PVNS,Loose bodies,

1. PIGMENTED VILLONODULAR
SYNOVITIS,SYNOVIAL
CHONDROMATOSIS & LOOSE
BODIES
Dr.Darshan.C.K
JSS Medical College

3. PVNS
 Synonyms:(PVNS, xanthoma, xanthogranuloma, fibroxanthoma, giant cell
tumor of tendon sheath, benign synovioma, villous arthritis.)
 It is a proliferative condition of the synovium characterized by
monoarticular involvement (Knee) & the presence of inflammation and
hemosiderin deposition in the synovium.

4. History
 PVNS was first described in 1852 by Flandry F, Hughston JC.
 Originally thought to be a neoplastic process because of its growth
pattern, capacity to erode surrounding bone and joint tissue, and
high recurrence rate after resection.
 In 1941, Jaffe et al presented the pathologic entity as a synovitis,
thereby shifting the focus from a neoplastic process to an
inflammatory one.
 Recent observations of cytogenetic abnormalities demonstrate that
its pathogenesis remains unresolved.

5. Etiology
 1.Unknown
 2.Trauma
 3. local metabolic activity
 4.Neoplastic process.
 5.Inflammatory process

6. Etiology
A) Trauma:
 Some author suggest that it occurs as a result of trauma and subsequent recurrent local
hemorrhage to the affected joint.
 Hemophiliac synovial pathology differs from PVNS, in that it lacks lipid laden histiocytes
and giant cells, which are considered classic indications of PVNS
 The theory of repeated trauma and hemarthrosis as an explanation for PVNS has fallen
out of favor.

7. Etiology
B) Abnormal local metabolic activity:
 suggested as an inciting event for the inflammation seen in PvNS, but it has been an
inconsistent finding.
C) Neoplastic
 The presence of trisomy 7 and clonal DNA rearrangements & presence of DNA
aneuploidy.
 Pointers to neoplastic aetiology
-invasive character of diffuse pigmented villonodular synovitis
-aneuploidy by DNA analysis and chromosomal rearrangements

8. Etiology
 Many chromosomal abnormalities have been detected.
-Dysregulation of apoptosis with high cytoplasmic levels of B cell lymphoma
protein 2(Bcl2)
- mitochondrial dysfunction with high levels of humanin genes further support a
neoplastic origin.
 Humanin genes, anti-apoptotic peptides encoded in the mitochondrial genome that
act against Bax (bcl-2-associated X protein), are strongly expressed in diffuse
pigmented villonodular synovitis, but barely detected in localized pigmented
villonodular synovitis.

9. Etiology
 There also are more CD57 (natural killer) cells in diffuse pigmented villonodular synovitis
contrasting with more CD3 and CD20 cells in localized pigmented villonodular synovitis.
 Macrophages, more common in diffuse pigmented villonodular synovitis, have
osteoclastic differentiation and proinflammatory cytokines including tumor necrosis
factor a (TNF-a)
D) Inflammatory
 Analysis of cell populations in PVNS strongly support for its being a chronic
inflammatory process .Findings were based on the presence of a cell marker for
inflammation within a heterogeneous population of mononuclear cells.

10. Clinical Presentation
 IncidenceThe estimated annual incidence of pigmented villonodular synovitis is
1.8/million
 A monoarticular process that often involves the large joints.
 Site :The knee is the most commonly involved joint, but others include the hip, ankle,
shoulder, and elbow.
 Age often appears in the 3rd decade of life.
 Sex: no sex based predilection.
 slowly progressive and tend to be episodic.
 Early mild pain is insidious

11. Clinical Presentation
 Later limitation of motion, contracture, and joint locking can occur.
 Joint effusion is common and aspiration may yield brownish fluid due to chronic
hemorrhage or, less often, fresh blood.
 When joint involvement is diffuse, there may be warmth and tenderness.
 PVNS most often is intra-articular and monoarticular.
 involvement of a bursa is termed pigmented villonodular bursitis. Symptoms are
non-specific

12. Occurs in two forms:
 Localized (LPVNS)
 Diffuse (DPVNS)
 LPVNS and DPVNS, the two entities exist along a continuum of one disease
process.
 Histologically, LPVNS and DPVNS are similar, however, they differ in their Gross
apprance ,Clinical presentation, Prognosis, Response to treatment.

