9    Joints

Introduction and Synopsis

Anatomy of the Synovial Joints

A synovial joint consists of (Fig. 9.1):

• epiphysis (articular end of the bone),
  
• articular cartilage,
  
• joint capsule,
  
• joint fluid.

These entities together with muscles, tendons, and ligaments form an anatomic unit.

The epiphyses of the articulating bones: The trabecule of the epiphyseal and metaphyseal spongiosa commonly follow characteristic courses (trajectories) along lines of compression forces.

The cortex of articulating bones gradually decreases in width toward the joint. Where bone is covered by articular cartilage, the cortex is reduced to a very thin osseous layer that appears radiographically as a delicate line, referred to as the subchondral bone plate. It can be seen free of any superimposed structures along convex articular surfaces.

Articular cartilage: With few exceptions, this consists of hyaline cartilage, which is nourished by diffusion from the joint fluid. In the calcified zone of the cartilage, small vessels arising from the subchondral bone region have been detected as well. Healthy cartilage is strikingly elastic and serves the role of shock absorber. With normal use, a liquid film always remains between the articulating cartilage surfaces.

Joint capsule: By enveloping the joint, the capsule creates an intra-articular and extra-articular space. It inserts at the epiphysis of the articulating bone slightly outside the cartilage cover, creating an intra-articular area not covered by cartilage, referred to as the bare area.

The joint capsule consists of an outer, predominately collagenous connective tissue, the fibrous capsule, and an inner synovial lining, also referred to as the synovial membrane. The synovial lining also covers all of the intra-articular osseous structures except the articular cartilage. It secretes synovial fluid, determines the fluid’s components, and phagocytizes any foreign material, such as organisms or cartilage fragments.

Fig. 9.1 Anatomy of the synovial joint.

Synovial fluid: The synovial fluid is the ‘grease’ of the joint and supplies nutrients to the articular cartilage by diffusion.

Signs of Joint Diseases on Radiography and CT

Radiographic Signs of the Peripheral Joints and Their Role in the Differential Diagnosis

Soft-tissue Swelling (Fig. 9.2)

Soft-tissue swelling is recognized by an altered silhouette and by displaced or obliterated fat planes.

• The characteristic sign of active arthritis is the voluminous fusiform soft-tissue swelling, often with a bulged and indistinctly outlined joint capsule. Under favorable circumstances, it might become visible only several days after the onset of the arthritis and is then the only radiographic ‘early sign’ (only in the hands).
  
• In osteoarthritis, soft-tissue swelling is less voluminous and becomes rather nodular at the fingers. If it is accompanied by an inflammatory component (active osteoarthritis), an ‘arthritic’ soft-tissue swelling develops.
  
• In periarticular soft-tissue inflammation (bursitis, tenosynovitis, infection), soft-tissue swelling is asymmetric but can still be uniform at the fingers and toes (Fig. 9.2b).

Juxta-articular Osteoporosis (Fig. 9.3)

This indicates juxta-articular bone loss. It appears as heterogeneous to patchy demineralization, indistinct spongiosa texture, and decreased number of trabeculae. These findings have a gradual transition to the variably wide homogeneous band of demineralization involving the opposing articulating end of the bone.

• As part of an arthritis, it is referred to as the ‘collateral phenomenon’. The arthritis induces bone resorption by means of neurocirculatory reflexes, increased perfusion, and activated osteoclasts. This process, which is not visible until weeks after the onset of the inflammation, indicates direct bone destruction.
  
• This is an unusual finding in osteoarthritis.
  
• Disuse osteoporosis is not confined to the juxta-articular areas. Since longstanding arthritis leads to pain-induced immobilization of the joints, these types of osteoporosis frequently overlap.
  
• The osteoporosis of sympathetic reflex dystrophies (in particular with Sudeck disease) is, like the soft-tissue swelling in these conditions, a diffuse phenomenon and not confined to the joints. Elevated inflammatory serum parameters are not associated with these diseases.
  
• Bone marrow edema syndrome involves only one of the bones on each side of the joint (most commonly the femoral head) and is confined to one joint. The diagnosis can be established by MRI and scintigraphy.

Loss of the Subchondral Bone Plate (Fig. 9.4)

Loss of the subchondral bone plate precedes erosions (‘pre-erosion’ according to Dihlmann). The cause can be either a trophic demineralization (from hyperemia) or a direct effect of pus or pannus (‘direct sign’).

• Absence of a subchondral bone plate is a specific sign of arthritis. In particular, this applies whenever the mineral content of the bones is well preserved in the remaining skeletal regions. Partial loss of the joint silhouette is more indicative of arthritis than complete loss, as the latter can also represent a normal variant.
  
• This is observed in osteoarthritis only with extensive destruction.
  
• Systemic demineralization (e.g., hyperparathyroidism, rickets, osteomalacia) is associated with destruction of the subchondral bone plate.
  
• Cell death of osteonecrosis close to the joint causes fractures of the subchondral bone plate.
  
• Bone marrow edema syndrome (‘transient osteoporosis’) causes loss of the subchondral bone plate as in arthritis, but the finding is generally monoarticular, and the joint space is not narrowed.

Erosion (Fig. 9.5, 9.6)

An erosion is a confined osseous defect involving the articulating end of the bone (‘joint socket’). Seen in profile, it is a defect, and seen end on, it appears as a ‘cyst.’ Depending on the activity of the disease process, the erosion can have an indistinct, distinct, or even sclerotic border.

• In arthritis, the erosions begin at the ‘bare areas’ and, consequently, are located in the region of the capsular insertions. If a tenosynovitis is present, superficial defects relatively distant from the joint can appear in the region of the inflammatory tendon sheath. Some locations are a relatively specific indication of a synovial origin of the disease.
  
• In osteoarthritis, the erosions occur primarily centrally as pressure erosions. (The abnormal pressure load due to articular destruction can induce osseous resorption.)
  
• Gouty erosions are often located away from the joint (they are not ‘erosions’ in the true sense of the definition) and can be quite large.

