877

Review

Pigmented Villonodular Synovitis of Synovial Joints:

Clinical, Features Pathologic, and Radiologic

Robert

H. Dorwart12 K. Genant1 William H. Johnston4 James M. Morris3

Harry

of pigmented villonodular synovltis presentation of this unusual entity is a noncalcified capsular soft-tissue mass of the knee, without bony abnormalities. When pigmented villonodular synovitis occurs in other joints, it is often accompanied by cystic bone erosions. This important radiographic finding might mislead one to an improper diagnosis of neoplasia or infection. This review reveals insufficient emphasis in the radiologic literature on the high incidence of bone lesions in joints affected by pigmented villonodular synovitis. A mechanism for the development of bone cysts is proposed. Clinical, pathologic, radiologic, and therapeutic considerations are discussed.
of large synovial joints are presented. The typical plain-film

The clinical, pathologic,

and radiologic

features

Received

October

28,

1983;

accepted

after re-

vision May 30, 1984.

The opinions or assertions contained herein are the private views of the authors and are not to be construed as official or reflecting the views of the Department of Defense or the LfrtifOrmed Services lkiiversity of the Health Sciences. I Department of Radiology, University of Californb School of Medicine, San Francisco, CA 94143.

Pigmented villonodular synovitis (PVNS) was defined by Jaffe et al. in 1941 [1]. They emphasized the histologic similarity of PVNS involving the synovia of joints to the tenosynovial tumorlike lesions of bursae and tendon sheaths. They further indicated that the origin of such abnormalities is probably inflammatory, rather than neoplastic, and classified the synovial lesions into localized nodular and diffuse forms. Since that landmark article, several species of patients with PVNS of synovia have been reported [2-8], all confirming the overwhelming occurrence of this entity in the knee joint (about 80% of cases). Other joints that may be affected by PVNS, in decreasing order of frequency, include the hip, ankle, small joints of the hands and feet, shoulder [2, 4, 6, 9-1 1 ], and elbow [12-14]. The high incidence of bone lesions associated with PVNS is well documented in the orthopedic literature [6, 7, 9, 1 2-1 8], but only two [2, 1 9] of several articles in the radiologic literature [9, 20-24] stress this important association. We review the clinical, pathologic, and radiologic features of this unusual entity. The incidence of bone lesions in large synovial joints has been tabulated. (The small joints of the hand, wrist, and feet have been excluded from this analysis, as have been all cases with primary tendon-sheath involvement.) Pertinent pathologic and radiologic illustrative material is presented, and a mechanism for the development of bone erosions and cysts is proposed.

Address reprint requests to H. K. Genant. 2 Present address: Department of Radiology, tkiiformed Services lkiiversity of the Health Sdences, School of Medicine, Bethesda, MD 20814. 3 Department ofOrthopaedic Surgery, lhiiversity of California School of Medicine, San Francisco, CA
94143.
4

Clinical

Features case of PVNS

Department

of Pathology,

Uiiversity

of Califor-

nia School of Medicine, San Francisco, CA 94143. Current address: Department of Pathology. Kaiser Foundation Hospital, Los Angeles, CA 90027. AJR

143:877-885, October 0361 -803x/84/i 434-0877

C American Roentgen

1984

Ray SOciety

is found in a young adult, age 20-50, equally likely a duration of symptoms and signs before presentation is 2-3 years. Pain, limitation of motion, and minimal to mild joint swelling, heat, and tenderness are the most common presenting complaints. The disease is usually slowly progressive. Monarticular involvement of the knee occurs in about 80% [4, 7, 25]. Involvement of more than one joint is rare [26, 27]. Laboratory findings including blood count and sedimentation rate are normal, and joint fluid is most often serosanguineous [2, 4, 22, 25, 26]. The clinical manifestations of PVNS are more variable than the above descriptions

The usual

man or woman. The average

878

DORWART

ET AL.

AJR:143,

October

1984

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Fig. 1 and contains giant cell
solid

-Pathology of early PVNS. A, Hyperplastic synovium consists of fingerlike masses of fibrous stroma. H and E, x32. B, Fibrous stroma foamy macrophages, lymphocytes, and plasma cells. Multinucleate lies at upper left, and golden brown hemosiderin lies within cytoplasm

of synovial hemosiderin reaction, xl ingrowth of

lining cells and macrophages. H and E, x200. c, Blue-staining lies free in stroma or in cytoplasm of macrophages. Prussian blue 30. D, Rice body consists of mass of fibnn showing peripheral flbroblasts, most apparent at upper right. H and E, x32.

