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Eugene

W. CaIdwell

Lecture

Common Disorders of Synovium-Lined Pathogenesis, Imaging Abnormalities,

Donald Resnick1

Joints: and Complications

A variety of common disorders affect the synoviumlined articulations of the appendicular skeleton. Each is characterized by unique imaging abnormalities that allow the radiologist, in most instances, to suggest a single accurate diagnosis. This article contains a review of the pathogenesis, imaging abnormalities, and complications of some of these disorders. Although each process is examined with both conventional and sophisticated imaging techniques, emphasis is clearly placed on close radiographic-pathologic correlation. Indeed, the radiograph (or alternative image) should be viewed as a mirror, reflecting underlying gross and microscopic pathologic abnormalities. If one understands the disease, one can interpret the imaging findings with a great deal more confidence and accuracy.
Anatomic Considerations

The structure of a synovial joint differs fundamentally from that of a cartilaginous or fibrous joint [1]. The articular capsule

surrounding a synovial joint consists of a thick outer layer, the fibrous capsule, and a more delicate inner layer, the synovial membrane (Figs. 1A-i C). The fibrous capsule binds together the apposing bones, and it is firmly adherent to the penosteum of these bones. The highly vascular synovial membrane lines the nonarticular portions of the synovial joint and any intraarticular ligaments or tendons. At the marginal areas of the joint, the synovial membrane covers the intracapsular osseous surfaces that are clothed by penosteum or perichondnum but are without cartilaginous surfaces (Fig. 1 D). These regions are designated bare or unprotected portions of the joint and are important in the pathogenesis of marginal osseous erosions that accompany synovial inflammatory disorders (discussed later). Small fingerlike projections, or villi, normally may be apparent on the inner surface of the synovial membrane in certain regions of the articular cavity. Irritation or inflammation of the synovium leads to excessive villous formation. The functions of the synovial membrane include the secretion of a mucoid substance into the synovial fluid; the removal of substances from the articular cavity via capillaries, venules, or lymphatic channels; and, owing to the presence of loose synovial folds, villi, and marginal recesses, the facilitation of joint motion [2, 3]. The articulating surfaces of the bone are covered by a layer of glistening connective tissue, articular cartilage, whose function includes transmission and distribution of high loads, maintenance of contact stresses at acceptably low levels, movement with little friction, and shock absorption [4]. The

Received June 30, 1988; accepted after revision July 26, 1988. Presented as the Caidwell Lecture at the annual meeting of the American Roentgen Ray Society, San Francisco, CA, May 1988. 1 Department of Radiology, Veterans Administration Medical center and University of California, San Diego, Medical Center. Address Resnick, Dept. of Radiology, Veterans Administration Medical center, 3350 La Jolla Village Dr., San Diego, CA 92161. AJR 151:1079-1093, December 1988 0361 -803X/88/1 51 6-1 079 American Roentgen Ray Society

reprint

requests

to D.

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Fig. 1.-Anatomy of the synovial joint. A, Fundamental components of synovium-lined joint include fibrous capsule (FC), synovial membrane (S), and articular cartilage (C) with subjacent bone plate. At margins of joint, synovial membrane is applied to bone without protective cartilage (arrows). B, In certain sites, an additional structure is a disk (D), or meniscus, which may partially divide joint into two cavities. An example of such a joint is the knee. C, Elsewhere, disk may completely D, Photomicrograph (x200) reveals divide joint cavity. An example of such a joint is the stemoclavicular joint. periphery of synovium-lined joint where articular cartilage ends and synovium is applied directly to bone (arrow).

articular cartilage generally is hyaline in type, although in certain locations such as the acromioclavicular, sternoclavicular, temporomandibular, and apophysealjoints, fibrocartilage can be identified. The cartilage is devoid of blood and lymphatic vessels and nerves, and it derives its nutrition principally from diffusion of fluid from the synovial cavity. This feature explains the relative preservation of the cartilaginous surfaces in instances of ischemia of subchondral bone (i.e., ischemic necrosis of bone) and the atrophy of cartilage that accompanies disuse or immobilization of a limb. It should be noted, however, that small blood vessels do pierce the subchondral bone plate and extend into the deepest stratum of cartilage, and, additionally, a vascular ring is located within the synovial membrane at the periphery of the cartilage. The latter source of vascularity may explain the occurrence of peripheral osteophytes, which are characteristic of such disorders as osteoarthrosis. A subchondral endplate consists of trabeculae of variable thickness that curve around the inferior surface of the articular cartilage [5]. The calcified zone of cartilage, designated the tidemark, is located just superficial to the endplate. This tidemark anchors the collagen fibers of the noncalcified portions of the cartilage and, in turn, is anchored to the subchondral endplate. In certain articulations (such as the knee; wrist; and sternoclavicular, acromioclavicular, temporomandibular, and costovertebral joints), a fibrocartilaginous (or fibroelastic) disk or meniscus may be found attaching to the fibrous capsule (Figs. lB and 1 C). This disk may partially (e.g., knee) or completely (e.g., wrist or sternoclavicular joint) divide the articular cavity. Although the precise function of these intraarticular disks is not clear, it has been suggested that they serve as shock absorbers, distribute force over a larger surface, influence the degree of articular motion, enhance joint lubrication, and protect the articular surface [6].

Labra represent circumferential cartilaginous folds that are evident in certain joints, such as the hip and glenohumeral joint. Labra are attached to the peripheral portion of the articulation, thereby deepening the joint cavity and increasing congruity of the adjacent articular surfaces. In certain locations, such as the elbow, intracapsular fat pads are present, serving as cushions that absorb forces generated across the joint and, perhaps, distributing lubricants within the joint cavity. Traumatic Synovial Lipohemarthrosis Effusion, Hemarthrosis, and

A joint effusion appearing within the first few hours after an acute traumatic episode usually is related to a hemarthrosis; nonbloody effusions usually appear 1 2-24 hr after an injury [7]. It has been suggested that trauma may lead to a subtle increase in vascular permeability as well as to gross disruption of blood vessels, both factors contributing to posttraumatic hemarthrosis [8]. The detection of intraarticular blood after an injury requires careful clinical and radiographic examination to exclude occult fracture or ligamentous injury, although hemarthrosis also may accompany hemophilia and other bleeding disorders, pigmented villonodular synovitis, intraarticular neoplasms (such as hemangiomas), neuroarthropathy, and anticoagulant therapy. On standard radiographs, bloody or nonbloody effusions occurring after trauma lead to displacement of intraarticular fat pads and edema of extraarticular fat planes. Examples of these findings include ventral and posterior displacement of fat pads about the distal portion of the humerus in instances of elbow trauma (Fig. 2), bulging of extracapsular fat about the traumatized hip of a child, distortion of the suprapatellar and prefemoral fat planes owing to enlargement of the suprapatellar pouch in the injured knee, and displacement and obliteration of the fat plane overlying

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served in patients without fracture, probably related to significant cartilaginous or ligamentous injury [1 4], the discovery of both intraarticular fat and bone marrow spicules is reliable evidence of an intraarticular fracture, the fat being released from the marrow after cortical violation [1 5]. The radiographic detection of lipohemarthrosis relies on a horizontal-beam technique in which a fat-blood fluid level becomes visible [1 6]. This finding is seen most often in the knee (in association with fractures of the femur, tibia, patella, or fibula) or the glenohumeraljoint (in association with dislocations or humeral fractures), although it may be evident in other locations, such as the elbow [17].

