Pigmented villonodular synovitis (PVNS) is a benign but locally aggressive proliferative disease of synovial tissue. Current terminology designates it 'tenosynovial giant cell tumor.' Diffuse (formerly PVNS) and focal (formerly giant cell tumor/localized nodular synovitis) forms exist. Most commonly affects the knee (80%). On MRI, 'blooming' artifact on T2* gradient-echo sequences due to hemosiderin deposition is PATHOGNOMONIC. Lobulated synovial mass showing low signal on both T1 and T2 due to hemosiderin is characteristic. Treatment is usually synovectomy, with high recurrence rate especially in the diffuse form (30-50%).
Age Range
20-50
Peak Age
35
Gender
Equal
Prevalence
Rare
PVNS is a neoplastic process characterized by monoclonal proliferation of synovial cells. CSF1 gene translocation [t(1;2)] has been identified in some tumor cells — CSF1 overexpression chemotactically attracts surrounding macrophages and monocytes → 'landscape effect' with massive synovial growth. Pathophysiological mechanism of hemosiderin deposition: proliferative synovial tissue is hypervascular with recurrent micro-hemorrhages → erythrocytes are phagocytosed by synovial macrophages → hemoglobin degradation → hemosiderin (iron-protein complex) accumulation → brown-yellow pigmentation. MRI hemosiderin T2* blooming effect: hemosiderin has strong paramagnetic properties (iron Fe3+) → creates local magnetic field inhomogeneity → accelerates spin dephasing → shortens T2* → marked signal loss on gradient-echo sequences ('blooming'). This is pathognomonic for PVNS when combined with intraarticular lobulated synovial mass.
Marked signal loss (blooming) in intraarticular synovial mass due to paramagnetic hemosiderin on T2* gradient-echo. Pathognomonic for PVNS.
On T2* gradient-echo (GRE) or susceptibility-weighted imaging (SWI), marked signal loss ('blooming') is seen in the synovial mass. Blooming causes the lesion to appear larger than its true size because paramagnetic hemosiderin affects surrounding tissue signal. This finding is pathognomonic for PVNS. On spin-echo sequences, blooming is less pronounced because refocusing pulse partially corrects susceptibility effects.
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Marked blooming artifact is seen in the synovial mass on T2* gradient-echo sequence, consistent with hemosiderin deposition and pathognomonic for pigmented villonodular synovitis.
The synovial mass shows low signal intensity on both T1 and T2-weighted images — hemosiderin causes signal loss on both sequences. The mass shows lobulated and villous morphology. In diffuse form, entire joint synovium is thickened and nodular. On contrast images, heterogeneous enhancement (vascular component enhances, hemosiderin-rich areas remain low signal).
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Intraarticular lobulated synovial mass shows low signal on both T1 and T2, suggesting hemosiderin deposition consistent with pigmented villonodular synovitis.
Subchondral bone erosions appear as low signal areas on T1-weighted images. Bone erosions are especially common in 'tight' joints (hip, ankle) — synovial mass cannot expand and causes bone invasion. Erosions are less common in the knee due to larger joint space. Erosions are usually well-defined with sclerotic margins.
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Subchondral bone erosions are noted, consistent with the locally aggressive behavior of pigmented villonodular synovitis.
CT shows well-defined subchondral bone erosions and intraarticular soft tissue density mass. Due to hemosiderin, the mass may show slightly higher density than soft tissue (40-60 HU). CT better shows bone erosion size and location than MRI but MRI is superior for synovial mass characterization and hemosiderin detection.
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An intraarticular soft tissue mass with accompanying subchondral bone erosions is noted on CT.
On post-contrast T1 fat-sat, the synovial mass shows heterogeneous enhancement: vascular proliferative component enhances while hemosiderin-rich areas remain low signal. This heterogeneous pattern is characteristic for PVNS.
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The synovial mass shows heterogeneous enhancement on post-contrast images, with coexistence of vascular proliferative and hemosiderin-rich components consistent with PVNS.
Criteria
Involvement of entire joint synovium.
Distinct Features
Diffuse synovial thickening, large effusion, bone erosions common. Recurrence 30-50%. Total synovectomy needed.
Criteria
Single nodular lesion, usually pedunculated.
Distinct Features
Better prognosis, lower recurrence (5-15%). Local excision sufficient. Hoffa fat pad most common location (knee).
Criteria
Focal form developing in tendon sheath. Fingers most common location.
Distinct Features
Soft tissue mass in fingers. Same hemosiderin findings on MRI. Excision, low recurrence.
Distinguishing Feature
Synovial chondromatosis shows pathognomonic intraarticular calcified loose bodies with ring-and-arc calcification, absent in PVNS; PVNS shows hemosiderin blooming
Distinguishing Feature
Ganglion cyst is a homogeneously bright cystic lesion on T2 without hemosiderin; PVNS shows T1/T2 low signal and blooming
Distinguishing Feature
Bursitis shows T2 hyperintense fluid-filled bursa without hemosiderin blooming, while PVNS shows T2* blooming in synovial mass
Urgency
routineManagement
surgicalBiopsy
NeededFollow-up
6-monthPVNS treatment is planned by form and extent, requiring histopathologic confirmation. Focal form (localized nodular synovitis): arthroscopic local excision is sufficient — recurrence rate is low (5-15%) with excellent prognosis. Hoffa fat pad focal nodule in knee is the most common presentation. Diffuse form: total synovectomy is required — usually a combination of arthroscopic anterior + open posterior synovectomy (especially in knee). Recurrence is high in diffuse form (30-50%) with incomplete synovectomy being the most important risk factor. Recurrent diffuse PVNS treatment options: (1) revision synovectomy + adjuvant external beam radiotherapy (20-36 Gy — reduces recurrence to 15-20%), (2) yttrium-90 radiosynovectomy (intra-articular radioactive agent injection — synovial ablation), (3) CSF1 receptor inhibitor pexidartinib (TURALIO — FDA approved 2019) — CSF1/CSF1R signaling plays a role in PVNS pathogenesis and pexidartinib reduces tumor volume by 39% (ENLIVEN trial). Pexidartinib requires REMS program due to serious hepatotoxicity risk. In advanced cases (severe bone destruction, functional loss), total joint replacement (TKR/THR) may be required. Follow-up: 6-monthly MRI for recurrence assessment — reappearance of T2* blooming is the early finding of recurrence. In extra-articular form (giant cell tumor of tendon sheath), local excision in fingers is the standard treatment.
Surgical synovectomy (open or arthroscopic) is the primary approach for PVNS treatment. Recurrence rate in diffuse form is 30-50%. Focal form (giant cell tumor) has lower recurrence rate. Radiotherapy may be used as adjuvant to reduce recurrence. CSF1R inhibitors (pexidartinib) are a new treatment option for inoperable or recurrent cases.