13. LPVNS
 most often affects the flexor tendons of the fingers
 Localized pigmented villonodular synovitis at this site is termed a giant-cell
tumor of the tendon sheath
 is second only to the ganglion cyst in incidence.
 frequently involves the toes and less often the knee and ankle
 Less common than DPVNS
 characterized by a pedunculated, lobular lesion localized to one area of the
synovium.

14. LPVNS
 LPVNS lesions occur more common in the anterior compartment.
 Most cases lesions arise at the meniscocapsular junction.
 The synovium in the region of the anterior horn of the medial meniscus is the mc
site of involvement.
 Pt often present with suspicious meniscal pathology.
 Additionally, involvement of the infrapatellar fat pad, suprapatellar pouch,
intercondylar notch, ant horn of the lateral meniscus, medial and lateral recesses of
the knee have been reported.
 LPVNS has a favorable prognosis.

15. DPVNS
 More common form
 often presents with global joint involvement
 most of all synovium of the joint is invovled
 Swelling and pain are more pronounced than in LPVNS
 DPVNS tends to have a more rapidly destructive course
 poorer prognosis.
 can present with extra-articular extension, either at the time of primary diagnosis
or as recurrent disease.
 can involve any synovial joint but is most common in large joints: knee, hip,
ankle, shoulder, and elbow in decreasing order of frequency.

16. DPVNS
 Spinal involvement is rare.
 Extra-articular DPVNS can encroach on major neurovascular structures,
making surgical excision more challenging and complete excision difficult.
 Despite treatment, the recurrence rate for DPVNS is reportedly as high as
46%.
 The end result can be the need for total joint arthroplasty

17. DIFFERENTIALS
• Tuberculosis,
• Synovial osteochondromatosis,
• Hemophilic arthropathy,
• Synovial hemangioma,
• Secondary osteoarthritis and Amyloid arthropathy
• early osteoarthritis, rheumatoid arthritis, a meniscal tear

18. Pathology
 The gross appearance of the localized form ranges from a mottled red-brown to
yellow-brown
 single, large, lobulated mass originating from the synovium of the knee.
 The diffuse type thickens the synovium resulting in tangled folds, fronds, and
nodules with progressive encroachment on the joint space, bony erosion, and
extra-articular extension.
 Microscopically-villous hypertrophy of synovium
 Definitive diagnosis requires histological confirmation of biopsy material

19. Photograph shows the typical appearance of
diffuse intraarticular disease, which appears
brown (*) owing to hemosiderin deposition and
has villonodular protrusions (arrowheads).

20. Histology
 proliferating oval mononucleated synovial cells appearing as a mixture of fibroblasts and
histiocytes, irregularly distributed multinucleated giant cells with phenotypical features of
osteoclasts,
 islands of hemosiderin-loaded macrophages and foam cells
 intra- and extracellular deposition of hemosiderin
 an inflammatory infiltrate containing large numbers of T8 lymphocytes
Histology differential diagnosis
 nonossifying fibroma
 benign fibrous histiocytoma.

21. Histology
 Photomicrograph shows the villonodular fronds
with overlying synovial tissue (solid arrowheads).
 Brownish areas represent extensive hemosiderin
deposition.
 Inset photomicrograph demonstrates golden
brown globular cytoplasmic intracellular
hemosiderin (open arrowheads).

22. Histology
 Photomicrograph of localized
extraarticular PVNS shows
abrupt transition between the
nodular tumor (*) and fibrous
pseudocapsule (between
arrowheads).
 Inset photomicrograph
shows both multinucleated
giant cells (straight arrow)
and reniform mononuclear
histiocytoid cells (curved
arrows).