Internal
.-

Derangement

Fig. 2.-Positive fat-pad sign of elbow. Sagittal section of cadaveric elbow after intraarticular injection of air outlines characteristic elevation of anterior and posterior Intracapsular, extrasynovial fat pads (arrowheads), leading to radiographically evident lucent shadows that are strong cvidence of an effusion.

the pronator quadratus muscle and about the carpal scaphoid in cases of wrist trauma [9-1 1 ]. Furthermore, widening of the interosseous space due to accumulation of fluid can follow intraarticular trauma [12]. Although such radiographic changes provide only indirect evidence of intraarticular fluid and do not identify the composition of the fluid, MR imaging delineates more specifically the nature of the fluid and, indeed, can document the presence of hemorrhage owing to a predictable sequence of chemical degradation of hemoglobin in extravasated blood [13]. Bloody synovial fluid-containing fat droplets can be noted both grossly and microscopically after trauma to a joint. Although a hemorrhagic effusion containing fat may be ob-

Any of the normal components of a synovium-lined articulation, whether they be menisci (or disks), labra, or cartilage, may be injured as a result of acute trauma or chronic stress. Injury to intraarticular disks has been recognized in virtually each location where such disks are found. Meniscal abnormalities in the knee traditionally have been detected with arthrography. In the hands of a skilled radiologist, the accuracy rate of diagnosing (or excluding) medial meniscal tears may reach 99% and that of lateral meniscal tears can approximate 93% [1 9]. Although arthroscopy provides similar accuracy when performed by an expert orthopedic surgeon, it is more invasive than arthrography. Recent evidence indicates that MR imaging is extremely sensitive and specific in the detection of meniscal tears [1 9, 20], as well as in the detection of injuries to other intraarticular and periarticular structures, if the interpreter is aware of diagnostic pitfalls [21 ]. The application of fast imaging techniques will make MR more efficient and less costly in the diagnosis of meniscal injuries in the knee [22, 23]. The intraarticular disk or fibrocartilage of the wrist may be the site of perforation due to acute trauma or chronic degeneration. Highly accurate delineation of such disruption is provided by arthrography, especially when it is combined with careful monitoring with fluoroscopy, cineradiography, or the digital subtraction method [24] and, perhaps, with the multi-

Fig. 3.-Normal and abnormal intraartlcular disk of temporomandibular joint. A, Normal. Observe normal position of disk (arrows) between mandibular condyle (C) and articular fossa of temporal bone on TI-weighted sagfttal MR image, 600/20 (TR/TE). B, Abnormal. Anterior displacement of disk (arrow) is evident on similar MR image, 600/20.

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compartmental injection technique [25]. Whether MR imaging will provide similar diagnostic accuracy is not yet clear, although the introduction of surface coils specifically designed for MR examination of the wrist surely will aid in this regard. Dysfunction of the temporomandibular joint resulting from meniscal displacement, perforation, or both has been the subject of much attention. In recent years, many reports have been published defining the efficacy of arthrography [26-28], CT [29, 30], and MR imaging [31 -37] in the evaluation of this common clinical problem. Arthrography appears to represent the gold standard in the diagnosis of meniscal perforation; CT is best suited to the evaluation of intraarticular and periarticular osseous structures; and MR, owing to its noninvasive nature, is superior in defining the precise position of the meniscus and thereby delineating abnormal meniscal displacement (Fig. 3). The application of cine MR should further the assessment of dynamic abnormalities in temporomandibular joint function. The relationship of injuries of the anterior or posterior portion of the glenoid labrum to dislocations of the anterior or posterior glenohumeral joint, respectively, is well known. Indeed, the abnormality of the anterior glenoid labrum, known as the Bankart lesion, initially was believed to be the principal pathogenic factor in recurrent anterior glenohumeral joint dislocations [38], although recent emphasis has been placed on the entire capsular mechanism as the most important factor permitting such dislocations [39]. Researchers have not yet agreed on which imaging method is most suitable for the delineation of labral (and capsular) abnormalities of the glenohumeral joint, although considerable information is provided by computed arthrotomography (Fig. 4A) in which the glenoid labrum, glenohumeral ligaments, and articular recesses can be clearly defined [40, 41]. Although MR imaging appears accurate in the assessment of the rotator cuff and the related shoulder impingement syndrome [42-44], the value of MR in the diagnosis of abnormalities of the glenoid labrum and glenohumeral ligaments is not yet clear [45].

Less well recognized is the occurrence of tears and cystic deformation of the acetabular labrum in adults with persistent hip pain [46, 47]. These abnormalities may be accompanied by acetabular dysplasia and osteoarthrosis of the hip [48], as well as soft-tissue and intraosseous ganglia [49]. Although acetabular dysplasia, a radiolucent paraacetabular soft-tissue mass, or an intraosseous cystic lesion may be shown by routine radiography, more definitive diagnosis is provided by arthrography (Figs. 4B and 4C), CT, or MR imaging. Transchondral fractures generally relate to shearing, rotatory, or tangentially aligned impaction forces [50]. Acute injuries can produce fragments consisting of cartilage alone (chondral fractures) or cartilage and bone (osteochondral fractures). Obviously, a purely cartilaginous fracture produces no direct radiographic abnormalities, whereas one containing calcified cartilage and bone becomes apparent owing to varying degrees of radiodensity. Secondary radiographic signs, consisting of soft-tissue swelling and a joint effusion, can be apparent with either chondral or osteochondral fragments. Fluoroscopy, conventional or computed arthrotomography, and MR imaging are among the methods that can be used to define the nature and location of the fracture more accurately [51 52]. In the search for intraarticular chondral or osteochondral bodies with any technique, the propensity for such bodies to lodge in normal recesses or dependent portions of the joint (e.g., subscapular recess of the glenohumeral joint, acetabular fossa of the hip, and olecranon fossa of the elbow) should be remembered.
,

Synovial

Inflammatory

Diseases

There are a number of articular disorders that are characterized by prominent inflammation of the synovial membrane. Among these, rheumatoid arthritis and the seronegative spondyloarthropathies (psoriasis, Reiter syndrome, and ankylosing

Fig. 4.-Abnormal labra. A, Glenoid labrum. Transaxial CT scan after intraarticular injection avulsion of portion of posterior glenoid margin (arrowhead) in patient B and C, Acetabular labrum. Initial radiograph (B) shows findings acetabulum. Arthrogram (C) reveals contrast opacification of cyst and

of air reveals avulsion of anterior portion of labrum with with multidirectional instability of the shoulder. of osteoarthrosis of the hip with cystic lesion containing horizontal tear (arrowhead) in acetabular labrum.

piece bone

of bone in lateral

(arrow) aspect

and of

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spondylitis) must be emphasized. Indeed, in rheumatoid arthritis, the earliest recognizable pathologic abnormality is acute synovitis, which is characterized by vascular congestion and edema of the synovial membrane, precipitation of fibrin, and cellular accumulation (erythrocytes, polymorphonuclear leukocytes [especially lymphocytes], and subsequently plasma cells and multinucleated giant cells). These microscopic abnormalities result in a macroscopically evident thickened and injected synovial membrane, synovial villous formation, and joint effusion (Fig. 5). This pathologically evident synovial stage of rheumatoid arthritis is accompanied by characteristic radiographic abnormalities [53]. Accumulation of intraarticular synovial inflammatory tissue, increase in intraarticular fluid, capsular distension, and surrounding soft-tissue edema lead to one of four early radiographic findings of the disease, fusiform soft-tissue swelling. In response to hypere-

mia provoked by synovial inflammation and to relative disuse of the involved joint(s), a second early radiographic feature of the disease, periarticular osteoporosis, becomes apparent. This finding may be less evident in adult men and in individuals who are physically active. With recurrent or more prolonged inflammation, the synovium soon spills from the marginal pockets of the joint and grows toward and extends over the surface of the articular cartilage. Enzymatic destruction of the chondral coat then leads to the third early radiographic feature of rheumatoid arthritis, diffuse loss of interosseous space. The fourth radiographic feature, marginal erosion of bone, relates to the location of inflammatory synovial tissue, or pannus, in peripheral portions of the joint where bone does not possess protective cartilage. Although these four radiographic abnormalities-fusiform soft-tissue swelling, periarticular osteoporosis, diffuse loss of