Fig. 9.2 a Arthritis of the metacarpophalangeal joint with localized fusiform soft-tissue swelling. b Soft-tissue infection, however, shows diffuse soft-tissue swelling. Notice the demineralization of the phalanges.

Fig. 9.3 a Juxta-articular osteoporosis in rheumatoid arthritis. For comparison: the osteoporosis in Sudeck disease (b) involves all bones.

Fig. 9.4 Loss of subchondral bone plate in rheumatoid arthritis.

Fig. 9.5 a Acute erosion from rheumatoid disease. b Same erosion with marginal sclerosis formed after methotrexate therapy and, as a result, less distinctly demarcated.

Fig. 9.6 Erosion and its differential diagnosis.

• Destruction caused by an adjacent tumor presents as a solitary, broad erosion without any additional joint changes.

Circumscribed Osteolytic Foci (‘Subchondral Cysts,’ ‘Geodes’) (Fig. 9.7)

These are round, partially confluent defects in the articular ends of the bone. In arthritic conditions, they are also referred to as ‘signal cysts’.

• In rheumatoid arthritis, they are rarely larger than 1 cm. Marginal sclerosis develops only after therapy. To consider a subchondral cyst as a direct sign of arthritis, the finding must be seen in context with other direct signs.
  
• Subchondral cysts in osteoarthritis (‘detritic cyst’) usually are multiple, are located in the load-bearing zone, can be larger than 1 cm, and always have marginal sclerosis.
  
• Sharply demarcated subchondral osteolytic defects are found in metabolic diseases such as amyloidosis or pyrophosphate arthropathy. A fusiform soft-tissue swelling is frequently present. The joint space, however, is of normal width. Intraosseous gouty tophi may have a variety of appearances. Punched-out defects can occur alone or together with ovoid osteolytic lesions, and they can be septated or trabeculated.
  
• In pigmented villonodular synovitis (PVNS), the osteolytic changes arise from the articular margins. They are usually multiple and almost always have sclerotic margins. Joint-space narrowing and juxta-articular osteoporosis are absent (see page 376).
  
• In the intraosseous ganglion, the connection to the joint space is not always visible (see page 374).

Joint-space Narrowing (Fig. 9.8)

This indicates cartilage destruction.

• In arthritis, the narrowing is uniform and involves the entire joint space or large portions of it.
  
• In osteoarthritis, the joint-space narrowing is characteristically confined to a segment of the joint, most severely affecting the weight-bearing zones. This is an early sign of osteoarthritis.
  
• Joint-space narrowing also occurs in chondrocalcinosis. Additional chondral calcifications assist in the differential diagnosis.

Subchondral Sclerosis (Fig. 9.9)

This is a reactive osteosclerosis formed by a coarse, often disorganized framework of lamellar bone.

• It is unusual in arthritis and, if present, is usually observed after reparative intervals in chronic arthritic inflammation.
  
• Subchondral sclerosis is a characteristic sign of osteoarthritis.

Lamellar Periosteal Reaction (Fig. 9.10)

Single or multiple metadiaphyseal lamellar reactions are often present and often occur in the vicinity of the affected joints.

• It is observed close to the joint in some types of arthritis (particularly in seronegative spondylarthritis and juvenile rheumatoid arthritis), probably as a result of a periosteal edema.
  
• Other differential diagnoses are osteoarthritis, tumors, hematologic conditions, chronic venous insufficiency, and post-traumatic conditions.

Reactive Bone Apposition (Fig. 9.11)

Reactive bone apposition occurs as osteophytes and protuberances. The shape and distribution of these are often clues to differential diagnostic considerations.

• Some types of arthritis tend to have a rather pronounced osseous proliferation (e.g., psoriatic arthritis), which must be distinguished from marginal sclerotic transformation of erosions after arrest of the disease process.
  
• Even in early stages of osteoarthritis, osteophytic apposition takes place. This characteristically occurs at the bone-cartilage interface of the weight-bearing parts of the joint.

Mutilation and Ankylosis (Fig. 9.12)

Joint destruction can progress to mutilation and end in ankylosis with fibrous or osseous bridging.

• Some types of arthritis tend to have early mutilation (e.g., psoriatic arthritis). More often, mutilation and ankylosis occur in the later stages of the diseases.
  
• In osteoarthritis, except for the Charcôt joint, they are observed only after longstanding disease.

Fig. 9.7 Subchondral cysts of different sizes. These represent ‘signal cysts’ in both cases: a Psoriatic arthritis, b ‘geode-type’ rheumatoid arthritis.

Fig. 9.8 Concentric (a) and eccentric (b) joint-space narrowing in longstanding juvenile rheumatoid arthritis (a) and osteoarthritis (b).

Fig. 9.9 Subchondral sclerosis indicates degenerative joint disease. a Preserved joint space, very subtle osteophyte formation. b Marked osteoarthritis of the knee.

Fig. 9.10 Widening of the phalanges due to periosteal reaction in psoriatic arthritis.

Fig. 9.11 Osteophytic overgrowth of different degrees at an interphalangeal joint (a) and knee (b).

Fig. 9.12 a, b Mutilation. Typical ‘pencil-in-cup’ type in (b). c Osseous ankylosis of a proximal interphalangeal joint.

Radiographic Signs at Specific Joints

Spine

Anterior spondylitis (Romanus lesion): This represents the focal destruction of the anterior or posterior borders of the vertebral body and is similar to an erosion. The Romanus lesion is an early manifestation of an inflammation affecting the spine (Fig. 9.14). This defect is almost always surrounded by a broad sclerosis, producing a rather typical triangular sclerosis referred to as shiny corner sign (Fig. 9.13). It can occur with or without associated focal destruction.

Squared and rounded vertebra: Inflammatory destruction of the anterior surface of the vertebral body (anterior spondylitis) does not produce the classic Romanus lesion, but instead leads to loss of the anterior vertebral border. This results in squaring of the vertebral body due to flattening of its normally concave anterior surface (more often seen in the lateral than in the AP projection). Postinflammatory squaring can also develop differently; periosteal reaction with or without anterior spondylitis can fill the anterior concavity. Progression of anterior spondylitis causes destruction of the superior and inferior vertebral corner, resulting in a rounded vertebra (Fig. 9.15).