23. Diagnosis
 Not always obvious clinically.
 Various imaging modalities and lab investigations are often necessary to exclude
other conditions and narrow the diagnosis
 Radiograph
 Synovial fluid examination
 MRI
 Thallium scan

24. Diagnosis
A. Radiograph
 With early disease, radiographs may be normal or show only joint effusion
 Soft tissue may be distinctive when hemosiderin deposition results in high density,
but calcification & periosteal reaction is rare
 With progression marginal erosions and cysts become visible
 well-defined erosions with a sclerotic margin and tend to be prominent in joints
with tight capsules such as the hip, elbow, and wrist.
 Long-standing disease also can result in corticated bone deformities
 Lack of joint space narrowing and osteophytes differentiate pigmented
villonodular synovitis from degenerative joint disease

25. Diagnosis
Radiological DD
 synovial osteochondromatosis when calcifications are absent
 tuberculous arthritis,
 hemophilia
 synovial hemangiomas

26. Diagnosis
B) Ultrasonography
 proliferative synovitis, loculated joint effusions complex heterogeneous echogenic
masses, and markedly thickened synovium
 Doppler shows increased blood flow in these vascular lesions.
c) Computed Tomography
 erosions and cysts of bones
 Soft-tissue density is high when there is hemosiderin deposition.
 High attenuation characteristics

27. CT arthrogram showing femoral head
erosions

28. Diagnosis
D) MRI
 Modality of choice for diagnosing
 Highly sensitive and specific.
 Low signal intensity ("dark on dark“)on T1 & T2 images due to
haemorrhage & haemosidderin deposition
 Helpful in determining the extent of disease involvement and
distinguishing DPVNS from LPVNS.
 Typical MRI findings for LPVNS include a periarticular or synovial
nodular mass with varying degrees of bone erosion

29. Diagnosis
 In DPVNS, there is a poorly localized mass or diffuse synovial thickening
with varying degrees of periarticular erosions.
E) Thallium Scan
 Increased TI-201 uptake in PVNS.
 TI-201 uptake may prove to be a useful diagnostic modality, particularly
in patients in whom there is no clear distinction between recurrent
disease and early osteoarthritis..

30. Localized intraarticular PVNS of the knee in a 40-year-old woman with knee pain. (a)Lateral radiograph
shows an ill-defined area of soft-tissue opacity that replaces the normal Hoffa fat pad (arrows). (b,
c) Sagittal proton-density–weighted (b) T1-weighted fat-suppressed postcontrast (c) images reveal the
localized intermediate-signal-intensity soft-tissue mass (*), which has prominent diffuse enhancement.

31. Sagittal proton-density–weighted fat-suppressed (d) and gradient-echo (e) images show overall
increased signal intensity of the intraarticular soft-tissue mass (*). The gradient-echo image (e) also
shows focal hypointense areas (arrowheads), findings that represent the blooming artifact from
hemosiderin. (f) Photograph of the resected specimen shows the brownish appearance caused by
hemosiderin.

32. Diffuse PVNS of the knee in a 45-year-old man; multiple recurrences of PVNS ultimately led to
amputation. (a) Lateral radiograph shows a large suprapatellar effusion and soft-tissue
fullness about the knee (*). There are extrinsic erosions with marginal sclerosis (arrowheads) on
both sides of the knee joint and patellofemoral degenerative changes. (b) Photograph of the
sagittally sectioned gross specimen demonstrates the large mass throughout the knee joint (*).
The prominent brownish areas (curved arrows) result from more prominent hemosiderin
deposition. Extrinsic erosions (straight arrows) of the femur (F) and tibia (T) are also seen

33. (c,d) Sagittal T1-weighted (c) and gradient-echo (d) MR images reveal a large amount of low-
signal-intensity tissue (*) with posterior extension (curved arrows) that replaces the entire knee
joint. Extrinsic erosions of the femur and tibia with low-signal-intensity margins are also seen
(straight arrows)..

34. Diagnosis
F) Synovial fluid examination
 Joint aspiration gives fluid that ranges in colour from yellow or straw, with deep
xanthochromia from previous haemorrhage, to brown-stained or frankly bloody.
 Reports of synovial fluid analysis are sparse but findings point to inflammation
and which include
 slight elevation of protein,
 reduced glucose,
 low to moderate leucocyte count.

35. Management
 The goal is to eradicate all abnormal synovial tissue, thus removing the source of
pain and reducing the risk of joint destruction and recurrence.
 A combination of surgical and nonsurgical approaches may be necessary
Radiation Therapy
Results are often mixed in PVNS. Delivered by two methods
 external beam radiation,
 intra-articular radiation synovectomy.