Fig. 5.-Rheumatoid arthritis: pathologic overview. 1, Normal joint. Observe articular cartilage and synovial membrane. At edges possess protective cartilage. 2, Very early abnormalities of rheumatoid arthritis consist of synovial proliferation 3, Slightly later stage. Inflamed synovial tissue or pannus (arrow) extends across soft-tissue edema, and osteoporosis are seen. Small osseous erosions at margins 4 and 5, More advanced stages. Large marginal and central erosions and cysts 6, Advanced rheumatoid arthritis. Fibrous ankylosis of the joint dominates.

of articulation

(arrowheads),

synovium

abuts

on bone

that

does

not

(open arrows), soft-tissue edema (solid arrows), cartilaginous surface, leading to chondral erosion. of joint are apparent (arrowheads). are noted (arrowheads).

and osteoporosis. Capsular distension,

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interosseous space, and marginal erosions of bone-are considered classic early manifestations of rheumatoid arthritis (Fig. 6), they may not all be evident on initial radiographic examination, and, furthermore, additional alterations also may be seen, especially in more advanced disease. Multiple subchondral lucent areas (termed cysts, pseudocysts, or geodes [54]) typically are small and without sclerotic margins, and they correspond to intraosseous extension of inflamed synovium. Rarely, prominent subchondral cysts in rheumatoid arthritis occur in the absence of both articular space loss and osteoporosis, and the resulting radiographic features resemble those of gout [55]. In long-standing rheumatoid arthritis, intraarticular fibrous (and, less commonly, bone) ankylosis, subchondral bone sclerosis, and bone fragmentation leading to osseous bodies in the joint may be observed [56]. As in rheumatoid arthritis, the predominant target area in the synovial joint in the seronegative spondyloarthropathies appears to be the synovial membrane (Fig. 7) [53]. As opposed to the situation in rheumatoid arthritis, however, the synovial inflammatory changes in the seronegative spondyloarthropathies are of less intensity. Because of this, it might be expected that the degree of osteoporosis and the extent of osseous erosion in the seronegative spondyloarthropathies will be limited when compared with those of rheumatoid arthritis. In general, this is true, although some patients, particularly those with psoriasis, can have striking osteolysis, perhaps related to cortical atrophy resulting from a noninflammatory proliferation of the periosteum [57]. Although cartilaginous destruction can proceed from superficial extension of inflamed synovial tissue in the seronegative spondyloarthropathies (as in rheumatoid arthritis), buds of granulation tissue also may erode cartilage from beneath, especially in ankylosing spondylitis [58]. Thus, the central osseous structures are eroded by superficial or subchondral pannus, and the peripheral osseous structures are destroyed by inflamed synovium in the recesses of the articulation. Furthermore, fibroplasia followed by cartilaginous metaplasia and chondroossification in the seronegative spondyloarthropathies may lead to intraarticular bone ankylosis. Indeed, the detection of osseous fusion at sites other than the carpal and tarsal bones is unusual in rheumatoid arthritis. The proclivity to osseous

fusion of certain synovial joints in the seronegative spondyloarthropathies can be related to abnormalities occurring at the capsuloligamentous attachments, indicative of a generalized enthesopathy (a word derived from enthesis, meaning a site of ligamentous or tendinous attachment to bone) [59]. Although the presence of intraarticular bone fusion and the relative absence of periarticular osteoporosis are important radiographic signs of the seronegative spondyloarthropathies that differ from the classic manifestations of rheumatoid arthritis, one further radiographic abnormality in seronegative spondyloarthropathies is even more useful in the differential diagnosis. This abnormality is a remarkable tendency for bone formation, especially in the form of irregular excrescences, or whiskers, at the margins of the joint, adjacent to sites of erosion (Fig. 8). The exact cause of new bone formation in these disorders, which also may consist of periostitis in the shafts of the small tubular bones in the hands and feet, is not clear [60], although the inflammatory abnormalities in the involved articulations may be intermittent, perhaps allowing time during clinical remission in which reactive bone healing can occur. In any of the synovial inflammatory disorders, inflammation of synovium-lined bursae and tendon sheaths can be observed also. For example, in rheumatoid arthritis, bursal involvement may be seen in more than 5% of patients, particularly in the popliteal region of the knee and in the olecranon, subacromial (subdeltoid), and retrocalcaneal bursae (Fig. 9), as well as about the wrist and foot. Tenosynovitis is especially prominent on the dorsum of the hand, fingers, and foot. Inflamed bursae and tendon sheaths fill with exudate, enlarge, and form clinically detectable soft-tissue masses. Radiographs show that they displace or obscure adjacent fat planes and lead to subjacent osseous resorption. Certain complications of the synovial inflammatory diseases deserve emphasis. Synovial cysts are a well-known manifestation of these disorders. They probably relate to elevation of intraarticular pressure that occurs as a response to the accumulation of joint fluid (Fig. 1 0). Owing to the creation or enlargement of an opening between the inflamed articulation and a surrounding synovial sac, egress of joint fluid occurs that serves to decompress the articulation [61 ]. Rheumatoid

Fig. 6.-Rheumatoid arthritis: sequential radiographic abnormalities in metacarpophalangoal joints. A, Earliest abnormalities consist of soft-tissue swelling (solid arrows), penarticular osteoporosis, loss of a portion of subchondral bone plate on metacarpal head (open arrow), and minimal joint-space narrowing. B, With progression, increase in soft-tissue swelling (arrows) and osteoporosis are associated with marginal erosion of metacarpal heads (open arrow).

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ci
Fig. 7.-Seronegative spondyloarthropathles: pathologic overview. 1, Normal synovial joint. 2, Early changes consist of synovial inflammation (open arrows) and soft-tissue edema (solid arrows). Osteoporosis 3, Subsequently, synovial inflammatory tissue or pannus extends across and beneath chondral surface (arrows), disruption. 4 and 5, Later stages. Marginal and central osseous erosions develop (arrowheads). Associated bone proliferation 6, Finally, lntraartlcular bone ankylosis may develop. may not be evident. leading to cartilaginous (arrows) becomes evident. erosion or

synovial cysts are observed most often in the popliteal region; however, they also may arise in the calf, ankle, plantar aspect of the foot, wrist, elbow, and shoulder [53]. About the hip (Fig. 1 1), such cysts simulate inguinal hernias on physical examination. Arthrography remains the most popular imaging method for diagnosis of synovial cysts, and needle puncture with opacification of the joint (rather than of the cyst) is the preferred injection technique because a valvular mechanism may exist between the cyst and the articulation, allowing the flow of fluid to proceed in one direction only (from the articulation to the cyst) [62]. Sonography, scintigraphic arthrography, CT, and MR imaging also can be used in the evaluation of synovial cysts [63-66]. Because rheumatoid arthritis and related synovial disorders may involve tendons, tendon sheaths, and ligaments, malalignment is an expected complication [53]. Tendinitis, teno-

synovitis, and ligamentous laxity lead to characteristic patterns of subluxation and angulation, including fibular deviation of the toes at the metatarsophalangeal joints, ulnar deviation of the fingers at the metacarpophalangeal joints, boutonniere and swan-neck deformities of the digits, and atlantoaxial subluxation in the spine. In rheumatoid arthritis, such malalignment usually is accompanied by significant intraarticular abnormalities, including bone erosion. When subluxation is seen in the absence of intraarticular erosions, collagen vascular disorders, especially systemic lupus erythematosus, are a more likely diagnosis than rheumatoid arthritis. An insufficiency type of stress fracture is also a well-known complication of rheumatoid arthritis and related diseases. In rheumatoid arthritis, osteopenia, most likely representing osteoporosis and occurring in either a generalized or a periarticular distribution, may relate to hypervascularity, disuse, cor-