would indicate. As outlined by Byers et al. [4], the age range of patients affected by this entity is 1 1 -70 years, with peak incidence in the 21-30 year group. The duration of symptoms ranges from 6 months to as long as 25 years [28]. Pain is the most frequent complaint; it is characteristically severe and incapacitating during exacerbations of swelling, and dull or absent during periods of presumed disease inactivity. Swelling or a synovial mass is often noted when the knee, ankle, and elbow are involved but is unusual as a presenting complaint when the shoulder or hip are affected by PVNS [3, 5, 6, 12, 1 5, 28]. Limitation of motion may occur in about one-half of

patients [28], and a mechanical locking phenomenon is often described by those patients having knee involvement with the localized or nodular variety of PVNS [29]. Only occasionally is a history of trauma elicited [3, 5, 28, 30].

The findings

on physical

examination

correspond

to the

presenting complaints and stage of disease activity. These include limitation of motion, which is usually minimal but which may be severe; joint enlargement, due to joint effusion and/ or synovial masses; and tenderness on palpation [3, 5, 6, 12,

28, 30]. The joint effusion

occasionally clear

is usually

serosanguineous

but is

[1 1], and joint

fluid has a high cholesterol

AJR:143,

October

1984

PIGMENTED

VILLONODULAR

SYNOVITIS

879

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-.-.

:.

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..

...
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..

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;
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..-

. ..-.

.:m-=
-

:-.-..

.
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I

Fig. 2. -Pathology of late PVNS. A. Synovium retains papillary configuration but is considerably more fibrous and less cellular. H and E, x32. B, Within fibrous stroma are perivascular aggregates of mononuclear cells and golden-

brown hemosidermn pigment. Note absence of foamy

acterize early lesion. H and E, x200.

macrophages

that char-

content, although cholesterol [12].

the

patient

does

not

have

high

serum

Pathology The typical pathologic features of PVNS are indicated by the name [1 28, 31 -36]. Grossly, the synovium has a mossy or nodular texture, spongy cut surfaces, and a rusty, redbrown, or yellow-brown color. Microscopically, the synovium is composed of fingerlike or rounded masses of fibrous stroma covered by hyperplastic lining cells (fig. 1A). Large numbers of foamy macrophages in the stroma account for the yellow coloration (fig. 1 B), and the rusty or brown color is due to hemosiderin deposits in the stroma and in the cytoplasm of macrophages and synovial lining cells (fig. 1 C). This hemosiderin is a breakdown product of hemoglobin, and its presence signifies old hemorrhage. Multinucleate giant cells (fig. 1 B) vary in number, are derived from macrophages and synovial lining cells, and may also contain hemosiderin. Although PVNS is considered a benign inflammatory process, mitotic figures with a normal configuration are easily found in the proliferating fibroblasts, macrophages, and synovial lining cells. Masses of fibrin often adhere to the synovial surfaces or may lie free in the spaces between surfaces. Rice bodies consist of larger, rounded masses of fibrin that lie free in the joint-space (fig. 1 D). These rice bodies may undergo organization, with ingrowth of fibroblasts and capillaries, which convert the fibrin to fibrous tissue. Articular cartilage and the underlying bone are unremarkable in this active phase of PVNS. The pathologic spectrum of PVNS parallels the clinical features. With time, the cellularity of the synovium diminishes and the degree of fibrosis increases (fig. 2). Although the villi
,

and nodules of synovium shrink as this occurs, the villonodular pattern evident in the earlier stages persists. Thus, even in the late stages, PVNS is sufficiently distinctive to permit differentiation from the relatively mild changes evident with
degenerative arthritis.

As the stroma phages decrease

Lymphocytes and

becomes more fibrous, the foamy macroin number and may ultimately disappear.
plasma cells remain in lesser numbers,

often
persists,

lying

in a perivascular distribution. Hemosiderin also although much of the pigment present initially usually

disappears.

Bone The

Changes radiographic
with

of PVNS affectation is the localized nodular variety of PVNS, the plain films will usually be normal. Bone mineralization is normal with nodular and diffuse varieties of PVNS. Involvement by the diffuse type will result in noncalcified periarticular (intracapsular) soft-tissue masses (figs. 3 and 4). There may be small erosions of the subchondral bone in the early phases of this disease (fig. 4). Bone changes begin with erosion of the articular cartilage, often near the chondroosseous junction, with subsequent extension of the process through the cartilage and the underlying cortical bone into the cancellous bone. This gives rise to the juxtaarticular cysts evident radiographically, which are surrounded by fibrous tissue. Some of these bone changes are illustrated in our other report [1 11. Other large synovial joints besides the knee can be involved. The hips are the next most frequently involved joints.
correlate the pathology just described. If the

findings

in the

active

phase

880

DORWART

ET AL.