36. Management
External beam radiation
 external beam radiation therapy can be highly useful in managing refractory cases
of PVNS or in those with extensive extra articular involvement.
 No significant advantage has been reported to using adjuvant external beam
radiation compared with surgical synovectomy alone.
 Serious potential complications associated with external beam radiation, include
 Skin reactions
 Poor wound healing
 Joint stiffness
 sarcomatous transformation

37. Management
Intra-articular radiation synovectomy
 it as an adjuvant treatment modality in PVNS.
 that intra-articular radiation therapy may be useful in the management of PVNS,
particularly in patients with documented postoperative residual disease that is still
intra-articular.
 Caution with the use of intra-articular radiation therapy is Radionecrosis of the soft
tissues,Mild febrile and painful reactions.
 Development of postradiation sarcoma and increased risk of other malignancies as a
result of total body radiation exposure

38. SURGICAL Management
Arthroscopic Treatment of PVNS
 Arthroscopy has been associated with Better functional results and Lower rates of postoperative
stiffness than open techniques.
 Arthroscopic synovectomy in the knee offers excellent visualization of Anterior compartment as
well as the medial and lateral recesses.
 Posterior compartment synovectomy can be performed,
Localized PVNS
 Arthroscopic partial synovectomy is preferred surgical option for LPVNS.
 Limited or partial synovectomy necessitates débridement of the PVNS mass along with a rim of
surrounding healthy synovium
 Anterior compartment lesions are addressed via standard AL and AM portals.
 Posterior compartment lesions require PM or PL accessory portals to ensure adequate
visualization and access to the entire lesion.
 Recurrence is rare after limited local treatment of LPvNS lesions

39. Arthroscopic Treatment of PVNS
Diffuse PVNS
 In DPVNS the posterior compartment is typically involved and requires a surgeon who
is comfortable with the placement of accessory posterior arthroscopic portals
 Patients with large popliteal masses or extra-articular involvement generally are not
candidates for an exclusively arthroscopic approach.
 Thorough, complete synovectomy is the treatment of choice for DPVNS.
 In addition to the risk of recurrence, arthroscopic excision carries with it a theoretical
risk of
 Joint seeding and Portal contamination
 Extensive joint involvement and
 Extraarticular spread may result after failed arthroscopic management
 Subcutaneous contamination of an arthroscopic portal from DPVNS (rare)

40. Open Surgical Management
 Open arthrotomy and complete synovectomy is the standard surgical treatment
for DPVNS.
 In the knee, this is performed through a combined anterior and posterior
approach.
 Preferred anterior approach is through a midline incision and antromedial
parapatellar arthrotomy.
 The incisions must be extensive enough to allow flexion of the knee and lateral
inversion of the patella.
 This approach permits adequate exposure to the anterior aspect of the knee to
perform the synovectomy.

41. Open Surgical Management

42. Open Surgical Management

43. Summary
 Treatment of each patient must be based on the
 Type of PVNS (ie, local or diffuse),
 Presence or absence of extra-articular disease,
 Level of experience of the surgeon.
 MRI should be performed on any person in whom the diagnosis of PVNS is being
considered.
 The presence of extra-articular involvement suggests a more aggressive form of DPVNS,
which should be managed with an aggressive open surgical approach rather than with
arthroscopic surgery
 LPVNS responds well to arthroscopic resection

44. Summary
 Moderately extensive intra-articular DPVNS can be managed with total
synovectomy with results equivalent to those of open synovectomy.
 Unless a surgeon has a very good understanding of the use of accessory portals
and arthroscopic technique total synovectomy, it is very difficult to treat DPVNS
with arthroscopy alone.
 For the less experienced arthroscopist, open anterior and posterior synovectomy
offers better results and lower recurrence rates.
 Total joint arthroplasty for persistent recurrent disease or in cases demonstrating
end-stage arthritis is a viable option
 External beam radiation is no longer used due to its complications