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ticosteroid or salicylate therapy, unknown causes, or combinations of these factors. Localized skeletal and whole-body retention of bone-seeking radiopharmaceutical agents confirms an increase in bone turnover in patients with this disease [67-70]. Fractures may occur after minimal trauma or spontaneously in spinal sites (e.g., compression fractures of ver-

tebral bodies) or extraspinal locations (Fig. 1 2). Insufficiency fractures in the tubular bones in the lower extremity are particularly characteristic, especially in combination with osteoporosis, corticosteroid therapy, angular deformity, and flexion contracture [71]. Erosive abnormality of bone related to the rheumatoid process itself also can lead to fracture and deformity [72]. Thus, pathologic fractures are observed through the odontoid or olecranon process, the scaphoid bone in the wrist, the proximal portion of the humerus, and the acetabulum. Massive osteolysis is a rare finding of unknown pathogenesis that has been observed in rheumatoid arthritis [53]. The humeral and femoral heads, the small bones of the hands and
Fig. 10.-Mechanisms of decompression of joints with raised intraarticular pressure. Three p0tential pathways are subchondral cystic lesions (1), synovial cysts (2), and sinus tracts or fistulae (3).

Fig. 8.-Seronegative spondyloarthropathies: bone formation or whiskenng. In a patient with ankylosing spondylitis, observe superficial osseous erosion with adjacent bone proliferation (arrows), producing an irregular osseous outline. Osteoporosis is not apparent.

Fig. 9.-Rheumatoid arthritis: retrocalcaneal bursal involvement. A, Soft-tissue swelling (arrows) represents fluid-filled, distended retrocalcaneal bursa. B, Subjacent osseous erosion (arrowhead) can be seen subsequently. C, Photograph of sagittal section of posterosupenor aspect of calcaneus shows irregular (arrowheads).

synovial

lining

of bursa

(arrow)

and

adjacent

bone

erosion

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Fig. 11.-Rheumatoid arthritis: synovial cyst of hip. Transaxial CT scan delineates Iobulated synovial cyst (arrows) anterior to right hip. Observe extensive erosions of femoral neck.

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Fig. 12.-Rheumatoid arthritis: insufficiency fracture of calcaneus. Note vertically oriented, irregular bend of sclerosis (arrows).

wrists, and the elbow region usually are involved. Affected patients typically have severe disease, extensive abnormality of the cervical spine, and neurologic deficit, suggesting that neuroarthropathy may be one important factor in the pathogenesis of such osteolysis. Additional complications of rheumatoid arthritis include rheumatoid nodules, sinus tracts (fistulous rheumatism), vasculitis, and periarticular injury (e.g., rotator cuff disruption) [53].

Crystal

Deposition

Diseases

Three common crystal deposition diseases affect jointsmonosodium urate crystal deposition disease (gout), calcium pyrophosphate dihydrate (CPPD) crystal deposition disease, and calcium hydroxyapatite crystal deposition disease-although combinations of these three processes may occur in a single individual (e.g., mixed calcium phosphate crystal deposition disease). Of these disorders, CPPD crystal deposition disease has unique importance to the radiologist because it is often the radiologist who provides the initial diagnosis of this condition [73]. Although occurring as a hereditary disorder or in association with other processes (of which primary hyperparathyroidism and hemochromatosis are most important), CPPD crystal deposition disease generally is sporadic in nature, affecting middle-aged and elderly patients. Initial reports of CPPD crystal deposition disease stressed the occurrence of pseudogout attacks; however, this disease has the ability to mimic a variety of other conditions, including rheumatoid arthritis, osteoarthrosis, and neuroarthropathy [74]. Indeed, in the vast majority of patients, CPPD crystal deposition disease is asymptomatic and the diagnosis is suggested on the basis of typical abnormalities observed on radiographs obtained for unrelated reasons. Two such abnormalities are most characteristic: abnormal calcification and structural joint damage (pyrophosphate arthropathy). Calcification reflects the accumulation of CPPD crystals in various articular and periarticular tissues (Fig. 13). The mechanisms by which CPPD crystals are precipitated in these tissues is unknown [75]. CPPD crystal deposition generally is

first observed in cartilage, although deposits may be recognized in other articular structures, such as synovium and capsule, as well as in penarticular tissues, such as tendons and ligaments [74]. Rarely, the crystals are identified as distant sites, such as the dura mater and ligamentum flavum. In the cartilage, the earliest site of crystal deposition probably is about the chondrocyte Iacunae in the midzonal area [76]. Chondrocalcinosis is the term applied to the radiographic or pathologic documentation of cartilage calcification. Although chondrocalcinosis rarely can be related to the deposition of other types of crystals, such as calcium hydroxyapatite crystals, widespread cartilage calcification usually is indicative of CPPD crystal deposition. Chondrocalcinosis in CPPD crystal deposition disease is most common in the knees (Fig. 1 4), wrists (Fig. 1 5), symphysis pubis, elbows, and hips. Indeed, a radiographic survey consisting of frontal radiographs of the wrists, knees, and pelvis is an effective technique in screening for chondrocalcinosis or other forms of calcification in this disease [74]. Chondrocalcinosis may involve fibrocartilage or hyaline cartilage. Fibrocartilaginous calcification, which is most common in the menisci of the knee,

Fig. 13.-Calcium pyrophosphate dihydrate crystal deposition disease: sites of calcification. Doposits may be located in hyaline cartilage (1), fibrocartilage (2), synovial membrane (3), or joint capsule (4).

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Fig. 14.-Calcium pyrophosphate dihydrate crystal deposition disease: calcification in knee. Radiograph (A) and photograph (B) of sagittal section of knee reveal hyaline cartilage and fibrocartilage calcification as well as calcification in capsule and adjacent ligaments.

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Fig. 15.-Calcium pyrophosphate dihydrate crystal deposition disease: calcification in wrist. Radiograph (A) and photograph (B) of coronal section of wrist show chondrocalcinosis (arrow. heads) in torn triangular fibrocartilage; calcification of intraarticular ligaments, including the scaphoiunate ligament (arrow); joint-space narrowing and bone sclerosis in trapezioscaphoid space; and a lunate cyst.

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triangular cartilage of the wrist, anulus fibrosus of the intervertebral disk, and acetabular and glenoid labra, appears as thick, shaggy, irregular, radiodense areas, particularly within the central aspect of the joint cavity [73]. Hyaline cartilage calcification, which is most common in the wrist, knee, elbow, and hip, is thin and linear, creating a radiodense line that usually is parallel to and separated from the subjacent subchondral bone. Calcification within the synovial membrane in CPPD crystal deposition disease is observed most often in the wrist, knee, and metacarpophalangeal and metatarsophalangeal joints. Such calcification, which usually but not invariably is accompanied by chondrocalcinosis, leads to cloudlike radiodense shadows at the margins of the joint that may simulate idiopathic synovial osteochondromatosis [77]. Capsular calcification in this disease typically is observed in the elbow and metatarsophalangeal articulations, appearing as fine or irregular radiodense deposits that span the interosseous space. An association of capsular calcification with flexion contracture remains speculative [74]. Common locations of tendinous and ligamentous calcification in CPPD crystal deposition dis-

ease are the Achilles, triceps, supraspinatus, and quadriceps tendons, the calcifications appearing as thin and linear radiodense foci that extend for a considerable distance from the bone margin. These tendinous calcifications simulate those evident in calcium hydroxyapatite crystal deposition disease but may appear more extensive. Finally, soft-tissue deposition of CPPD crystals is most common about the elbow, wrist, and pelvis. Rarely, tumorous soft-tissue calcific collections resembling gouty tophi are observed [78]. Structural joint damage, or pyrophosphate arthropathy, is both common and characteristic in this disease (Fig. 16). Although the arthropathy usually is accompanied by abnormal calcification, this association is not universal [74]. Many of the radiographic alterations of pyrophosphate arthropathy, such as joint-space narrowing and subchondral sclerosis, resemble those of osteoarthrosis; however, careful analysis of pyrophosphate arthropathy reveals five features that, even in the absence of abnormal calcification, aid in its differentiation from osteoarthrosis [74, 79]: 1. Unusual articular distribution. -Although arthropathy is encountered in weight-bearing articulations, such as the hip

