Pigmented villonodular synovitis (PVNS) is a benign but locally aggressive proliferative disorder of synovial tissue. Hemosiderin deposition is the pathological hallmark, manifesting as low signal on all MRI sequences (blooming artifact). The knee joint is most commonly affected (75%). Bone erosions on both sides of the joint and prominent joint effusion are characteristic.
Age Range
20-50
Peak Age
35
Gender
Equal
Prevalence
Uncommon
PVNS develops from neoplastic proliferation of synovial tissue due to translocation of the CSF1 (colony stimulating factor 1) gene (t(1;2)). Neoplastic cells recruit monocytes and macrophages to the joint through CSF1 overexpression; these cells phagocytose hemoglobin through iron metabolism and accumulate hemosiderin. Hemosiderin — an iron-containing pigment — causes marked signal loss (blooming artifact) on T2* and gradient echo MRI sequences due to the superparamagnetic properties of iron atoms. Recurrent intra-articular hemorrhages lead to joint effusion and synovial hypertrophy, while proliferating synovial tissue erodes subchondral bone on both sides — known as 'kissing erosions' or 'erosions on both sides of joint,' which is characteristic of PVNS. Relative preservation of joint cartilage is an important distinguishing finding from degenerative arthritis.
Synovial mass showing low signal on all MRI pulse sequences (T1, T2, T2*, STIR). This finding results from the superparamagnetic effect of hemosiderin deposition and is pathognomonic for PVNS. When evaluated together with blooming artifact on gradient echo sequences, diagnostic certainty is very high.
On T2-weighted sequences, the synovial tissue demonstrates markedly low signal due to hemosiderin deposition. While normal synovial tissue produces intermediate-to-high T2 signal, hemosiderin-laden tissue in PVNS paradoxically shows low signal. It may present as nodular or diffuse synovial thickening. This 'dark on all sequences' pattern is the most diagnostic MRI finding of PVNS.
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On T2-weighted series, the intra-articular synovial tissue demonstrates markedly low signal due to hemosiderin deposition, consistent with pigmented villonodular synovitis.
On gradient echo (GRE/T2*) or susceptibility weighted imaging (SWI) sequences, hemosiderin deposition creates prominent blooming artifact — the lesion appears larger and darker than its true size. This is the most sensitive MRI finding for PVNS diagnosis. The degree of blooming is directly proportional to the amount of hemosiderin.
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On gradient echo sequences, prominent blooming artifact is noted in the synovial lesion, suggesting dense hemosiderin deposition.
On T1-weighted series, synovial tissue demonstrates low to intermediate signal intensity. Hemosiderin deposition also causes signal loss on T1 but not as dramatic as on T2. Focal T1 hyperintense foci may be seen in the presence of intracellular methemoglobin (subacute hemorrhage). Hemorrhagic joint effusion shows slightly increased T1 signal compared to simple effusion.
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On T1-weighted series, low to intermediate signal synovial thickening is noted within the joint, with focal high signal foci indicating subacute hemorrhage.
On post-contrast T1 series, synovial tissue demonstrates prominent homogeneous enhancement. Hemosiderin deposition and enhancement coexist within the same tissue — overall enhancement is observed despite hemosiderin foci on post-contrast series. Fat-saturated post-contrast series best demonstrate synovial hypertrophy and enhancement pattern. Diffuse type shows widespread, localized type shows focal nodular enhancement.
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On fat-saturated post-contrast series, prominent diffuse synovial enhancement is demonstrated.
On STIR sequence, joint effusion shows prominent hyperintense signal but is not homogeneous due to hemorrhagic component. Fluid-fluid levels may be visible — serous fluid (hyperintense) above, hemosiderin-rich fluid (hypointense) below. Synovial hypertrophy shows heterogeneous signal on STIR; low signal in hemosiderin foci and high signal in cellular areas coexist.
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On STIR sequence, prominent joint effusion with fluid-fluid levels is demonstrated, indicating the presence of hemorrhagic component.
On CT, subchondral bone erosions are seen on both sides of the joint (such as femoral and tibial condyles) — 'kissing erosions'. Erosions have sharp sclerotic margins and show pressure-type resorption, different from aggressive bone destruction. The joint space is relatively preserved. High-density hemosiderin deposition within synovial tissue may be visible as increased density on CT.
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On CT, sclerotic-margined subchondral erosions are seen on both sides of the knee joint (femoral and tibial condyles) with relatively preserved joint space — 'kissing erosions' pattern consistent with PVNS.