45. Summary
 Infliximab (anti-TNF-a) in patients with recurrent pigmented villonodular
synovitis has been reported to control the reactive synovitis without
affecting the size of the neoplasm.
 Long-term follow-up is essential since recurrence can occur many years
after initial treatment
 After recurrence, treatment consists of repeat synovectomy usually with
intra-articular yttrium-90 or dysprosium-165.
 These radionuclides are used to destroy small amounts of residual
abnormal tissue and avoid the disadvantages of a Complete synovectomy

46. SYNOVIAL CHONDROMATOSIS
Synovial chondromatosis is a benign condition
characterized by development of cartilaginous or
osteocartilaginous bodies within synovial
membranes of joints, bursae or tendon sheaths as a
result of metaplasia of synovial fibroblasts
Also is termed synovial osteochondromatosis,
synovial chondrometaplasia, articular ecchondrosis,
and synovial chondrosis

47. SYNOVIAL CHONDROMATOSIS
 Synovial chondromatosis has been divided into primary and
Secondary forms.
 Primary synovial chondromatosis, represent chondroid metaplasia
in the subserous layer on inner surface of capsule of a joint with
resultant formation of multiple intraarticular chondral bodies.
 An identical process can also involve the synovium that extends
along tendons and bursae and is frequently referred to as
tenosynovial or bursal chondromatosis, respectively
 Secondary synovial chondromatosis is associated with joint
abnormalities, such as mechanical or arthritic conditions, that
cause intraarticular chondral bodies

48. Pathology
 Gross pathology- thickened synovial lining with multiple shiny blue-white
glistening cartilage nodules- cobble stone appearance
 synovium is moist, folded and hyperaemic
 Loose bodies noted-average 1-2 cm in diameter
 The cartilage nodules are attached by a synovial pedicle- provides
nutritional support, allows hypertrophy and endochondral ossification
 After separation the synovial fluid provides nutrition but the osseous
portion dies

49. Histology
 Metaplastic synovial fibroblasts produce nodules of hyaline cartilage
 Nodules undergo endochondral ossification with woven and lamellar bone
 The hyaline cartilage in primary synovial chondromatosis is often
hypercellular with atypical histologic features, including multinucleation,
nuclear crowding, nuclear enlargement and hyperchromasia, and mild
myxoid changes
 Dystrophic mineralization can also occur centrally within the lobules.

50. Metastasis
 No metastasis is noted
 No sarcomatous change
 Malignant degeneration to chondrosarcoma or de novo intra
articular chondro sarcoma can occur- incidence less than 1%

51. Clinical features
 Male to female ratio- 1 : 1.4
 Middle age adults affected
 Not hereditary
 10 percent have bilateral involvement

52. CLINICAL PRESENTATION
 Low grade chronic pain
 Limitation of movement
 Limp & locking of joint
 Localised tenderness & swelling due to effusion
 degenerative disease Is ultimately a common sequel

53. X-ray
 Initial stages- effusion & juxta articular osteoporosis
 multiple intraarticular chondral bodies with "ring-and-arc chondroid mineralization and
extrinsic erosion of bone on both sides of the joint
 With hypertrophy, opacities become larger with peripheral linear densities
MRI
 MRI shows chondromas usually helps establish the diagnosis, and the images
the true extent of the disease.
 High signal intensity on t2 weighted images due to hyperplasia of synovium

56. Synovial chondomatosis- shoulder joint

57. Synovial chondomatosis- hip joint

58. Management
 The treatment of choice for primary synovial chondromatosis, either intraarticular or
extraarticular (bursal or tenosynovial), is surgical resection
 The overall recurrence rate for intraarticular disease in larger series appears to range
from 3% to 23%, and recurrence may be related to incomplete resection in many
cases
 controversy exists regarding the extent of surgical treatment required whether
removal of chondral bodies alone is sufficient or whether associated synovectomy is
also necessary.