Andersson lesion, type A (inflammatory type): This is an inflammatory reaction with focal destruction of the disk and vertebral body. It is characterized by irregularities along the end plates, usually accompanied by extensive sclerotic zones. Differentiation from mechanically induced osteochondrosis (predilection for L4 – S1) is sometimes difficult.

Andersson lesion, type B (noninflammatory, pseudodegenerative type): This is a pseudarthrosis following a diskovertebral fracture of the demineralized and extensively ossified, stiff axial skeleton (as occurs in ankylosing spondylitis, Fig. 9.119).

Syndesmophytes: These are ossifications of the outer fibers of the anulus fibrosus, caused by a progressive inflammatory process. Initially, they are thin, vertical outgrowths along the contour of the disk. With progression, the syndesmophytes thicken and involve the anterior longitudinal ligament and paravertebral soft tissues. The end result is the ‘bamboo spine’.

Spondylophytes: These are ossifications of the vertebral margins caused by disk degeneration, but might be secondary to an inflammation. The submarginal spondylophyte arises at the insertion of the anterior longitudinal ligament, several millimeters from the diskovertebral junction. Initially, it grows horizontally and then vertically (forming a hook). The marginal osteophyte merges horizontally with the end plate.

In addition to these major types – syndesmophyte secondary to an inflammatory process and spondylophyte secondary to degenerative alterations – numerous intermediate types are encountered.

Parasyndesmophytes are asymmetric ossifications that are thicker than syndesmophytes and not vertically oriented but are curved or commashaped and separated (‘para-’) from the margin of the vertebral body. They occur in three types: steer-horn type; paradiskal elongated, thin type; and paradiskal ossicle.

The term mixed osteophyte is applied by some authorities to an osteophyte constituting a mixture of syndesmophyte and spondylophyte.

Any interpretation of these special types is difficult, and in assigning an etiology one should always consider further radiographic findings (Fig. 9.17).

Block vertebra: This can be a developmental abnormality or the result of a preceding inflammatory process.

Sacro-iliac (SI) Joints

Radiographic signs of sacroiliitis (‘variegated picture’ of Dihlmann, Fig. 9.16):

• thinning of the subchondral bone plate,
  
• erosions (more severe on the iliac side than on the sacral side),
  
• joint-space widening (irregular),
  
• densification,
  
• osseous bridging, later osseous ankylosis,
  
• capsular and ligamentous calcifications.

Fig. 9.13 ‘Shiny corner’ in anterior spondylitis.

Fig. 9.14 MRI of a Romanus lesion. a The T2-weighted SE sequence shows triangular edema at the anterior-superior corner of a vertebral body. Strong enhancement after the administration of contrast medium. b T1-weighted SE sequence.

Fig. 9.15 Squaring and rounding of the vertebral body due to anterior spondylitis.

Fig. 9.16 ‘Variegated picture’ of sacroiliitis.

Fig. 9.17 Comparison of the different ossifications between vertebral bodies. a Syndesmophyte, thin ossification, vertical growth. b Parasyndesmophyte, separated from the margin of the vertebral body. c Parasyndesmophyte of the ‘Steer-horn type.’ d Degenerative spondylophytes.

Sonography

When tendons and muscles are examined, the acoustic anisotropy of the muscular and collagenous fibers must be taken into consideration. Due to the internal orientation of these structures, the echogenicity changes with the angulation of the probe. Differences in echogenicity caused by this effect should not be misinterpreted as lesions (Fig. 9.18).

Any report of sonographic findings should include the following aspects:

Location: Anatomic location and contact with neighboring structures.

Echogenicity: Anechoic, hypoechoic, hyperechoic.

Margin: Sharp, indistinct, partially sharp, partially indistinct.

Acoustic quality behind the lesion: Acoustic enhancement, acoustic shadowing.

Most Important Sonographic Differential Diagnoses:

Anechoic lesions: Cysts, ganglions, effusions.

Caution: Hematomas, abscesses, and, rarely, tumors can be anechoic.

Hypoechoic lesions: Hematomas, abscesses, granulation tissue, many lipomas (characteristic ‘pennate’ structures), many benign and almost all malignant tumors, many tendon tears. Some effusions or cysts can also contain echogenic fluid.

Echogenic lesions: Lipomas, tendon ruptures (reflecting interfaces), calcifications or ossifications (typical acoustic shadowing), defects at the bone surface (e.g., erosions, Hill-Sachs deformity).

What Questions Can Be Answered by Sonography of Joints and juxta-Articular Structures?

• Differentiation between intra-articular effusion and periarticular soft-tissue edema,
  
• Differentiation between effusion and tumor,
  
• Detection of a synovial cyst,
  
• Diagnosis of a tendon tear,
  
• Diagnosis of a tenosynovitis,
  
• Detection of osseous involvements (erosion) in arthritis,
  
• Detection of bursal involvement in arthritis.

Scintigraphy

The three-phase bone scan with Tc 99 m diphosphonate is performed with anterior and lateral views. The strength of bone scanning is that it provides an overview of disease manifestations in the skeleton, yielding information critical for the differential diagnosis. The most important indications are:

• In suspected rheumatoid arthritis patients who do not fulfill the American Rheumatology Association (ARA) criteria for rheumatoid disease and who have negative radiographic findings, to search for inflammatory foci and to determine the distribution pattern (major differential diagnosis is osteoarthritis),
  
• Exclusion of other disorders that affect bone, such as metastases.

Fig. 9.18 Because of acoustic anisotropy of fibers, the echogenicity of lamellated structures (here: normal rotator cuff) depends on the angle of the interrogating sound beam. This effect must be distinguished from pathologic differences in echogenicity.

MRI

Image Analysis

Soft-tissue contrast is determined by the selected pulse sequences and is characteristic for each individual structure and for the joint content (Fig. 9.19).