AJR:143,

October

1984

Fig.
woman.

3.-Typical
Obvious

PVNS
synovial

of

knee in 22-year-old
masses with

soft-tissue

lobulated margins. No calcifications bones are grossly normal.

or ossifications;

Fig. 4.-Advanced PVNS of knee in 16-year-old girl with 10-year history of intermittent pain and joint swelling. Displacement of suprapatellar muscle-fat planes secondary to poorly defined synovial masses. Bony mineralization is normal, and no calcification is seen. Irregular cartilage loss of medial and patellofemoral compartments is accompanied by subchondral lucencies (arrows).

TABLE

1 : Summary of Reports of Pigmented Villonodular Synovitis, Diffuse and Nodular Varieties, Involving Large Synovial Joints
Report

TABLE

2: Distribution
Joint

of Bone Lesions

in PVNS
Erosive Bone Lesions. no. (%)

Knee

Hip

Shoulder

Elbow
. . . . . . . 2(i) i(i) i(i) . . . . . . . . . . . . . .

Ankle

Total No of Cases

[2] [3J
[5] [6] [9]

28(6)
. . . . . . . .

7(7)
4(2)

1(0)
. . . . . .

Hip
i(0) ... ... 1(i) ... ...

40

37(93)

Shoulder
Elbow Ankle Subtotal (without knee)
. . .

8
8 9 65

6 (75)
5 (63) 5 (56) 53 (82)

i9(2) 1(1)
. . . . . .

4(4) 4(4)
. . . . . .

1(i)
2(i) 2(2)

. .

..

1101

[11], this report [i2j

. .

2(0)
. . . .

2(2)
1(i)

2(2)
. . . . . . . . .

1(i)
... ... . .

Knee
Total
Note-Summary

81
i46
of data from table 1.

2i (26)
74(5i)

[13]

2(2)
. . .

2(2)
. . .

[i4J

us]
1181
[19j [20]
[2iJ
. . . . .

3(3)
. . . . . .

3(3)
4(4) 2(i) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2(1) . . . . . . 1(0) 1(i) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ... ... ... ... ... ... ... i(0) i(0) ... 2(i) . . . . 2(2) . . . . . . . . . . . . . .

4(0)

1221 [24]
[26]

1(0) 5(0)
2(0)

3(3)
1(0)
. . .

i(i)
. 1(1) . . 1(1)

127]
(30]

[36] 1371 1381 139]

[40j

i(0)
. . .

3(0)
. . . . . . . . . . . .

1(i) 1(1)
1(1) . . . . i(i) .

[42] [43J (44] [45]

[46J [47]

14i]
. . . . .

2(0)

1(i)
i(1)

1(1)
. . .

i(i)

Note -Only of radiographic

those reports that include photoradiographs findings are listed. Numbers in parentheses with bone cysts and/or cortical erosions.

or contain detailed descnptsons indicate total number of joints

The shoulder, ankle, and elbow are occasionally involved. Table 1 is a summary of English-language reports on PVNS, with categorization by affected joint. We excluded lesions that primarily affected periarticular tendons and those affecting the small joints of the hand, wrist, and feet, since the latter lesions are nearly always tendinous in origin. It is evident that the incidence of bone changes is significant in joints other than the knee. However, an accurate determination of the incidence of bone changes is difficult to achieve, since not all published series provide sufficient information. This tabulation probably includes strong bias toward cases with bone lesions, since examples of PVNS without bone lesions are probably less likely to be reported. Byers et al. [4] reported a 15% incidence of bone lesions but did not provide information regarding specific joints affected by PVNS. Similarly, of 1 14 cases, Jones et al. [48] reported 1 1 (1 0%) with bone changes. Only one (4%) of 24 patients whose knee joints were affected with PVNS had bone cysts on plain films, as reported by Johansson et al.

AJR:143,

October

1984

PIGMENTED

VILLONODULAR

SYNOVITIS

881

Fig. 5.-Bone erosion of PVNS of hip in 25-year-old man. Large space is preserved, and no hypertrophic bone changes are evident.

cystic

erosion

(arrows)

of anterolateral

aspect

of neck

and inferior

part of head of femur. Joint-

Fig. 6.-Chronic

PVNS

of ankle

in 25-year-old

man.

Lobulated

articular

soft-tissue

mass

accompanied

by subchondral

lucencies

in talus and distal

fibula

(arrows).