60. Management
 Milgram advocated synovectomy to treat active phase 1 disease
(intrasynovial disease without chondral bodies).
 synovectomy with removal of chondral fragments for phase 2
disease (transitional form with intrasynovial disease and chondral
bodies)
 removal of the multiple chondral bodies alone and no synovectomy
for phase 3 disease (late inactive disease with chondral bodies but
no synovial abnormality)

61. Prognosis
 Good prognosis
 Synovial chondromatosis and synovialosteochondromatosis -remain uncommon,
benign and self limited conditions

62. LOOSE BODIES
 Loose bodies are fragments of cartilage or bone that freely float inside
the knee joint space.
 They can be the result of an injury or from generalized wear and tear
over time.
 Depending on the severity of the condition, there can be one or many
loose bodies inside the joint.
 stable (they don’t move about inside the joint)
 unstable (they float through the inside of the joint) which can cause pain
or loss of motion
 The loose bodies can vary in size from a few millimeters (such as the
size of a small pill) to a few centimeters (the size of a quarter).

63. Symptoms
 The feeling of something moving in knee.
 Intermittent joint locking
 clicking
 Knee pain
 swelling

64. LOOSE BODIES
CLASSIFICATION OF LOOSE BODIES
A. FIBROUS LOOSE BODIES
 Traumatic i e. organization from haemorrhage into villus
 pathological-in association with tuberculosis, syphilis and osteoarthritis
B. FIBRINOUS LOOSE BODIES
 Traumatic-after haemorrhage
 pathological in association with tuberculosis and chronic synovitis.
C. CARTILAGINOUS LOOSEBODIES.
 Traumatic separation of whole or part of an intraarticular fibro-cartilage
eg.meniscus

65. LOOSE BODIES
D. OSTEO CARTTLAGINOUSLOOSE BODIES
 Pathological
 osteochondritis dissecans,
 detachment of osteophytes in osteoarthritis,
 separation of sequestrum in acute osteomyelitis.
synovial chondromata
 Traumatic- fracture of the tibial spine.
E. MISCELLANEOUS LOOSE BODIES
introduced foreign body
 lipoma
 secondary carcinoma.

66.  X-ray: A loose body is typically diagnosed with an x-ray. In most cases, the traumatic
loose body has a bone chip with it or a big chunk of cartilage easily seen on an x-ray.
 MRI: The best way to see the location and character of loose body is with an MRI.
When the loose body is just cartilage or in the case of synovial chondromatosis, a
MRI is the best non radiation diagnostic tool to asses the whole knee joint. It is a
useful preoperative tool to see size, number and location of the loose bodies.
 CT scan: This is rarely used but can give details about the loose body when fracture
or bone fragments are expected.

67. LOOSE BODIES
 Diagnosis of presence of loose body inside the knee joint is made by history of
recurrent locking at different angles.
 There will be associated findings according to the cause of loose bodies.
 The most difficult part is to differentiate injury to the meniscus with the
presence of loose bodies inside the joint.
 This difference is easier when the loose body is radio-opaque ie. bony or
osteo-cartilaginous or radioopaque foreign bodies. This requires only X-ray for
diagnosis.

68. LOOSE BODIES
 Two conditions should be kept in mind which are often
misdiagnosed as bony loose bodies in the knee joint
 Fabella -a sesamoid bone in the lateral head of the gastroenemius
 Pellegrini-Stieda's disease in which calcification occurs in the tibial
collateral ligament after partial avulsion from the medial condyle of
the femur

69. Treatment
 Non-surgical management - physical therapy and anti-inflammatory drugs can
be used to help with the symptoms and to keep the joint flexible.
 Arthroscopy: The gold standard today is to remove possibly all loose bodies by
arthroscopy, popularly known as “clean out “arthroscopies.
 It is minimally invasive and allows surgeon to thoroughly examine the knee for
loose body and allows to asses any damage to cartilage and treat the condition,
hence it is best Diagnostic and therapeutic modality available
 Open arthrotomy: This is less common due to the availability of arthroscopy but
it can be done when the loose bodies are very large and numerous or there is
associated complete synovial involvement

71. REFERENCES
 CAMPBELL'S OPERATIVE ORTHOPAEDICS
 TUREK TEXT BOOK OF ORTHOPAEDICS.
 BONE TUMORS BY JOSEPH M. MIRRA.
 ATLAS OF ORTHOPAEDIC PATHOLOGY BY WOLD AND UNNI
 THE RADIOLOGY OF SKELETAL DISORDERS
 DUKE RADIOLOGY-CASE REVIEW

72. T
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