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Fig. 16.-Calcium pyrophosphate dihydrate crystal deposition disease: pyrophosphate arthropathy. A, Metacarpophalangeal joints. Collapse of bone (arrows) is noted about metacarpophalangoal joints. B, Wrist. In addition to chondrocalcinosis and synovial and llgamentous calcification (arrow. heads), note considerable narrowing of radlocarpal joint (arrow) and mldcarpal compartment with cyst formation and sclerosis. Also note stepladder appearance with proximal migraton of scaphoid and distal migration and tilting of the lunate.

and knee, it also is apparent in sites (such as the wrist, elbow, and glenohumeral joint) that are less commonly involved in osteoarthrosis. 2. Unusual intraarticular distribution-In certain articulations, the distribution of pyrophosphate arthropathy is distinctive. Examples of this include selective involvement of the radiocarpal or trapezioscaphoid region of the wrist, the patellofemoral compartment of the knee, and the talocalcaneonavicular articulation of the midfoot. 3. Prominent subchondral cyst formation-In pyrophosphate arthropathy, cysts may be numerous and large. They typically are subchondral in location; clustered in a group; and surrounded by sclerotic, smudged, and indistinct margins [80]. When large, they may fracture or simulate neoplasm [81]. 4. Destructive bone changes that are severe and progressive-Extensive and rapid subchondral bone collapse and fragmentation and single or multiple intraarticular osseous bodies may occur in pyrophosphate arthropathy. The resulting radiographic findings resemble those of neuroarthropathy. 5. Variable osteophyte formation-Although large and irregular bone excrescences are noted about some involved joints in CPPD crystal deposition disease, elsewhere significant structural articular damage may be unaccompanied by any osteophyte formation. The cause of pyrophosphate arthropathy is not clear. Despite strong evidence that calcification precedes arthropathy in many patients with CPPD crystal deposition disease, instances have been documented in which arthropathy develops in patients who have neither local (in the same joint) nor distant (in any joint) calcification on radiographic examination [73]. The absence of radiographically evident calcification in patients with CPPD crystal deposition disease and arthropathy may be related to the insensitivity of standard radiographic technique in showing small calcific collections or the disappearance of calcific foci with progressive destruction of the joint. The concept that the primary alteration of this disease is one of cartilage degeneration with secondary calcification provides a further explanation for the apparent absence of radiographically evident calcification in patients with pyrophosphate arthropathy. It has been suggested that crystal

deposition by tissue [82].

is favored deterioration

by age changes in normal cartilage or caused by preexisting joint disease

Osteoarthrosis Although the terminology applied to degenerative arthritis has not yet been established, at present degenerative joint disease is the best general phrase to describe degenerative alterations in any type of articulation (i.e., synovial, cartilaginous, or fibrous) [83]. The terms osteoarthrosis and osteoarthritis are reserved for degenerative disease of synoviumlined joints. Because in most of the affected articulations inflammatory changes are not pronounced, the suffix -osis appears more appropriate than -itis. The causes of this most common of synovial articular diseases apparently are diverse. Both systemic factors (such as genetics, advancing age, nutritional and metabolic status, physical activity and occupation) and local factors (such as trauma and preexisting articular disease or deformity) are important [83]. Traditionally, it has been thought that degenerative alterations begin in the articular cartilage with disruption of the cartilage matrix and degradation of the chondrocytes. However, an alternative theory emphasizes the initial role of subchondral bone abnormalities in the pathogenesis of osteoarthrosis [84]: It is suggested that thinness of the articular cartilage prevents it from assuming the major role in the dissipation of energy, and the force of impact loading is attenuated by subchondral bone as well as by joint capsule and muscular structures [85]. Overload produces microfractures of the trabeculae in the subchondral region; repair of these fractures subsequently leads to stiffness of the bone, a reduction in its shock-absorbing efficiency, and exposure of overlying cartilage to increasing force. No convincing evidence exists to suggest that alterations in the synovial membrane and joint lubrication are important in the initiation of degenerative joint disease. Osteoarthrosis in the weight-bearing articulations of the lower extremity leads to a predictable sequence of radiographic and pathologic events. It is apparent that either excess or diminished pressure is deleterious to cartilage, although the type and severity of the cartilaginous (and os-

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seous) response are different in the pressure and nonpressure segments of the articulation. The segmental nature of the abnormalities is one of the most characteristic features of osteoarthrosis. Initial abnormalities predominate in the pressure or stressed segment of the joint. Here, the cartilage appears discolored and thin and becomes roughened or coarsened [83]. Irregular crevices or cracks and larger regions of erosion also become evident. Denuded areas occur, uncovering the subchondral bone, and eventually, loss of entire segments of the cartilaginous coat may be observed. Vascular invasion may lead to numerous blood vessels in the subchondral marrow spaces and deeper portions of the original or regenerating cartilage [86]. The progressive loss of cartilage, evident on pathologic examination, accounts for one fundamental radiographic sign of osteoarthrosis: diminution of articular space. Characteristically, the loss of joint space predominates in the area of the articulation that has been subjected to excessive pressure. Thus, the joint-space narrowing is apparent in the superolateral aspect of an osteoarthritic hip and in the medial femorotibial space of an osteoarthritic knee. In certain sites, such as the interphalangeal and metacarpophalangeal joints of the hand and the sacroiliac joint, articular space diminution may be more uniform. With these few exceptions, however, the focal nature of the cartilaginous destruction and resulting loss of interosseous space are the

characteristics that distinguish osteoarthrosis from processes like rheumatoid arthritis that lead to diffuse chondral alterations. Two types of abnormality in the subchondral bone of the pressure segment of the joint represent important radiographic and pathologic characteristics of osteoarthrosis: eburnation and cyst formation. After cartilage loss, bone eburnation becomes evident in the closely applied osseous surfaces, apparently related to the deposition of new bone on preexisting trabeculae and to trabecular compression and fracture with callus formation [87]. The loss ofresilient cartilage heightens the abnormal stress on the hyperemic subchondral bone, leading to flattening and collapse of the articular surface. A close relationship exists between joint-space diminution seen on radiographs and bone sclerosis; although joint-space loss may initially occur in the absence of sclerosis, progressive obliteration of this space is accompanied by increasing prominence of bone sclerosis. The occurrence of subchondral cysts in the pressure segment of an osteoarthritic hip is well known. Such cysts are commonly multiple, of variable size, and pyriform. Communication of the cyst with the articular space is variable. The precise cause of these cysts is hotly debated, and two theories have emerged: synovial fluid intrusion and bone contusion (Fig. 17) [83]. According to the first of these theo-

B Fig. 17.-Osteoarthrosis: pathogenesis of subchondral cysts. Two fundamental theories are illustrated. A, Theory of synovial intrusion states that abnormal stress on cartilage (arrow) leads to cartilaginous degeneration. Synovial fluid is driven into subchondral bone through gaps in chondral surface and bone plate (arrowhead), producing cysts that initially communicate with joint. Subsequently, neck of cyst may become occluded with fibrous tissue. B, Theory of bone contusion also holds that cartilage loss occurs because of abnormal stress (arrow). Subsequently, fracture and vascular insufficiency of the bone itself (arrowhead) produce cysts that secondarily may communicate with the joint.