[8]. These three reports contain neither reproductions nor detailed descriptions of radiographs. In reports where photoradiographs and/or detailed descriptions of radiographs were provided, bone changes were more frequent. Tables 1 and 2 summarize this information. Of l46joints involved with PVNS, 74 (51 %) showed bone changes. Of 81 knees, 21 (26%) had cystic bone lesions, usually involving the tibial plateau and/or distal femoral condyles (fig. 4). An explanation for the less frequent involvement of the juxtaarticular bones of the knee is that the knee joint capsule is normally very capacious. The suprapatellar bursa provides a large space in which the tumorlike growths of PVNS may develop and into which space the joint effusions are spread [1 2, 21 ]. In combined series of joints other than the knee, 42 (84%) of 50 cases demonstrated bone lesions. These bone changes are mostly cystic lucent

defects usually having thin sclerotic rims [2, 3, 6, 26, 37]. The lucencies are usually 1 -2 cm in diameter and are sometimes Iobulated. Bone cysts often develop when the hip is involved (table 1 fig. 5). Similar juxtaarticular lucencies can be seen at the shoulder or ankle (fig. 6). Minor subarticular cortical erosions are occasionally seen (figs. 4 and 6). More advanced cortical erosions and bone destruction are rare (fig. 7) [2, 14, 18, 38] and probably are manifestations of end-stage joint disease. Only four cases are recorded where the progression of bone changes is documented radiographically [6]. All of these individuals had hip involvement manifested by joint-space narrowing and deformity of the femoral head. As pointed out by Schajowicz and Blumenfeld [1 7], no significant hypertrophic spurring occurred despite the severe femoral head
,

882

DORWART

ET AL.

AJR:143,

October

1984

Fig. 7.-Advanced
osteophyte formation.

destructive

arthropathy

of PVNS

in 35-year-old

woman.

Erosive

changes

in acetabulum,

femoral

head,

and femoral

neck.

No buttressing

or

deformity. Our analysis of reproductions of radiographs in reports cited in table 1 confirms that impression: Other cases
of significant femoral or humeral deformity and joint-space

narrowing without hypertrophic spurring were found [2, 3, 6, 1 3, 26, 38-40]; however, only six cases with associated
spurring are reported (one hip, four knees) [2, 1 5, 41]. Our

own material also confirms this observation: Despite moderately severe femoral or humeral head deformity, minimal or no hypertrophic spurring or buttressing is seen (fig. 7) [1 1]. Joint-space narrowing is an unusual manifestation of PVNS [2, 6, 1 8] and probably reflects superimposed degenerative joint disease. It is also very unusual to have more than one joint involved [1 9, 26, 27, 39]. Rare cases of extension into the retroperitoneal space via the psoas bursa [26, 37] and the iliopectineal bursa [1 5] have been reported. Calcification in the soft-tissue component was noted in only one case in the literature we reviewed [42]. Isolated cases of involvement of the joints of Luschka of the cervical spine [49], of the lumbar facet joints [50, 51 ], and of the temporomandibular joint [52] have been reported. Radiography Routine radiographic evaluation of PVNS has been confined to plain films and occasionally arthrograms. The probable reason for the relatively infrequent use of arthrography for evaluating this disorder is the nonspecificity of plain film findings. Reported findings on knee arthrograms include single or multiple nodular filling defects within the capsule of the affected joint and normal or minimally abnormal articular cartilage. Aspirated joint fluid is usually serosanguineous, and joint capacity is normal [5, 9, 1 8, 22, 24, 39, 44, 48]. We have
performed shoulder arthrography on a patient with PVNS,

There is only one report ofthe use of computed tomography (CT)for the radiographic evaluation of PVNS. Besides defining the prominent bony changes, CT provided excellent definition of the soft-tissue mass in this case [54]. Arthrosonography has been used in one instance, in which a complex echogenic mass within a distended suprapatellar bursa was described [45]. Etiology The origin of PVNS has been variously attributed to an inflammatory response to an unknown agent by Jaffe et al. [1], to repeated hemorrhage into the joint [29-33], to neoplasia (25, 55], to a disorder of lipid metabolism [1 4, 29], and to repeated minor trauma [30]. There is one reported case in a patient with abnormal cellular and humoral immunity [56]. More recently, Docken [30J has supported a proliferation of histiocytes as the basis for PVNS masses. No single explanation has been incontrovertibly proven, however. The pathogenesis of the bone cysts is also unproven. McMaster [1 5] and DeBruin and Rockwood [45] suggested that the cysts are created by the extension of villonodular tissue into the bone through the chondroosseous junction at the articular margins. Scott [1 3] found that the hypertrophied synovium invaded through vascular foramina of epiphyseal nutrient vessels. However, neither of these mechanisms adcounts entirely for the widespread distribution of subchondral cysts when pathologic and radiologic features are correlated. A third postulate is that of Chung and Janes [3], who proposed that the exuberant villonodular tissue and joint effusion cause high intraarticular pressure; in turn, focal areas of demineralization eventuate in cyst formation. Others have found high intraarticular pressures in joints involved with PVNS [1 3]. Reports of Baker cysts associated with PVNS of the knee joint are also supportive of the concept of elevated intraarticular pressures [30, 57, 58]. Pathologic specimens from one of our patients [1 1 demonstrated fine erosions of the surface of the articular cartilage. In another case, there was absence of the articular cartilage. In its place, there was vascular fibrous tissue that extended into the subchondral

