Tenosynovial giant cell tumour (TGCT) is a fibro-histiocytic soft-tissue tumour that involves anatomical structures covered by a synovial membrane (joints, bursae and tendon sheaths). It can also affect extra-synovial locations, such as subcutaneous and intramuscular lesions [1]. Common symptoms are pain, swelling, stiffness, and limited function, leading to decreased quality of life [2].
TGCT can be classified according to its site (intra- and extra-articular) and growth pattern [3]. In the 2013 World Health Organisation classification of soft tissue and bone tumours, localised-type (L-TGCT) and diffuse-type (D-TGCT) replaced the terminology “giant cell tumour of the tendon sheath” and “pigmented villonodular synovitis”, respectively [1]. There is no clear histological distinction between both subtypes, therefore, diagnosis is based on radiological diagnosis and clinical presentation [4]. TGCT is a rare neoplasm with incidence rates of 45 and 5 per million person-years for L-TGCT and D-TGCT, respectively. TGCT has a female predilection (♀:♂; 2:1) and affects a relatively young patient group mainly aged between 30 and 50 years, although it can occur at any age [5, 6].
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L-TGCT occurs in an extra-articular location in 90% of cases, involving tendon sheaths of the volar aspect of fingers (85%), followed by foot and knee locations (15%) [7]. These tumours primarily present as painless soft-tissue masses without joint dysfunction. The diffuse type originates predominantly in the intra-articular space of large joints such as the knee (70%) followed by the hip (15%) but often extends extra-articular [5]. The extra-articular D-TGCT form is mostly a secondary extension of intra-articular disease [8]. D-TGCT tends to present with chronic joint pain and swelling, often with progressive secondary osteoarthritis [2, 9]. D-TGCT represents a monoarticular disease, which means that in case of polyarticular involvement with similar MRI appearance, other diagnoses should be considered, such as gout, haemophilic or amyloid arthropathy.
TGCT subtypes share a common underlying pathogenesis, mainly related to a Colony-Stimulating Factor 1 (CSF1) translocation resulting in CSF1 overexpression. CSF1 overexpression causes an increase in neoplastic cells by binding to CSF1-receptors (CSF1R) and accumulating CSF1R presenting cells [10]. Histologically, TGCT shows an infiltrative growth pattern and comprises mononuclear cells, multinuclear osteoclast-like giant cells, macrophages and stromal hyalinization. Also, hemosiderin depositions are frequently observed [1].
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MRI is the imaging modality of choice for diagnosing and evaluating disease severity [11]. It gives insight into areas that are not amenable for arthroscopic evaluation. Thereby, MRI can provide a preoperative map of D-TGCT localisations to evaluate common blind spots before open synovectomy [8]. Achieving complete resection can be challenging, especially in extensive tumour growth. Incomplete resections are associated with a higher chance of tumour relapse [12, 13]. Other treatment modalities such as radiosynoviorthesis or external beam radiotherapy have been used to reduce relapse rates. However, evidence regarding the efficacy of these treatments is scarce [14, 15]. Furthermore, the role of radiotherapy for TGCT remains controversial because it may result in complications such as osteoarthritis in a young patient population [13]. With the arrival of CSF1R-inhibitors, a novel systemic therapy for D-TGCT patients not amenable to surgery, MRI is essential to select and follow-up on target lesions [16, 17].
In this educational review, we demonstrate the imaging features of D-TGCT and highlight blind spots and potential pitfalls on MRI.
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