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ries, elevation of intraarticular pressure promotes intrusion of synovial fluid into the subchondral bone through gaps in the articular surface, with secondary resorption of trabeculae [88]. Alternatively, proponents ofthe theory of bone contusion suggest that cysts are the result of violent impact between opposing osseous surfaces that do not possess protective cartilage, which leads to cystic necrosis of bone [89, 90]. Histologic data can be found that support the simultaneous occurrence of both synovial fluid intrusion and bone contusion [54]. To this point, cartilaginous and osseous changes occurring in the stressed segment of the joint have been emphasized. One of the characteristic radiographic and pathologic alterations of osteoarthrosis, however, occurs in the nonpressure segment of the articulation. Here, osteophytes develop as a revitalization or reparative response of the remaining cartilage [83]. The features of conversion of cartilage to bone in osteoarthrosis resemble those accompanying normal endochondral ossification with vascular invasion and erosion of the subchondral bone plate and calcified cartilage, and with deposition of osseous tissue on the eroded surface. Although the precise location of osteophytes depends on the specific site of osteoarthrosis and the particular characteristics of the developing joint degeneration, the largest outgrowths tend to occur at the marginal regions, appearing as osseous ledges that hang from the parent bone. Here, vascularization of the subchondral bone marrow produces calcification of the adjacent cartilage and the inception of endochondral ossification. The developing osteophyte generally contains spongy trabeculae and fatty marrow, and it is covered with articular cartilage. As it grows, it leaves behind remnants of the original calcified cartilage (and subchondral bone plate), which serve as indicators of the location of the original joint surface (Fig. 18). These remnants can be identified not only histologically but radiographically as zones of increased density.

The appearance of osteophytes in the central or interior portions of the articular space is a less well recognized manifestation of osteoarthrosis [83]. Their pathogenesis again relates to endochondral bone formation; in central areas in which remnants of articular cartilage still exist, hypervascularity of subchondral bone stimulates endochondral ossification. The resulting excrescences, which are most pronounced in the hip and knee, are buttonlike or flat in configuration (Fig. 19) and often are demarcated at their bases by remnants of the original calcified cartilage. Central osteophytes lead to a bumpy articular contour on radiographic examination. When small and localized, the osteophytes may simulate the appearance of an intraarticular osseous body or cartilage calcification (chondrocalcinosis). In most cases, however, two features allow correct diagnosis: (1) continuity between the osteophyte and the underlying bone, and (2) ossification rather than calcification. In certain situations, the periosteal or synovial membrane may stimulate cartilage, leading to bone formation. This phenomenon is most characteristic in the femoral neck, where it is termed buttressing [91 , 92]. The medial aspect of the femoral neck typically reveals buttressing in osteoarthrosis of the hip (Fig. 1 8). Subsequently, continued bone formation may lead to a collar of osteophytes that extend partially or completely around the femoral neck. Buttressing of the femoral neck is not specific for osteoarthrosis; it has been observed in osteonecrosis, ankylosing spondylitis, and rheumatoid arthritis, and even with an adjacent osteoid osteoma. In certain locations, such as the interphalangeal joints of the hands, osteophytes may develop at the site of bone attachment of the joint capsule. In the hands, the resulting excrescences extend proximally, resembling the wings of a sea gull (sea-gull sign), and account for the clinically detectable Heberden and Bouchard nodes that are characteristic of the disease.

Fig. 18.-Osteoarthrosis: osteophyte formation. Photograph (A) and radiograph (B) of coronal section of femoral head reveal prominent osteophyte on its medial aspect (arrowheads). Observe curvilinear radiodense line that exists at base of osteophyte. Subchondral cysts (arrows) in lateral aspect of femoral head and buttressing of medial aspect of femoral neck are apparent also.

Fig. 19.-Osteoarthrosis: osteophyte formation. Photograph of distal femoral articular surface reveals buttonlike bone excrescence (arrow) representing central osteophyte. Such an outgrowth can be misinterpreted as an intraarticular body during radiographic examination. Marginal osteophytes also are apparent.

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Abnormalities of the synovial membrane are not prominent in most cases of osteoarthrosis. In the presence of severe cartilaginous and osseous alterations, however, the changes in the synovial membrane may become more severe, with the occurrence of large villi that extend between the bone surfaces [83]. One factor that may aggravate synovial inflammation in osteoarthrosis is cartilaginous or osseous debris that has originated from the articular surfaces and has become embedded in the synovial membrane, acting as a local irritant. Additional factors that may be responsible for synovial inflammation in this disease are crystal deposition (CPPD or calcium hydroxyapatite), hemorrhage, and amyloidosis [9395]. Although the precise relationship of amyloid accumulations and osteoarthrosis is not clear, local deposits of amyloid have been identified in many constituents of osteoarthritic joints, including the articular cartilage, fibrocartilage, capsule, and synovial membrane. Rarely, synovial abnormalities in osteoarthrosis may become so severe that they resemble those occurring in rheumatoid arthritis. In the interphalangeal joints of the hand (and, rarely, the foot), such synovial inflammation is present in inflammatory (erosive) osteoarthrosis (osteoarthritis) [96-98]. In this disease, accurate radiographic diagnosis is provided by the combination of bone proliferation and bone erosion. The erosions predominate in the central portions of the articulation in the form of sharply marginated, etched defects [83]. Although the pathogenesis of such erosions is not certain, they differ in location from the marginal osseous erosions that characterize other inflammatory diseases, such as rheumatoid arthritis. The central erosions of inflammatory osteoarthritis may relate to collapse or pressure atrophy of subchondral bone rather than to direct attack of inflamed synovial tissue on bone.

pronator 1 1 . Bledsoe

quadratus muscle: a radiologic RC, Izenstark JL. Displacement

sign. Radiology 1964;82:879-886 of fat pads in disease and injury

ACKNOWLEDGMENT I thank W. B. Saunders

reproduction of illustrations

Co. of Philadelphia,
from Diagnosis

PA, for allowing

and Joint
,

the

of Bone

Disor-

ders, 1988, 2nd ed., edited by D. Resnick and G. Niwayama 73, 83].

