L4–L5 neuroforamen, Fig. 10.62).

If it is not possible to label a certain vertebral level unequivocally, this must be taken into consideration when annotating the film and explicitly stated in the report since confusion as to an exact level, e.g., for a planned surgical procedure, could have catastrophic consequences.

Technique

Radiography. Images of the spine should, wherever possible, be obtained with the patient standing. Oblique views allow demonstration of the facet joints and the neural foramina. However, it is not possible to optimally demonstrate both of these anatomical structures simultaneously as they have different angles in the sagittal plane ( Fig. 10.63). See Chapter 10.3.8 for functional studies.

CT. CT is better suited to displaying bony changes than is radiography because it is not hampered by overlapping structures. This is particularly important when assessing the facet joints, the neural foramina and the width of the spinal canal. A maximal slice thickness of 2 mm is recommended. The ability of modern CT devices to produce isotropic voxels allows for high-quality reconstructions at all levels. Axial and sagittal reconstructions, in a bone and soft tissue algorithm, are routinely obtained, with the axial reconstructions being acquired parallel to the intervertebral disks in cases of degenerative disease. Exact measurements of osseous features (e.g., spinal canal stenosis) should only be performed using bone windows since measurement errors are too great otherwise.

Myelography/CT Myelography. Currently, myelography is usually combined with CT myelography. Its use is largely confined to the preoperative assessment of patients in whom it is uncertain whether the changes detected on CT or MRI adequately explain their symptoms. This technique is able to more accurately display the degree of root or spinal cord compression ( Fig. 10.64). With disk herniation, therefore, a good filling of the nerve root sheath argues against significant nerve root compression. Myelography without CT can provide important additional information since it allows for a dynamic examination in functional positions (flexion, extension).

Discography. This involves “pressurizing” a disk by injecting radiographic contrast directly into the nucleus pulposus under fluoroscopic or CT guidance and assessing the patient’s pain response to this provocative test. In cases of multilevel disease or in patients with discordant or equivocal findings on sectional imaging studies relative to the clinical examination, discography may identify the exact disk level responsible for the patient’s symptoms. Discography is very rarely performed because it often does not add significant information to the clinical picture and there is some evidence that it may be harmful to the injected disks.

MRI. MRI is the method of choice for detecting disk herniation. With the option of multiplanar reconstructions, CT achieves adequate accuracy in the lumbar spine but it is clearly inferior to MRI in the cervical spine. Calcification within the intervertebral disk or spinal ligaments and bony changes, on the other hand, are the much better assessed with CT. If CT or MRI of the spine is obtained, supplementary radiographs only rarely add any useful information.

MRI is primarily indicated for acute radicular symptoms with neurologic deficits; multiplanar reconstruction CT with or without intrathecal contrast (myelography) is an alternative imaging option when MRI is not available.

Newer MRI techniques are providing additional physiological and functional information, beyond the current anatomical imaging. This has not yet established itself, however, in daily clinical practice.

Fig. 10.62 Anatomical relationship of lumbar nerve roots to their respective neural foramina.

Fig. 10.63 Oblique view of the cervical spine to assess the neural foramina.

10.3.2 Clinical Presentation of the Degenerative Spine

Back pain is the main reason for time lost from work in Western industrialized nations. With low back pain, psychosocial factors should be considered in addition to true somatic abnormalities with regard to pathogenesis and disease prognosis. This also impacts the use of diagnostic investigations and treatment: problem-solving skills, anxiety-related avoidance behavior, passive pain behavior, pessimistic attitudes, social situation, care level, job satisfaction, and entitlements for pension and/or insurance claims all need to be considered.

Degeneration of spinal segments per se is not painful. Initiating factors for pain include irritation associated with dysfunction and segmental hypermobility. On the other hand, degenerative processes based on bony, ligamentous, or discogenic causes can lead to mechanical compromise of neural structures.

The main causes of back pain secondary to degenerative spinal disease are, apart from facet joint osteoarthritis, Modic 1 changes and irritation of the posterior longitudinal ligament, e.g., in association with disk herniation. These usually manifest clinically as load-dependent symptoms. Associated or isolated pain of musculoligamentous origin should not be ignored and needs to be included in differential diagnostic considerations.

Fig. 10.64 CT myelography displaying facet joint osteoarthritis and associated bony spinal canal stenosis.

Disk herniations produce radicular symptoms secondary to nerve root compression, which may also be related to bony narrowing of the neuroforamina or the spinal canal from spondylarthritis or uncovertebral osteoarthritis. Radicular compression results in venous congestion, edema, and ultimately intra- and perineural fibrosis. The segments L3–S1 are by far the most commonly affected, followed by the cervical spine, especially C5–C7. Usually sensory disturbances predominate in the form of radicular pain, dysesthesia, and possibly hypoesthesia. Paralysis is classified clinically according to degrees of strength, ranging from 0/5 (no movement) to 5/5 (normal strength) ( Table W10.1).

Radicular distribution allows a precise clinical determination of level ( Table 10.1 and Fig. 10.65).