Signal patterns of pathologic processes:

• lesions in the bone and bone marrow due to inflammation, tumor, or trauma: the signal intensity is decreased on T1-weighted images and increased on T2-weighted images,
  
• ossifications and calcifications: the signal intensity is decreased on T1-weighted and T2-weighted images,
  
• degeneration and tears involving tendons, ligaments, and fibrocartilage: the signal intensity is increased on T1-weighted and T2-weighted images,
  
• edema: the signal intensity is decreased on T1-weighted images and increased on T2-weighted images,
  
• tumor, synovitis, pannus, traumatic lesions after administration of contrast medium: enhancement with increased signal intensity on the T2-weighted images,
  
• tumors and inflammation enhance. Degenerative changes show no or only faint enhancement.

Which Questions Can MRI of the Joints and Adjacent Structures Answer?

• noninvasive diagnosis of cartilage/fibrocartilage defects (menisci),
  
• numerous questions after trauma,
  
• diagnosis of tendon ruptures, tenosynovitis, and synovial cysts,
  
• early diagnosis of subchondral osteonecrosis and insufficiency fractures,
  
• early diagnosis of synovitis/pannus,
  
• early detection of osseous involvement in arthritis,
  
• differentiation between intra-articular effusion and periarticular soft-tissue edema and synovitis/pannus,
  
• differentiation between septic arthritis and osteomyelitis,
  
• exact topographic display of the lesion (e.g., concomitant involvement of the joint or bursa in rheumatoid arthritis),
  
• diagnosis of joint tumor or articular involvement of bone tumors,
  
• diagnosis of compression of the spinal cord in rheumatoid arthritis of the upper cervical spine,
  
• early diagnosis of sacroiliitis.

Fig. 9.19 MRI of the knee. Normal sagittal plane of a T2-weighted TSE sequence.

Arthritis versus Osteoarthritis (Overview)

Pathogenesis of Osteoarthritis and Its Radiographic Features

The cause of osteoarthritis is defective cartilage, with the cartilage in part damaged by mechanical or metabolic processes. In many cases, however, the etiology remains unclear (see page 308–312 for further details).

In the course of degenerative alterations, cartilage destruction leads to uneven mechanical loading, with overloading and subsequent destruction of still spared intact cartilage (Fig. 9.20).

The primary result of cartilage destruction is narrowing of the load-bearing zone of the joint space. The lack of the shock-absorbing cartilage increases the impact load of the subchondral bone, resulting in small areas of osteonecrosis, which become hypervascular toward the marrow space. The hypervascularity leads to increased osteoblastic activity and trabecular thickening, ultimately resulting in a sclerosis. Since the bone cannot withstand the continued overload, trabecular microfractures occur and, ultimately, the trabecular structures collapse. This leads to the formation of so-called ‘detritic cysts’, which strictly speaking are not cysts, but are designated as such because of their radiographic appearance. It is still unresolved whether they are formed solely by subchondral compression fractures or by joint fluid extending into the trabecular space or both. A connection to the joint capsule can be detected only in some cases. The composition of the cyst contents (myxoid, proteoglycans, articular cartilage fragments, and metaplastically formed cartilage) suggests a combination of both mechanisms. Within the cyst, vascularized fibro-cartilage tissue can form and lead to enhancement on MRI. On conventional radiography, the subchondral cysts appear as localized osteolytic lesions that are more-or-less surrounded by a pronounced sclerotic rim (Fig. 9.22).

Fig. 9.20 Conceptual overview of the pathophysiology of osteoarthritis.

Fig. 9.21 Conceptual overview of the pathophysiology of inflammatory arthritis.

In contrast to the zones of increased compressive stress, the peripheral portions of the joint are subjected to less stress. Due to regional growth factors, enchondral bone formation produces osteophytes. This may be thought of as an attempt by the bone to broaden the load-bearing area of the joint.

Pathogenesis of Arthritis and Its Radiographic Appearance

Arthritis has a vast number of causes (Fig. 9.21). They all have in common that they induce an inflammation of the synovial lining that is responsible for the disease process. This explains the similarity of the morphologic articular changes, regardless of the particular cause.

Any individual arthritis, in contrast, is characterized by its clinical course and age of onset, as well as by the distribution of the lesions in the skeletal system (‘distribution pattern’) and joints.

Synovitis with thickening of the synovial lining and hyperemia initially causes joint effusion and periarticular edema that are clinically and radiographically apparent as soft-tissue swelling. The effusion can cause joint-space widening, with potential damage to the joint capsule (e.g., due to recurrent inflammation). Furthermore, the hyperemia allegedly is a major cause of juxta-articular osteoporosis (arthritic collateral phenomenon).

Arising from the synovial lining as well as in the subchondral region, vessels and soft tissues proliferate and form granulation tissue (‘pannus’). The pannus and inflammatory effusion erode joint cartilage and also bone not covered by the protecting cartilage layer (‘bare area’) adjacent to the capsular insertion, This leads to the formation of erosions. In the course of the disease, cartilage destruction progresses, and pannus extends from the peripheral and subchondral sites towards the joint, initially leading to the destruction of the subchondral bone plate and eventually to erosions and osteolytic defects (Fig. 9.23).

With progression of the disease process, cartilage and bone are further destroyed (resulting in joint space narrowing), eventually leading to complete destruction with mutilation and misalignment. This affects small joints quite frequently. With complete destruction of the joint, the disease arrests since the inflammation has subsided. In this stage, the reparative processes can produce an initially fibrous and later osseous bridging of the former joint resulting in ankylosis.

A long chronic process may show sclerosis around the erosions and cysts representing signs of repair. This enables differentiation between old and acute lesions.

Fig. 9.22 Large subchondral cyst in the acetabular roof in osteoarthritis of the hip. The radiograph shows a sclerotic rim around the osteolytic area. b Strong contrast enhancement of the cyst content on MRI (T1-weighted TSE with fat suppression) indicates vascularized tissue.

Fig. 9.23 Schematic comparison of the most relevant signs of erosive osteoarthritis and inflammatory arthritis.

Fig. 9.24 Schematic comparison of erosive osteoarthritis and psoriatic arthritis.

Enthesopathies (Fibro-ostosis and Fibro-ostitis)

Fibro-ostosis

Locations: Calcaneus (posterior and plantar calcaneal spur), greater trochanter, ischial tuberosity, olecranon, and iliac crest (Fig. 9.26). Other locations are less common.