[1 53,

REFERENCES
1 . Resnick D, Niwayama G. Articular anatomy and histology. In: Resnick D, Niwayama G, eds. Diagnosis of bone and joint disorders, 2nd ed. Philadelphia: Saunders, 1988:631-644 2. Davies DV. The structure and functions of articular synovial membrane. Br MedJ 1950;1:92-95 3. Hasselbacher P. Structure of the synovial membrane. C/in Rheum Dis 1981;7:57-69 4. Ghadially FN. Structure and function of articular cartilage. C/in Rheum Dis 1981;7:3-28 5. Jaffe HL. Metabolic, degenerative and inflammatory diseases of bones and joints. Philadelphia: Lea & Febiger, 1972:80 6. Bamett CH, Davies DV. MacConaill MA. Synovia/ joints: their structure and mechanics. Springfield, IL: Thomas, 1961 7. Wilkinson A. Traumatic haemarthrosis of the knee. Lancet 1965;2:13-.15 8. Weinberger A, Schumacher HR. Experimental joint trauma: synovial response to blunt trauma and inflammatory reaction to intraarticular injection of fat. J Rheumato/ 1981;8:380-389 9. Butt WP, Lederman H, Chuang S. Radiology of the suprapatellar region. C/in Radio/ 1983;34:511-522 10. MacEwan DW. Changes due to trauma in the fat plane overlying the

of the elbow: a new radiographic sign. Radiology 1959;73:717-724 1 2. Weston WJ. Joint space widening with intracapsular fractures in joints of the fingers and toes of children. Austra/as Radio! 1971;15:367-371 13. Gkxiiori JM, Grossman RI. Mechanisms responsible for the MR appearance and evolution of intracranial hemorrhage. RadioGraphics 1988;8:427-440 14. Gregg JR, Nixon JE, DiStefano V. Neutral fat globules in traumatized knees. C/in Orthop 1978;132:219-224 15. Lawrence C, Seife B. Bone marrow in joint fluid: a clue to fracture. Ann Intern Med 1971;74:740-742 16. Arger PH, Oberkircher PE, Miller WT. Upohemarthrosis. AiR 1974;121 :97-1 00 17. Yousefzadeh DK, Jackson JH Jr. Lipohemarthrosis of the elbow joint. Radiology 1978;128:643-645 18. Nicholas JA, Freiberger RH, Killoran PJ. Double contrast arthrography of the knee. Its value in the management of 225 knee derangements. J Bone Joint Surg [Am) 1970;52-A:203-220 19. BeIlon EM, Keith MW, Coleman PE, Shah ZR. Magnetic resonance imaging of internal derangements of the knee. RadioGraphics 1988;8:95-1 18 20. Mink JH, Levy T, Crues JV Ill. Tears of the anterior cruciate ligament and menisci of the knee: MR imaging evaluation. Radiology 1988;167: 769-774 21 . Herman U, Beltran J. Pitfalls in MR imaging of the knee. Radiology 1988;167:775-781 22. Tyrell RL, Gluckert K, Pathna M, Medic MT. Fast three-dimensional MR imaging of the knee: comparison with arthrography. Radiology 1988;166:865-872 23. Haggar AM, Froelich JW, Hearshen DO, Sadasivan K. Maniacal abnormalities of the knee: 3DFT fast-scan GRASS MR imaging. AiR 1988;150: 1341-1344 24. Resnick D, Andre M, Kerr R, Pineda C, Guerra J, Atkinson D. Digital arthrography of the wrist: a radiographic-pathologic investigation. AiR 1984;142:1 187-1190 25. Levinsohn EM, Palmer AK, Coren AB, Zinberg E. Wrist arthrography: the value of the three compartment injection techniques. Skeletal Radio! 1987;16:539-544 26. Kaplan PA. Computed tomography vs arthrography in the evaluation of the temporomandibularjoint. Radiology 1984;152:825-827 27. Katzberg RW, Dolwick ME, Helms CA, Hopens T, Bales DJ, Coggs GC. Arthrotomography of the temporomandibular joint. AJR 1980;1 34: 995-1003 28. Loft CW, Wilson DJ, Juniper RP. Temporomandibular joint arthrography: dynamic study by videorecording. Clin Radiol 1988;39:73-76 29. Thompson JR, Chnstiansen EL, Hasso AN, Hinshaw DB. The temporomandibular joint: high-resolution computed tomographic evaluation. Radiology 1984;150: 105-110 30. Manzione JV, Seltzer SE, Katzberg RW, Hammerschalg SB, Chiango BF. Direct sagittal computed tomography of the temporomandibular joint. AJNR 1982;3:677-679 31 . Westesson P-L, Katzberg RW, Taflents RH, Sanchez-Woodworth RE, Svensson SA. CT and MR of the temporomandibular joint: comparison with autopsy specimens. AJR 1987;148: 1165-1171 32. Kaplan PA, Tu HK, Williams SM, Lydiatt DD. The normal temporomandibularjoint. MR and arthrographic correlation. Radiology 1987;165: 177-1 78 33. Schellhas KP, Wilkes CH, Fntts HM, Omlie MR, Heithoff KB, Jahn JA. Temporomandibularjoint: MR imaging of internal derangements and post34. 35. operative changes. AiR 1988;150:381-389 Burnett KR, Davis CL, Read J. Dynamic display of the temporomandibular joint meniscus using fast-scan MR imaging. AiR 1987;149:959-962 Hardy CJ, Katzberg RW, Frewy RL, Szumowski J, Totterman 5, MUeller OM. Switched surtace coil system for bilateral MR imaging. Radiology 1988;167:835-838 Wilk RM, Harms SE. Temporomandibular joint. Multislab, three-dimensional Fourier transformation MR imaging. Radiology 1988;167:861-863 WaIter E, HUls A, Schmelzle R, Kiose U, KUper K, Kalender WA. CT and MR imaging of the temporomandibular joint. RadioGraphics 1988;8: 327-348 Bankart ASB. The pathology and treatment of recurrent dislocation of the shoulderjoint. Br J Surg 1938;26:23-29 Turkel SJ, Panio MW, Marshal JL, Girgis FG. Stabilizing mechanism preventing anterior dislocation of the gleno-humeral joint. J Bone Joint

36. 37.

38. 39.