and the findings were similar to those described in the knee [11]. Arteriography has been used in rare cases suspected dinically to be synovial sarcoma [5, 1 8, 53]. Findings are nonspecific and include neovascularity, slight arteriovenous shunting, and blush. Thus, arteriography is not helpful in differentiating the two entities [5, 18].

AJR:143,

October 1984

PIGMENTED

VILLONODULAR

SYNOVITIS

883

Fig. 8.-Rheumatoid arthritis. A, Large, noncalcified periarticular soft-tissue mass (arrow). B, Cystic bone lesions in humeral head. C, Arthrogram. Appearance due to profusion of rice bodies indistinguishable from PVNS. Diagnosis must be based on clinical and laboratory data.

bone. Extension ofthe synovial mass into a large bone erosion was demonstrated on the gross pathologic specimen of a patient with PVNS of the hip [47]. These findings lend support to the postulate of Chung and Janes [3]. The surface erosions in the articular cartilage and subchondral bone are manifested radiographically as subchondral lucencies, and the expanded erosions appear as bone cysts.

Differential

Diagnosis

Synovial sarcoma is the primary differential consideration when the diagnosis of PVNS is raised on the basis of clinical and radiographic findings. Both entities may exhibit lobulated synovial soft-tissue masses, normal bone mineralization, and a normal-appearing joint [48]. However, if the lesion is entirely or partly outside of the joint capsule, if there are scattered and irregular calcifications within the mass, and/or if bone destruction is present, then the diagnosis of synovial sarcoma is likely [20]. Cavanagh and Schwamm [23] provide an excellent discussion of the differential diagnostic considerations when cystic

bone changes are found in PVNS. These include rheumatoid arthritis, tuberculous arthritis, osteoarthritis, angiomas of osseous origin, amyloidosis, fibrous dysplasia, and multiple enchondromatosis. In addition, on the basis of findings of Resnick et al. [59], pseudogout or calcium pyrophosphate dihydrate deposition disease should be included in this extensive list. Repetition of the excellent discussions in both of these references is not necessary, but a brief discussion of the differentiation of osteoarthritis and rheumatoid arthritis from PVNS is appropriate, because of the frequent occurrence of

these entities.

Osteoarthritis or degenerative joint disease is found in an older population and affects multiple joints, especially the small joints of the hands, wrists, feet, and ankles. When osteoarthritis does involve large joints such as the knee, hip, and shoulder, cystic bone lesions may be encountered. Useful in differentiating degenerative joint disease from PVNS are the presence of a juxtaarticular soft-tissue mass and the generally normal-appearing joint space with PVNS. Hypertrophic spur formation or buttressing, as is often seen when osteoarthritis affects the large joints, will be absent or minimal with PVNS. The differentiation of rheumatoid arthritis from PVNS may be more difficult, as this erosive arthropathy will cause bony erosions secondary to synovial pannus formation and chronically elevated intraarticular pressures [59]. The synovial proliferations, when associated with a profusion of rice bodies, may mimic the appearance oflobulated synovial masses, both on plain films and arthrograms (fig. 8). The lack of hypertrophic bone formation with rheumatoid arthritis is another similarity

884

DORWART

ET AL.

AJR:143, October

1984

to PVNS. However, polyarticular involvement, synovial fluid, biochemical analyses, erythrocyte sedimentation rate elevations, and periarticular demineralization will establish the diagnosis of rheumatoid arthritis. The arthrographic appearance of diffuse PVNS is that of multiple lobulated filling defects within a normally distensible joint. However, there are other diagnostic considerations when these arthrographic findings are noted, including hype,plastic synovitis secondary to inflammatory arthritides such as adult rheumatoid arthritis, juvenile rheumatoid arthritis, hemophilia, and chronic indolent infection [60-641. We have encountered a case of rheumatoid arthritis with marked synovial hyperplasia and a profusion of rice bodies that had the same appearance on shoulder arthrography as PVNS (fig. 8). In addition, chronic indolent infectious synovitis might be expected to have a similar appearance on arthrograms [64]. Multiple loose bodies within the joint space, as in secondary chondromatosis, might also mimic PVNS on an arthrogram, but loose bodies are generally ossified, and the affected joint shows characteristics of degenerative joint disease that are more prominent than those changes seen with PVNS. Primary synovial chondromatosis may uncommonly present with noncalcified, nonossified intraarticular masses demonstrable only by arthrography [64-66]. Finally, synovial masses have been reported in the rare entities of lipoma arborescens [67] and synovial hemangiomas [681.