A distinction is made between the following types of low back pain with regard to the time course of back pain:

• Acute low back pain: less than 6 weeks.

• Subacute low back pain: more than 6 weeks up to 12 weeks.

• Chronic or chronic recurrent low back pain: longer than 12 weeks.

Furthermore, a distinction should be made between the following types of low back pain:

• Nonspecific low back pain: No clear indications of a specific cause are evident.

• Specific low back pain: A cause is identified (e.g., infection, tumor, osteoporotic fracture, disk herniation, spondylarthrosis, spinal canal stenosis, etc.).

“Red flags” are symptoms or previous illnesses that serve as warning signs for a specific underlying cause, possibly requiring urgent treatment. A radiculopathy, for example, would also be considered a “red flag.”

Caution

Acute conus medullaris and cauda equina syndromes (pain, flaccid paralysis, saddle anesthesia, absent reflexes, sphincter dysfunction, urinary and fecal incontinence, absent pyramidal signs) are a spinal emergency necessitating immediate diagnostic evaluation with imaging. The cause is often a massively prolapsed disk, less commonly a hematoma, a decompensated spinal canal stenosis, or, even less frequently, tumor or infection.

Possible causes of the discrepancy between clinical presentation and radiographic findings are manifold:

• Many morphological alterations, such as osteochondrosis, facet joint osteoarthritis, disk herniations, and sometimes even higher-grade stenosis of the spinal canal and/or the neural foramina, are asymptomatic and therefore clinically irrelevant.

• Nerve root irritation is not only caused by mechanical compression. The causes of radicular pain have not yet been finally clarified; however, local biochemical alterations certainly play a significant role (changes of prostaglandin levels, increased levels of tumor necrosis factor, interleukin, and cyclooxygenase-2, etc.) with cascadelike inflammatory processes.

• Pain radiating, for example, from the facet, sacroiliac, or hip joints can create the impression of nerve root irritation (pseudoradicular pain).

• Anomalous nerve-root exit levels, transitional anomalies, and normal variants of innervation create the wrong clinical impression of a “false” level of the lesion.

Note

In order to avoid treating insignificant additional findings, the radiologist should refrain from giving a clinical opinion regarding the imaging findings without an adequate knowledge of the clinical presentation. A statement as to whether the imaging findings correlate with clinical symptoms presupposes sufficient knowledge regarding the clinical presentation.

10.3.3 Degenerative Disk Disease

Pathology. Disk degeneration results from the combined effects of mechanical and metabolic causes, which are mutually dependent and reinforce each other. Genetic factors also play a role.

The metabolism of the disk is maintained by diffusion, either from the bone marrow of the adjacent vertebral bodies via the subchondral bone lamella and the cartilaginous end plate or from the surrounding blood vessels via the anulus fibrosus. Age-related or degenerative alterations of the vertebral bodies and the cartilaginous end plates can interfere with the nutritive supply of the disks and exacerbate the degenerative changes. If this process emanates from the vertebral bodies, then it usually begins in the periphery where the cartilaginous plates are absent. Reparative tissue extends into the disk and may lead to revascularization of the disk (the disk is partially vascularized only up to the fourth year of life).

In the natural course of aging, the nucleus pulposus loses its capacity to take up water and its inner pressure is reduced. Degenerative damage and deformity of the cartilaginous end plates and leakage of disk material through the end plates (Schmorl’s nodes) result in a loss of intradiscal pressure and increased mechanical loading of the anulus fibrosus and facet joints. Additionally, the reduced perfusion of the end plates also results in impaired metabolism of the intervertebral disk. There is also a positive correlation between impaired arterial circulation due to arteriosclerosis and disk degeneration.

The degenerative process of the disk appears initially as horizontal bands in the nucleus pulposus; water content and integrity of the proteoglycans decrease and disk height is reduced. In later stages disk calcification ( Fig. 10.66) and gaping anular fissures parallel to the superior and inferior end plates may become evident. These cavities then fill with gas (nitrogen; “vacuum phenomenon”). In rare cases degradation of the disk can lead to fusion of two adjacent vertebral bodies.

During the process of degeneration and increased mechanical loading, splitting and fragmentation of the otherwise spirally arranged fibers of the anulus fibrosus occurs. The fibers can only resist the high pressure of the nucleus pulposus (~ 8 bar [800 kilopascals]) to a certain extent; the result is an anular tear ( Figs. 10.67 and 10.68). Recurrent overloading can result in abrupt or slowly developing displacement (herniation) of disk material beyond the margins of the disk space (see Fig. 10.67). This can occur in any direction, but herniations in dorsal and dorsolateral directions are of particular clinical importance since these are the sites where there is a risk of compression of neural structures.

Fig. 10.65 Peripheral dermatomes and key muscles of the most important lumbosacral nerve roots. However, keep in mind that the muscles also receive contributions from other nerves (e.g., the extensor digitorum longus is innervated mainly by L5, but also from L4 and S1).

Only gold members can continue reading. Log In or Register to continue