AJR:151,

December

1988

DISORDERS

OF SYNOVIUM-LINED

JOINTS

1093

Surg [Am] 1981;63-A:1208-1217 Rafli M, Firooznia H, Golimbu C, Minkoff J, Bonamo J. CT arthrography of capsular structures of the shoulder. AJR 1986;146:361-367 41 , Rafli M, Firooznia H, Bonamo JJ, Minkoff J, Goiimbu C. Athletic injuries: 40. 42. CT arthrographic findings. Radiology 1987;162:559-564 Kneeland JB, Middleton WD, Carrera GF, et al. MR imaging ofthe shoulder: diagnosis of rotator cuff tears. AJR 1987;149:333-337 Seeger LL, Gold RH, Bassett LW, Ellman H. Shoulder impingement syndrome: MR findings in 53 shoulders. AIR 1988;150:343-347 Kieft GJ, Bloem JL, Rozing PM, Obermann WR. Rotator cuff impingement syndrome: MR imaging. Radiology 1988;166:211-214 Kieft GJ, Bloem JL, Rozing PM, Obermann WR. MR imaging of recurrent anterior dislocation of the shoulder: comparison with CT arthrography. AJR 1988;150:1083-1087 (leo T, Hamabuchi M. Hip pain caused by cystic defomation of the labrum acetabulare. Arthritis Rheum 1984;27:947-950 Ikeda T, Awaya G, Suzuki 5, Okada Y, Tada H. Tom acetabular labrum in young patients. Arthroscopic diagnosis and management. J Bone Joint Surg [Br] 1988;70-B:13-16 Lagier R, Seigne JM, Mbakop A. Juxta-acetabular mucoid cyst in a patient with osteoarthritis of the hip secondary to dysplasia. Int Orthop 1984;8: 19-23 McBeath AA, Neidhart DA. Acetabular cyst with communicating ganglion. A case report. J Bone Joint Surg [Am] 1976;58-A:267-269 Milgram JW, Rogers LF, Miller JW. Osteochondral fractures: mechanisms of injury and fate of fragments. AJR 1978;130:651-658 Heare MM, Gillespy T Ill, Bittar ES. Direct coronal computed tomography arthrography of osteochondritis dissecans of the talus. Skeletal Radiol 1988;17:187-189 Mesgarzadeh M, Sapega AA, Bonkdarpour A, et al. Osteochondritis dissecans: analysis of mechanical stability with radiography, scintigraphy, and MR imaging. Radiology 1987;165:775-780 Resnick D, Niwayama G. Rheumatoid arthritis and the seronegative spondyloarthropathies: radiographic and pathologic concepts. In: Resnick D, Niwayama G, eds. Diagnosis of bone and joint disorders, 2nd ed. Philadelphia: Saunders, 1988:894-953 Resnick D, Niwayama G, Coutts R. Subchondral cysts (geodes) in arthritic disorders: pathologic and radiographic appearance of the hip joint. AiR 1977;128:799-806 Resnick D. Gout-like lesions in rheumatoid arthritis (letter). AJR 1976;127:1062 Resnick D, Gmelich JT. Bone fragmentation in the rheumatoid wrist: radiographic and pathologic considerations. Radiology 1975;1 14:31 5-321 Fassbender HG. Pathology of rheumatic disease. New York: SpringerVerlag, 1975:79 Paison EG, Goodfellow JW. Preankylosing spondylitis. Histopathological report. Ann Rheum Dis 1975;34:92-97 Ball J. Enthesopathy ofrheumatoid and ankylosing spondylitis. Ann Rheum Dis 1971;30:213-223 Resnick D, Niwayama G. On the nature and significance of bony proliferation in rheumatoid variant disorders. AiR 1977;129:275-278 Genovese GR, Jayson MIV, Dixon A St J. Protective value of synovial cysts in rheumatoid knees. Ann Rheum Dis 1972;31 :179-1 82 Rauschning W, Undgren PG. The clinical significance of the valve mochanism in communicating popliteal cysts. Arch Orthop Trauma Surg 1979;95:251-256 Lukes PJ, Heberts P, Zachrisson BE. tJtrasound in the diagnosis of popliteal cysts. Acta Radio! [Diagn] (Stockh) 1980;21 :663-665 Abdel-Dayem HM, Barodawala YK, Papdemetriou T. Scintigraphic arthrography. Comparison with contrast arthrography and future applications. C/in NucI Med 1982;7:516-522 Lee KR, Tines SC, Price HI, DeSmet AA, Neff JR. The computed tomographic findings of popliteal cysts. Skeletal Radiol 1983;10:26-29 Hull RG, Rennie JAN, Eastmond CJ, Hutchison JMS, Smith FW. Nuclear magnetic resonance (NMR) tomographic imaging for popliteal cysts in rheumatoid arthritis. Ann Rheum Dis 1984;43:56-59 Rosenspire KC, Kenedy AC, Steinbach J, Blau M, Green FA. Investigation of the metabolic activity of bone in rheumatoid arthritis. J Rheumatol 1980;7:469-473 Helfgott 5, Rosenthall L, Esdaile J, Tannenbaum H. Generalized skeletal response to 99m technetium methylene diphosphonate in rheumatoid arthritis. J Rheumatol 1982;9:939-941 Steven MM, Sturrock RD, Fogelman I, Smith ML. Whole body retention of

diphosphonate 70.

in rheumatoid

arthritis.

J Rheumatol

1982;9:873-877

71

Reid DM, Kennedy NS, Smith MA, Tothill P. Nuki G. Total body calcium in rheumatoid arthritis: effects of disease activity and corticosteroid treatmont. Br Med J 1982;285:330-332 Schneider R, Kaye JJ. Insufficiency and stress fractures of the long bones occurring in patients with rheumatoid arthritis. Radiology 1975;116: 595-599 Resnick D, Cone R. Pathologic fractures in rheumatoid arthritis: sites and mechanisms. RadioGraphics 1984;4:549-562 Resnick D, Niwayama G. Calcium pyrophosphate dihydrate (CPPD) crystal deposition disease. In: Resnick D, Niwayama G, eds. Diagnosis of bone andjoint disorders, 2nd ed. Philadelphia: Saunders, 1988: 1672-1 732 Resnick D, Niwayama G, Goergen TG, et al. Clinical, radiographic, and pathologic abnormalities in calcium pyrophosphate dihydrate crystal deposition disease (CPPD): pseudogout. Radiology 1977;122: 1-15 Heam PR, Russell GG. Formation of calcium pyrophosphate crystals in vitro: implications for calcium pyrophosphate crystal deposition disease (pseudogout). Ann Rheum Dis 1980;39:222-227 Reginato AJ, Schumacher HR, Martinez VA. The articular cartilage in familial chondrocalcinosis. Light and electron microscopic study. Arthritis Rheum 1974;17:977-992 Ellman MH, Krieger Ml, Brown N. Pseudogout mimicking synovial chondromatosis. J Bone Joint Surg [Am] 1975;57-A:863-865 Ling D, Murphy WA, Kyriakos M. Tophaceous pseudogout. AdA 1982;138:162-165 Utsinger PD, Zvaifler NJ, Resnick D. Calcium pyrophosphate dihydrate deposition disease without chondrocalcinosis. J Rheumatol 1975;2: 258-264 Martel W, McCarter DK, Solsky MA, et al. Further observations on the arthropathy of calcium pyrophosphate crystal deposition disease. Radiology 1981;141:1-10 Weinberg 5, Scott RA. Giant deode (subchondral cyst) in calcium pyrophosphate deposition disease of the wrist. J Can Assoc Radio! 1981;32:171-175 Dieppe PA. Crystal deposition and inflammation. Q J Med 1984;53: 309-316 Resnick D, Niwayama G. Degenerative disease of extraspinal locations. In: Resnick D, Niwayama G, eds. Diagnosis of bone and joint disorders, 2nd ed. Philadelphia: Saunders, 1988:1364-1479 Radin EL, Paul IL, Rose RM. Role of mechanical factors in pathogenesis of primary osteoarthritis. Lancet 1972;1 :519-522 Radin EL. The physiology and degeneration ofjoints. SeminArthritis Rheum 1972;2:245-257 Trueta J. Studies of the development and decay of the human frame. Philadelphia: Saunders, 1968:335 Todd RC, Freeman MAR, Pirie CJ. Isolated trabecular fatigue fractures in the femoral head. J Bone Joint Surg [Br] 1972;54-B:723-728 Landells JW. The bone cysts of osteoarthritis. J Bone Joint Surg [Br] 1953;35-B:643-649 Rhaney K, Lamb DW. The cysts of osteoarthritis of the hip. A radiological and pathological study. J Bone Joint Surg [Br] 1955;37-B:663-675 Ondrouch AS. Cyst formation in osteoarthritis. J Bone Joint Surg [Br] 1963;45-B:755-760 LLoyd-Roberts GC. The role of capsular changes in osteoarthritis of the hip joint. J Bone Joint Surg [Br] 1953;35-B:627-642 Martel W, Braunstein EM. The diagnostic value of buttressing of the femoral neck. Arthritis Rheum 1978;21 :161 -1 66 Egan MS, Goidenberg DL, Cohen AS, Segal D. The association of amylid deposits and osteoarthritis. Arthritis Rheum 1982;25:204-208 Ladefoged C. Amyloid in osteoarthritic hip joints: deposits in relation to chondromatosis, pyrophosphate, and inflammatory cell infiltrate in the synovial membrane and fibrous capsule. Ann Rheum Dis 1983;42: 659-664 Vigorita VJ. Pigmented villonodular synovitis-like lesions in association with rare cases of rheumatoid arthritis, osteonecrosis, and advanced degenerative joint disease: report of five cases. Clln Orthop 1984;183: 115-121 Cram DC. Interphalangeal osteoarthritis characterized by painful inflammatory episodes resulting in deformity of the proximal and distal articulations. JAMA 1961;175:1049-1053 Kidd KL, Peter JB. Erosive osteoarthritis. Radiology 1966;86:640-647 Utsinger PD, Resnick D, Shapiro RF, Wiesner KB. Roentgenoiogic, immunologic and therapeutic study of erosive (inflammatory) osteoarthritis. Arch Intern Med 1978;138:693-697

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