On diffusion-weighted imaging, the solid synovial component of PVNS shows variable diffusion restriction. Cellular areas demonstrate mild-to-moderate restricted diffusion (ADC: 1.0-1.5 × 10⁻³ mm²/s), while hemosiderin-dense areas complicate assessment due to susceptibility artifact. On DWI, PVNS can be distinguished from malignant synovial tumors (synovial sarcoma) by higher ADC values.
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On diffusion-weighted series, mild restricted diffusion is noted in solid areas of the synovial component, with susceptibility artifact present in hemosiderin-dense regions.
On CT, a synovial mass slightly higher density than soft tissue (50-80 HU) is seen within the joint. This increased density results from hemosiderin deposition. Lesion margins are defined by the joint capsule. Calcification is rare in PVNS; if present, alternative diagnoses (synovial chondromatosis) should be considered.
Report Sentence
On CT, a slightly hyperdense synovial mass compared to soft tissue is seen within the joint, consistent with hemosiderin deposition.
Criteria
Diffuse involvement of entire synovial membrane, in large joints (knee, hip, shoulder), aggressive clinical course, high recurrence rate (30-50%)
Distinct Features
On MRI, widespread thickening and hemosiderin deposition throughout the entire synovial membrane. Kissing erosions more common in diffuse type. Joint effusion is prominent. Surgical total synovectomy is required, but recurrence rate is high. CSF1R inhibitor (pexidartinib) therapy has FDA approval for diffuse type.
Criteria
Focal nodular lesion within joint, typically knee (Hoffa fat pad, intercondylar region), low recurrence rate (<10%)
Distinct Features
On MRI, single nodular lesion with variable hemosiderin content, no diffuse synovial thickening. Bone erosions are rare. Arthroscopic excision is sufficient. Localized type has better prognosis.
Criteria
Tendon sheath origin, most common in fingers and toes, small well-defined nodule, extra-articular
Distinct Features
Second most common soft tissue tumor in fingers and toes (after ganglion cyst). On MRI, hemosiderin content may be less than diffuse type. Well-defined, lobulated contour nodule surrounding adjacent tendons. Treated with surgical excision, recurrence 5-15%.
Distinguishing Feature
Synovial sarcoma shows heterogeneous high T2 signal ('triple sign' — cystic, solid, hemorrhagic); it lacks the diffuse low T2 signal and blooming artifact seen in PVNS. Synovial sarcoma is more common extra-articular and bone erosions are unilateral.
Distinguishing Feature
Synovial hemangioma shows bright (hyperintense) T2 signal with minimal hemosiderin deposition. Presence of phleboliths (calcified on CT) favors hemangioma. The 'dark on all sequences' pattern of PVNS is not seen in hemangioma.
Distinguishing Feature
Giant cell tumor (GCT) is a solid mass originating from the epiphysis in subchondral bone, not showing intra-articular synovial thickening. GCT may contain hemosiderin but synovial proliferation and kissing erosions are not seen in GCT. GCT typically produces unilateral bone lesion.
Distinguishing Feature
Lipoma arborescens (synovial lipomatosis) shows synovial villous proliferation but fat signal predominates (T1 hyperintense, signal loss on fat-suppressed sequences). The hemosiderin-related low signal of PVNS is absent. Lipoma arborescens is typically bilateral and associated with degenerative joint disease.
Urgency
semi-urgentManagement
Lokalize tip: artroskopik veya açık eksizyon. Diffüz tip: total sinovyektomi (açık veya artroskopik) ± radyasyon sinovyektomi. Refrakter diffüz tip: CSF1R inhibitörü (pexidartinib — FDA onaylı). İleri vakalarda total eklem replasmanı gerekebilir.Biopsy
NeededFollow-up
Cerrahi sonrası 6-12 aylık MRG takip (rekürrens %30-50 diffüz tipte). Gadolinyumlu MRG rezidü/rekürrens tespitinde altın standarttır.PVNS diagnosis is typically made by MRI; pathological confirmation shows hemosiderin-laden macrophages, giant cells, and synovial proliferation. Treatment of diffuse type is challenging; due to high recurrence rates after incomplete synovectomy, CSF1R inhibitor (pexidartinib) therapy is an important option in inoperable/refractory cases. It is administered under REMS program due to hepatotoxicity.
Treatment is surgical synovectomy (open or arthroscopic). Local recurrence rate is 30-50% in diffuse form (<10% in localized form). Total knee replacement may be considered in resistant cases. Radiotherapy and CSF1R inhibitors (pexidartinib) are used in recurrent or inoperable cases. Malignant transformation is very rare.