findings of PVNS (monarticular involvement of a young adult knee, normal joint, normal juxtarticular bones, synovial softtissue mass without caldifications) should be added (1) the frequent occurrence of subchondral and juxtaarticular bone cysts and (2) the relative lack of hypertrophic bone formation and buttressing. We recommend that PVNS be included in
the differential considerations when 1 -2 cm lucent bone sions with thin sclerotic margins are present in the vicinity leof

a joint capsule. More frequent use of arthrography might help detect cases that have only synovial changes. Unfortunately
synovial masses entity. Correlation are not in themselves of all the clinical aspects diagnostic of this and the histologic

features is usually required for definitive specimens are often available for analysis
ment of this disabling rare arthropathy

diagnosis. Tissue because the treatsurgical.

is primarily

ACKNOWLEDGMENTS We thank James LaCount, his photographic assistance, script preparation. Northridge Hospital Medical Center, for and Denice Nakano for help in manu-

REFERENCES
1.

Jaffe HL, Lichtenstein

novitis, bursitis

L, Sutro CJ. Pigmented

villonodular

sy-

Treatment Treatment of pigmented villonodular synovitis depends primanly on the severity of joint destruction and secondarily on the age of the patient. The treatment of choice in the early

and tenosynovitis. Arch Pathol 1941;3i :731-765 2. Smith JH, Pugh DG. Roentgenographic aspects of articular pigmented villonodular synovitis. AJR 1962;87: 1146-1156 3. Chung SMK, Janes JM. Diffuse pigmented villonodular synovitis of the hip joint. J Bone Joint Surg [Am] 1965;47:293-303 4. Byers PD, Cotton RE, Deacon OW, et al. The diagnosis and treatment of pigmented villonodular synovitis. J Bone Joint Surg

case (before

significant

cartilage

loss or bony erosion)

is as

complete a synovectomy as possible. Unfortunately, despite meticulous surgical treatment, the recurrence rate has been reported to be as high as 46% [4]. When the disease is advanced (severe pain and limited joint motion due to destruction of joint cartilage and/or bone erosion), arthrodesis or arthroplasty is indicated. In the older or sedentary patient, total replacement of major joints is indicated and will provide relief of pain and restore
acceptable motion. Controversy arises in treatment of the

[Br] 1968;50:290-305 U, Moberger G. Pigmented villonodular synovitis of joints. Acta Orthop Scand 1969;40:448-460 6. Pantazopoulos TH, Stavrou Z, Stamos C, Kehyaas G, Hartolfilakidis-Garofalidis G. Bone lesions in pigmented villonodular synovitis. Acta Orthop Scand 1975;46:579-592 7. Granowitz SP, DAntonio J, Mankin HL. The pathogenesis and long-term end results of pigmented villonodular synovitis. Clin Orthop 1976;i 14:335-351 8. Johannson JE, Ajjoub 5, Coughlin LP, Wener JA, Cruess RL. Pigmented villonodular synovitis of joints. Clin Orthop 5.
Nilsonne 1982;163:159-i66

younger patient with severe joint destruction. Because of the frequent reports offailure of totaljoint replacement, especially in the younger, active age group, serious consideration must be given to arthrodesis as an alternative to arthroplasty [19]. Another controversy in the treatment of PVNS is the use of irradiation. Larmon [25] strongly advocated its use. However, Atmore et al. [28] reported that there is no significant difference in long-term results between patients with surgery only and those with surgery and irradiation. Radiotherapy

9. Levin EJ, Gannon W. Diffuse villonodular synovitis of the shouldes. Radiology 1963;89: 1302-1304 iO. Snook GA. Pigmented villonodular synovitis with bony invasion. JAMA 1963;i84:424-425 1 1 Dorwart RH, Genant HK, Johnston WH, Morris JM. Pigmented villonodular synovitis of the shoulder: radiologic and pathologic
.

assessment.