Fibro-ostosis is usually asymptomatic. Inflammatory reaction due to overuse can cause pain and swelling (e.g., ‘epicondylitis’ in tennis players, golfers).

– Irregular calcifications of the tendons and ligaments (Fig. 9.25).

• New bone formation at the tendon insertions (spurs, excrescence, Fig. 9.26).

Insertion defects are possible at the site of muscle insertions. These contour defects (‘rarefying fibro-ostosis’) occur in the region of the pubic bone, ilium, and sacrum, as well as in the region of the femoral neck and humerus (Fig. 9.27).

Fibro-ostitis

• productive fibro-ostitis (new bone formation with specific radiographic features),
  
• rarefying fibro-ostitis (inflammatory insertion erosions, Figs. 9.28, 9.29).

Fibro-ostitis is a sign of inflammatory joint diseases, especially common in psoriatic arthritis, Reiter syndrome and ankylosing spondylitis.

The clinical findings consist of localized swelling and pain.

The productive fibro-ostitis produces new bone, which is irregularly outlined and has indistinct frayed borders.

The rarefying fibro-ositis is characterized by an indistinctly outlined osseous defect at the insertion of the tendon, ligament or capsule. Reactive sclerosis is common around the defect (Fig. 9.29).

‘Acute’ fibro-ostosis with inflammatory tissue reaction and fibro-ostitis in rheumatoid diseases are not always distinguishable on imaging studies, since both conditions show evidence of inflammation on bone scan (increased activity) and MRI (edema).

Fig. 9.25 a Anatomic specimen of a calcified ischiosacral ligament. Radiograph of the specimen (b) and cross-section of the specimen (c) reveal the spongiosal texture.

Fig. 9.26 Extensive classic fibro-ostoses (enthesopathic change) within the pelvis.

Fig. 9.27 Chronic calcifying fibro-ostosis at the insertion of the infraspinatus muscle, a Oblique projection. The T2-weighted SE sequence (b) indicates absence of inflammation in the region of the tendinous insertion (no edema).

Fig. 9.28 Enthesopathy (fibro-ostitis) at the insertion of the infraspinatus muscle in psoriasis.

Fig. 9.29 Rarefying fibro-ostitis at the calcaneal tuberosity in an 8-year-old boy with seronegative spondyloarthropathy, a Lateral view. b T1-weighted SE image.

Fig. 9.30 Enthesopathy without osseous involvement in seronegative spondyloarthropathy.

Degenerative Joint Diseases

Osteoarthritis of the Peripheral Joints

Distribution of Arthritic Changes

Primary osteoarthritic changes are found mainly in the spine and in the hip, knee, first metacarpophalangeal articulation, and interphalangeal articulations (Fig. 9.31). In contrast, the shoulder, elbow, foot, and ankle are infrequently involved. Osteoarthritic changes found in these joints should always be considered secondary in nature. Why primary arthritic changes rarely involve the ankles but commonly involve the hands is unknown.

Secondary osteoarthritic changes have preferred sites determined by the underlying joint disorder (see Table 9.2).

a) Damage to the Hyaline Articular Cartilage and Synovial Lining

Damage to the articular cartilage is called chondromalacia. The four stages in cartilage damage are:

I Cartilage edema (Fig. 9.32),

II Start of cartilage fragmentation with defects (Fig. 9.33),

III Cartilaginous fibrillation with large defects (Fig. 9.35),

IV Complete cartilage denudation.

In cartilage degeneration, the superficial zone of collagenous fibers is damaged first (in some cases accompanied by degradation of proteoglycans). The cartilage matrix, which consists mainly of hydrophilic proteoglycans, accumulates more water and becomes swollen, leading to cartilage edema. The resultant increased mechanical friction, together with the lost normal elasticity of the cartilage, leads to fragmentation of the cartilage substance with formation of defects.

Fragmentation and defect formation progress, producing the phenomenon known as fibrillation. This is the most frequently observed finding, since it also is the time when patients consult their physician because of increasing joint pain. Further progression leads to denudation of the articular surface (Fig. 9.34).

The synovial lining plays a major role in causing symptoms in osteoarthritis. Increased friction leads to mechanical and histochemical irritation (synovitis), and with time a chronic effusion with its complications may develop (e.g., synovial cysts). Morever, nourishment of the cartilage supplied by synovial fluid is compromised. This can be followed by shrinkage of the joint capsule, adding joint deformities to the altered cartilage coat and cortical bone end.

b) Subchondral Damage

Continued overloading quickly leads to small areas of marrow edema, microhemorrhage and microfracture, and even focal osteonecrosis. Edematous areas can resolve within a few weeks without any residue. However, hyperemia, cellular infiltration, and proliferation of fibrovascular tissues might develop in the otherwise highly vascularized and nerve-rich subchondral bone. These changes can also be fully repaired, but might leave behind defects in the form of subchondral cysts (filled with liquid, myxoid, fibrous, or cartilaginous material) or reparative bone and subchondral sclerosis. These ‘residues’ (cysts, subchondral sclerosis) interfere with the fluid exchange between the subchondral region and cartilage. The radiologic manifestations of these processes are local subchondral osteopenia, cysts, or sclerosis.

Fig. 9.31 Distribution pattern of primary degenerative osteoarthropathy at the peripheral joints.

Fig. 9.32 Sagittal MR arthrography of the knee, T1-weighted SE sequence. Cartilage edema along the retropatellar articular surface, indicating the first stage of damage to the articular cartilage.

Fig. 9.33 The start of cartilage fragmentation of the knee; indirect MR arthrography, gradient echo sequence. Stage II.

Fig. 9.34 Degenerative changes of the cartilage and subchondral region.

Fig. 9.35 Histologic section through the articular cartilage. Stage III.

c) Cartilage Repair

Erosive osteoarthritis (synonyms: inflammatory osteoarthritis, destructive osteoarthritis, Fig. 9.38) is a special form of osteoarthritis with swelling, redness and pain as found in synovial arthritis. The cardinal symptom is the radiographically detectable erosion. Distal and proximal interphalangeal joints are preferentially affected, but involvement of any joint is possible. An effusion (best shown by sonography) is always present. In destructive osteoarthritis, the erosions are more central than marginal and either progress to large cysts or become sclerotic.