AiR

1984;i43:886-888

may be reasonable for the older patient or for recurrence after synovectomy [3, 30, 58]. However, irradiation cannot be recommended for younger patients, because of possible carcinogenic effects and because ofthe high incidence of induced joint stiffness.
To conclude, other than the the rare entity knee. To the of PVNS may list of typical involve joints radiographic

12. Breimer CW, Freiberger RH. Bone lesions associated with villonodular synovitis. AJR 1959;79:618-629 13. Scott PM. Bone lesions in pigmented villonodular synovitis. J Bone Joint Surg [Br] 1968;50:306-3i 1 14. Torisu T, Iwabuchi R, Kamo V. Pigmented villonodular synovitis of the elbow with bony invasion. Clin Orthop 1973;94:275-280 15. McMaster PE. Pigmented villonodular synovitis with invasion of
bone. J Bone Joint Surg (Am] 1960;42:i 170-1183

16. Jaffe HL. Discussion. Of: McMaster PE. Pigmented villonodular synovitis with invasion of bone: report of six cases. J Bone Joint Surg (Am] 1960:42:1183

AJR:143,

October1984

PIGMENTED

VILLONODULAR

SYNOVITIS

885

1 7. Schajowicz F, Blumenfeld I. Pigmented villonodular synovitis of the wrist with penetration into bone. J Bone Joint Surg (Br]
1968;50:3i 2-317

1981;i

9:379-392

44. Kaufman RA, Towbin RB, Babcock DS, Crawford AH. Arthrosonography in the diagnosis of pigmented villonodular synovitis.
AJR 1982;1 39: 396-398

1 8. Van Rens TJG. Pigmented villonodular synovitis of the hip joint. Acta Orthop BeIg 1972;38:22i-232 19. Danzig LA, Gershuni DH, Resnick 0. Diagnosis and treatment of
diffuse pigmented villonodular synovitis of the hip. Clin Orthop

45. DeBruin
invasion

JA, Rockwood
of

CA. Pigmented
the knee

villonodular
joint. South

synovitis:
Med
123-

bone

involving

1966;59:466-468

1982;1 68:42-47

46. Shives TC, Ivin JC. Case report 140. SkeletalRadiol diagnosis
sarcoma
Johanson

1981;6:

20. Lewis

RW. Roentgen
synovial
LP,

of pigmented
of the knee

villonodular
joint.
and

sy-

i 26

novitis and 1947;49:26-38

Radiology
arteriog-

21

Rein

BI,

Bilodeay 1322-1327

P. Arthrography

47. Jergesen HE, Mankin HJ, Schiller AL. Diffuse pigmented villonodular synovitis of the knee mimicking primary bone neoplasm: a report of two cases. J Bone Joint Surg (Am] 1978;60:825829

raphy in pigmented
1964;92:

villonodular

synovitis

of the knee. Radiology

22. Greenfield

MM, Wallace MKM. Pigmented villonodular synovitis. Radiology 1969;93:845-85i 23. Cavanagh R, Schwamm HA. RPC of the month from the AFIP. Radiology 1971;iOO:409-4i4 24. Wolfe AD, Giuliano VJ. Double-contrast arthrography in the
diagnosis of pigmented 1976;i 10:793-799 villonodular synovitis of the knee.
Med

48. Jones FE, Soule EH, Doventry MB. Fibrous ovium (giant-cell tumor of tendon sheath,
synovitis). J Bone Joint Surg [Am]
1969;51

xanthoma
pigmented

of synnodular

:76-86

AJR

25. Larmon
Am

WA. Pigmented
141-150

villonodular

synovitis.

C/in North

1965;49:

26. Gehweiler

JA, Wilson JW. Diffuse biarticular pigmented villonodRadiology 1969;93:845-85i 27. Wagner ML, Spjut HJ, Dutton RV, Glassman AL, Askew JB. Polyarticular pigmented villonodular synovitis. AJR 1981;i36:82i -823 28. Atmore WG, Dahlin DC, Ghormley AK. Pigmented villonodular synovitis: a clinical and pathologic study. Minn Med
ular synovitis. 1956;39: 196-202

49. Kleinman GM, Dagi TF, Poletti CE. Villonodular synovitis in the spinal canal. J Neurosurg 1980;52:846-848 50. Campbell AJ, Wells IP. Pigmented villonodular synovitis of a lumbar vertebral facet joint. J Bone Joint Surg (Am] 1982;64: 145-i 46 51 Savitz MH, Katz 55, Goldstein H, Worcester D. Hypertrophic synovitis of the lumbar facet joint in two cases of herniated intervertebral disc. Mt Sinai J Med (NY) 1982;49:434-437 52. Rickert AR. Pigmented villonodular synovitis of the temporomandibular joint. Otolaryngo! Head Neck Surg 1982;90:668-670 53. Rosenthal Dl, Coleman PK, Schiller AL. Pigmented villonodular
.

synovitis:

correlation

of angiographic

and histologic

findings.

AiR

1980;1 35:581-585 54. Rosenthal DI, Aronow 5, Murray WT. Iron content of pigmented villonodular synovitis detected by computed tomography. Ra55. diology 1979;i33:409-41 1 Wright CJE. Benign giant-cell synovioma: cases. Br J Surg 1951;38:259-27i an investigation of 85

29. Goergen
novitis

TG, Resnick
of the knee:

D, Niwayama
of two

a report

G. Localized nodular sycases with abnormal arthro-

30. 31 32. 33.

34.
.

35.

grams. AJR 1976;i26:647-650 Docken WP. Pigmented villonodular synovitis: a review with illustrative case reports. Semin Arthritis Rheum 1979;9: 1-22 Key JA. Experimental arthritis: the reactions of joints to mild irritants. J Bone Joint Surg 1929;i 1:705-738 Young JM, Hudacek AG. Experimental production of pigmented villonodular synovitis in dogs. Am J Pathol 1954;30:799-81 1 Volz AG, Peltier LF. Experimental production of pigmented villonodular synovitis in rabbits. Surg Forum 1963;i4:452-453 McCollum DE, Musser AW, Rhangos WC. Experimental villonodular synovitis. South Med J 1966;59:966-970 Singh A, Grewal DS, Ghakravarti RN. Experimental production

of pigmented villonodular synovitis in the knee and ankle joints of rhesus monkeys. J Pathol 1969;98: 137-1 42 36. Shafer SJ, Larmon WA. Pigmented villonodular synovitis: a report

of seven cases. Surg Gynecol Obstet 1957;92:574-580

37. Minear WL. Xanthomatous joint tumors. J Bone Joint Surg (Am]

56. Kinsella TD, Vasey F, Ashworth MA. Pertubations of humoral and cellular immunity in a patient with pigmented villonodular synovitis. Am J Med 1975;58:444-448 57. Folman J, Aeis ND. Pigmented villonodular synovitis presenting as a popliteal cyst. !sr J Med Sci 1980;16:735-738 58. Wiss DA. Recurrent villonodular synovitis of the knee: successful treatment with Yttrium-90. Clin Orthop 1982;i 69: 139-i 44 59. Resnick D, Niwayama G, Coutts AD. Subchondral cysts (geodes) in arthritic disorders: pathologic and radiographic appearance of the hip joint. AiR 1977;i28:799-806 60. Weston WJ. The enlarged subdeltoid bursa in rheumatoid arthntis. Br J Radio! 1969;42:48i-486 61 Staple 1W. Extrameniscal lesions demonstrated by double-contrast arthrography of the knee. Radiology 1972;102:31 1-319 62. Dalinka MK, Bonavita JA. Arthrography. In: Practice of surgery,
.

Orthopedics

1. Hagerstown, 1972;i 02: 1 35-i

MD:

Harper

& Row,

1978:1-67

1951;33:451 -458 38. Goldman AB. Hip arthrography. Radiol Clin North Am 1981;19:329-348 39. Can CR, Berley FV, Davis WC. Pigmented villonodular synovitis of the hip joint. J Bone Joint Surg (Am] 1954:36: 1 007-i 013 40. Mallory TB, Castleman B, Parris EE. Case records of the Massachusetts General Hospital: case 301 31 N EngI J Med 1944;230:409-4i 2 41 Clark WS. Case records of the Massachusetts General Hospital: case37292. NEnglJMed 1951;245:ii2-i15 42. Lindenbaum BL, Hunt T. An unusual presentation of pigmented villonodular synovitis. Clin Orthop 1977;1 22:263-267 43. Weissman BN. Arthrography in arthritis. Radio! C/in North Am
. .

63. Salerno
Radiology 64.
Milgram Clin

NA, Menges
JW.

JF, Borns
38

PF. Arthrograms

in hemophilia.

The classification of loose bodies in human joints. 1977;124:282-291 65. Goldberg RP, Genant HK. Calcified bodies in popliteal cysts: a characteristic radiographic appearance. AiR 1979;131 :857-859 66. Prager AJ, Mall JC. Arthrographic diagnosis of synovial chondromatosis. AIR 1976;i27:344-346 67. Burgan DW. Upoma arborescens of the knee: another cause of filling defects on a knee arthrogram. Radiology 1971;1 01:583Orthop

584

68. Forrest

J, Staple TW. Synovial

hemangioma

of the knee. AiR

1971;1 12:51 2-516