Atrophic osteoarthritis is characterized by loss of cartilage (leading to joint-space narrowing) with absent or only minimal reactive changes (sclerosis, osteophytes). It tends to involve the hands (Fig. 9.47).

Fig. 9.36 Signs of degeneration seen here in a representative case of moderately severe osteoarthritis.

Fig. 9.37 Signs of degeneration seen here in a representative case of an advanced osteoarthritis.

Fig. 9.38 Resolution of a polyarthritis over 10 years. In 1985, the proximal interphalangeal joint of the middle finger is the only spared visualized joint. In 1991, an erosive arthritis with excessive erosions has developed here. Subsequently, the inflammatory component regresses, and a latent osteoarthritis has developed. The latent osteoarthritis of the remaining interphalangeal joints remains unchanged throughout the observation period.

Typical signs of osteoarthritis are – pain on weight bearing,

• limited range of motion,
  
• subluxation,
  
• subcutaneous soft-tissue nodules (Heberden nodes at the distal interphalangeal joints and Bouchard nodes at the proximal interphalangeal joints).

Imaging is used to confirm the diagnosis and to follow the clinical course. The radiographic findings often lag behind the clinical findings for years.

Technical consideration: To detect alignment abnormalities, radiographic films have to be obtained under weight bearing (standing).

Primary and secondary osteoarthritic changes have the same basic manifestation (Figs. 9.36, 9.37; also compare with pages 294–296):

• joint-space narrowing, especially of the weight-bearing portions,
  
• subchondral sclerosis,
  
• subchondral cyst formation,
  
• osteophytes,
  
• joint deformity with misalignment,
  
• chondrocalcinosis (Fig. 9.40),
  
• loose intraarticular bodies (‘joint mice’),
  
• insertional calcifications of ligaments, tendons, capsules.

Localized subchondral radiolucency, with or without joint-space narrowing, is an early diagnostic sign, but it is rarely encountered (Fig. 9.39).

The three-phase bone scan shows increased uptake caused by increased regional perfusion (= early phase) and by increased bone turnover (= late phase) (Fig. 9.42). The role of the bone scan is determination of the distribution pattern, which frequently assists in discriminating between arthritis and (active) osteoarthritis.

The pathologic changes of cartilage described above (cartilage edema, swelling, and fibrillation) can be visualized with MRI ‘cartilage sequences’ (T2-weighted gradient echo sequences with and without fat suppression) or by means of direct or indirect MR-arthrography of the major joints. Moreover, T2-weighted turbo (fast) spin echo sequences can also be used advantageously. The subchondral changes (microhemorrhages, microfractures, micronecrosis) are not well delineated because of their extremely small size.

See pages 108 and 316 for the MRI signs of the pathology of menisci and disks.

Osteoarthritis of Specific Joints

Osteoarthritis of the Knee

osteoarthritis of the knee (Fig. 9.41). To detect or exclude misalignments, views with the patient standing (with a vertically placed measuring device) are indicated. Degenerative meniscal changes are best detected with MRI.

PVNS (pigmented villonodular synovitis): This condition is dominated by large cystoid defects in the articular ends of the bone. In its early stages there is no joint-space narrowing.

Osteoarthritis of the Hip

In the hip, superolateral joint-space narrowing is more common than medioinferior narrowing (Fig. 9.43). Upright views of the hip show superolateral, superomedial or axial migration of the femoral head to the best advantage. Displacement of the femoral heads into the acetabulum with increasing depths of the acetabular cavity is referred to as acetabular protrusion. Besides dysplasias and other malformations (e.g., coxa vara and valgus), Paget disease and fibrous dysplasia should be added to the causes of secondary osteoarthritis already discussed.

An unusual variant of erosive osteoarthritis, the atrophic-destructive ‘osteoarthritis’ of the hip, leads to destruction of portions of the femoral head and, to a lesser degree, of the acetabulum, with relatively little reaction. This process takes place over months and mainly affects elderly women.

Fig. 9.39 Osteoarthritis of the knee joint.

Fig. 9.40 Chondrocalcinosis of the triangular fibrocartilage as part of degenerative joint disease.

Fig. 9.41 Osteoarthritis of the medial and lateral tibiofibular joints with a large subchondral cyst.

Fig. 9.42 Three-phase bone scan (late phase). Active osteoarthritis involving both knees, the right more than the left. Typical increase in activity in the weight-bearing zones.

Fig. 9.43 Osteoarthritis of the hips, (a) Superolateral narrowing with upward and lateral displacement of the femoral head, (b) Medioinferior narrowing.

Atrophic destructive osteoarthritis must be differentiated from Charcot joint: the neuropathic destruction also involves other joints of the affected extremity.

Osteoarthritis of the Shoulder

Primary osteoarthritis of the shoulder is rare. Secondary osteoarthritis (Fig. 9.44) develops on the basis of misalignment, trauma, Paget disease, dysplasias, acromegaly, and osteonecrosis, or as part of neurogenic, metabolic, and hematologic diseases. In the majority of cases, the glenohumeral and acromioclavicular articulations are equally involved. Acromioclavicular osteoarthritis can lead to the development of impingement syndrome with compression of the supraspinatus tendon.

Fig. 9.44 Osteoarthritis of the shoulder with deformity, osteophytes, and marked subchondral sclerosis.

Osteoarthritis of the Finger and Carpal Bones

Primary osteoarthritis of the distal (= Heberden) and proximal (= Bouchard) interphalangeal joints is the commonest osteoarthritis (Figs. 9.45, 9.46). The so-called ‘Heberden and Bouchard nodes’ are soft-tissue protuberances caused by underlying osteophytes. Osteoarthritis of the first carpal–metacarpal articulation frequently has an erosive component (Fig. 9.48). Osteoarthritis of the carpal bones mainly affects the scaphoid-trapezium-trapezoideum complex. A primary radiocarpal osteoarthritis is relatively rare.

In 1998, Dihlmann and Dihlmann described a subtype of osteoarthritis of the fingers, which they call osteoclastic osteoarthritis of the fingers. It is characterized by subchondral osteolytic areas that involve at least one-third of the length of the phalanx. These areas are larger than detritic cysts, which are confined to the articular end of the bone.

Secondary osteoarthritic changes can be observed together with chronic inflammatory conditions, acromegaly, and metabolic disorders such as hemochromatosis, diabetes mellitus, pseudogout (= CPDD).

Hemochromatosis leads to osteophytes with extensive cyst formation involving the metacarpophalangeal joints. This condition also often shows chondrocalcinosis.

Osteoarthritis of the Toes

The commonest causes of degenerative changes in the toe joints are malpositioned toes, especially the hallux valgus (Fig. 9.49). A striking finding of degenerative changes due to hallux valgus deformity is the often extreme hyperostosis and ‘cystoid’ osseous transformation in the first metatarsal head. Accompanying soft-tissue swelling (bursitis) is a frequent additional finding.

Fig. 9.45 Interphalangeal osteoarthritis. The ‘bird’s wing’ or ‘seagull’ appearance is caused by lateral osteophytes and central indentation.

Fig. 9.46 Prominent Bouchard osteoarthritis of the proximal interphalangeal joints, and also less pronounced Heberden osteoarthritis of the distal interphalangeal joints.

Fig. 9.47 Rare form of atrophic osteoarthritis. The joint spaces are asymmetrically narrowed.

Fig. 9.48 Osteoarthritis of the first carpometacarpal joint.

Fig. 9.49 Hallux valgus with mild degenerative changes.

Degenerative Changes of the Spine

The intervertebral disk consists of the nucleus pulposus, anulus fibrosus, and cartilaginous end plates (Fig. 9.50). Its major functions are to distribute axial loading and to keep surrounding ligaments taut. The degenerative process causes Assuring and fragmentation of the otherwise spirally intertwined collagenous fibers. The fibers might only partially withstand the high pressure of the nucleus pulposus (7 x atmospheric pressure). Repetitive overloading results most commonly in slowly developing herniation of the nucleus pulposus. However, acute herniations also rarely occur. In principle, the herniation can occur in any direction, but only posterior herniations are clinically relevant, since these are the only ones that compress the nerves or spinal cord, depending on whether the herniation is central or lateral in location.

Protrusion: Bulging of the disk (nucleus pulposus and anulus fibrosus). The nucleus pulposus extends into crevices of the inner zone of the anulus fibrosus and displaces fibers of the peripheral zone (Fig. 9.52).

Prolapse: Material of the nucleus pulposus leaves the anulus pulposus and extrudes through tears in the peripheral zone of the anulus fibrosus (Fig. 9.53).

Sequester: Displaced disk material is referred to as a sequestered fragment. This is usually accompanied by a tear in the posterior longitudinal ligament, but a sequestered fragment can remain subligamentous in location. Its differentiation from a prolapse is problematic, since it is only possible if discontinuation can be demonstrated between disk and sequester (rare) (Fig. 9.54).

Furthermore, disk material can herniate superiorly and inferiorly into the adjacent vertebral bodies. These herniations are called Schmorl’s nodes.

In the process of degeneration, the disk loses water and decreases in height (Fig. 9.51). Furthermore, calcifications may be seen within the disk.

As the degenerative process progresses, reparative osseous processes involving the disk begin at the periphery, where there are no cartilaginous plates. This reparative osseous tissue grows into the disk and can lead to revascularization of the disk (the disk is partially vascularized until the fourth year of life). It is conceivable that this process removes pre-existing disk herniations.

b) Changes of the Vertebral End Plates

The intervertebral disk is avascular in adolescents and adults and is nourished by diffusion from adjacent bone marrow and bordering ligaments.

In the process of natural aging, the nucleus pulposus loses its water retention capacity, and its internal pressure decreases. This shifts weight bearing from the center to the lateral, leading to ligamentous loosening, and the limited elastic vertebral bone adjacent to the disk is subjected to increased compressive loads. This can result in microedema, microhemorrhage, microfractures, and micro-necroses similar to the processes occurring in synovial joints.

This is followed by reactive changes with pseudo-inflammatory reactions in the subdiskal skeletal zones: hyperemia, and ingrowth of fibrovascular tissue. The outcome is subdiskal fibrosis and sclerosis as the bone attempts to counteract the increased axial pressure. The sclerotic bone is brittle and can collapse, resulting in tears and clefts and the formation of reparative connective tissue.

Instability with ligamentous loosening caused by the decreased pressure within the nucleus pulposus leads to reactive osseous proliferations, referred to as osteophytes, along the margin of the vertebral body (spondylosis deformans) and possibly to hypertrophy of the ligamenta flava. This process serves to counteract the instability. The same applies to the uncovertebral joints of the cervical spine (uncovertebral osteoarthritis or arthrosis). They prevent lateral displacement of the cervical vertebral bodies. The superiorly projecting uncinate processes are a peculiarity of the cervical spine and, in contrast to the dorsal and lumbar spine, form a vertical articulation. The uncovertebral joints are not synovial joints.

Fig. 9.50 Schematic drawing of the intervertebral disk and intervertebral foramen.

Fig. 9.51 Schematic drawing of disk degeneration, skeletal changes along the disk, and increasing intervertebral degenerative changes. Modified after Gutmann.

Fig. 9.52 Disk protrusion (GE sequence).

Fig. 9.53 Disk prolapse (GE sequence).

Fig. 9.54 Disk prolapse with interiorly dislocated sequestrum, sagittal CT reconstruction.

c) Changes to the Intervertebral Articulations

Degeneration of these joints is called facet (apophyseal) joint osteoarthritis. The atlanto-occipital and atlan-to-axial joints are also subject to the same process. The pathologic findings correspond to those of osteoarthritis (cartilage damage, subchondral sclerosis, and cyst formation). Characteristic abnormalities are deformed articular surfaces and massive osteophytic overgrowth that can lead to clinically relevant encroachment upon the intervertebral foramina (Figs. 9.55–9.57).

Synovial cysts consist of intraspinal, extradural protrusions of the joint capsule of osteoarthritically deformed intervertebral joints. They are invariably confined to the levels L3-S1 and contain joint fluid or, rarely, gas.

In the lumbar spine, especially at the L4/L5 segment, the degenerative changes can cause anterior gliding of a vertebra relative to its subjacent vertebra (degenerative or pseudospondylolisthesis, Fig. 9.58). This can cause spinal stenosis. In contradistinction, spondylolisthesis is caused by vertebral gliding because of a bilateral defect in the pars interarticularis (spondylolysis). Since in ‘genuine’ spondylolisthesis only the vertebral body glides, and the posterior vertebral arch, together with the spinal process, remains in place, the spinal canal is not narrowed. Etiologically, spondylolisthesis is generally congenital or traumatic (stress fracture).

d) Ligamentous Calcifications and Ossifications

Calcification and ossification of the longitudinal spinal ligaments (anterior and posterior ligaments, ligamentum flavum) are commonly encountered (Figs. 9.59, 9.60). Although this alteration increases after 50 years of age, it has a racial preference (increased incidence of calcifications in the posterior longitudinal ligaments in Asians) and shows quite a variable individual severity, suggesting not only simple ‘degeneration’ but also a genetic disposition. Diffuse idiopathic skeletal hyperostosis (DISH) has pathologic and radiographic findings that are identical to ligamentous calcifications and ossifications of other types, but it is nonetheless considered a distinct entity because of several unique features.

e) Stenosis of the Spinal Canal

In spinal stenosis, a distinction should be made between the central and lateral types. The lateral type involves lateral recess and intervertebral foramen. Congenital spinal canal stenosis is rare, and the acquired form is common.

Fig. 9.55 Massive narrowing of the C3-C4 intervertebral foramen by osteophytes of the facet joints and uncovertebral joints.

Fig. 9.56 Specimen of a cervical vertebra with uncovertebral and facet joint osteoarthritis, compared with the specimen of a normal cervical vertebra.

Fig. 9.57 2-D CT reconstruction of intervertebral foramina of both sides for comparison. The right intervertebral foramen is narrowed by a marginal osteophyte.

Fig. 9.58 Marked degenerative changes of the facet joints. In addition to narrowing of the intervertebral foramen, there is degenerative anterior slippage of the involved vertebrae (pseudo-spondylolisthesis).

Fig. 9.59 Ossification of the posterior ligaments (arrowheads) with fracture. The fracture is recognized by the discontinuity of the ligament and the widening of the disk space.

Fig. 9.60 Ossification of the posterior ligament with indentation of the spinal cord (myelo-CT).

A basic distinction must be made between – the usually chronic and diffuse ‘back pain’, caused by spondylosis deformans, facet joint osteoarthritis, and uncovertebral osteoarthritis. As with osteoarthritis of peripheral joints, restricted motion and pain on weight bearing dominate the clinical presentation;

Nerve root compression with radicular pain is caused by disk herniations, but also by osseous narrowing of the intervertebral foramina as part of facet joint osteoarthritis and uncovertebral osteoarthritis. The L3 to SI segments are the most frequently involved. In general, the sensory deficits dominate in the form of radicular pain, hypoes-thesia, and possible hypoalgesia. The strictly radicular distribution usually enables a precise clinical determination of the causative level (Table 9.3).

When correlating the radicular symptom complex with the expected radiographic findings, it should be kept in mind that the inferiorly extending lumbar roots begin medial to the cauda equina and then curve laterally to leave the spinal canal through the intervertebral foramen below the corresponding vertebral arch. This means that, for instance, L5 radicular pain can be caused by either a lateral or intraforaminal disk herniation at L5/S1 or a medial disk herniation at L4/L5. In the latter instance, a mixed symptom complex can be, but is not inevitably, present.

Disk Degeneration (Chondrosis, Osteochondrosis)

The basic findings of disk degeneration are (Figs. 9.61, 9.62):

• disk-space narrowing (= chondrosis),
  
• subchondral sclerosis (rarely osteoporosis),
  
• Schmorl’s nodes,
  
• spondylophytes,
  
• vacuum phenomenon,
  
• calcifications in the disk (nucleus pulposus).

The vacuum phenomenon is caused by the release of nitrogen into the degeneratively altered disk.

Osteochondrosis: The combination of altered ver tebral end plates (band-like sclerosis, contour ir regularities) and narrowed disk space.

The term ‘erosive’ osteochondrosis is used when the end plates show surface irregularities. ‘Serrations’ or contour defects (‘erosions’) are seen radiographically.

In these cases, differentiating this diagnosis from infectious spondylitis is difficult radiographically. A crucial discriminating criterion is the type of accompanying sclerosis: the subdiskal sclerosis is band-like in osteochondrosis and more focal in infectious spondylitis. Moreover, infectious spondylitis lacks other signs of disk degeneration. In cases of suspected infection superimposed on an (erosive) osteochondrosis, MRI is the preferred imaging modality.

Osteochondrosis and facet joint osteoarthritis of the cervical spine cause hypomobility, preferentially located at levels C5 to C7, frequently with hyper-mobility of higher cervical segments.

Hemispheric spondyloschisis: This term coined by Dihlmann describes a hemispheric spongiosal sclerosis in the anterior or middle third of the vertebral body above an intervertebral disk that appears radiographically normal or narrowed. We consider this a special manifestation of the (normally band-like) subchondral sclerosis as frequently seen with disk degeneration. Awareness of this special manifestation is important for the differential diagnosis when the apposing subdiskal end plate fails to show a sclerosis in the presence of a normal disk space. The hemispheric spongiosal sclerosis must be distinguished from increased density caused by infectious spondylodiskitis (use MRI). Osteoblastic metastases (Fig. 9.63) pose difficulty only if the spine shows additional degenerative changes together with a solitary metastatic lesion (rare).

Fig. 9.61 Degenerative changes of the lumbar spine with marginal osteophytes, end-plate sclerosis, and disk-space narrowing. The osseous appositions are most severe where the vertebral bodies show a decrease in height.

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