Teaching Case

A 22-year-old female with no significant history presents with pain and swelling of left middle finger for 13 months. Physical examination revealed fusiform swelling of the middle finger proximal phalanx, without a wound or erythema. Digital sensation was intact, with moderate limitation of finger flexion.

Radiographs of the left hand demonstrate an expansile lytic lesion of the proximal phalanx of the middle finger, with internal bony septations. The lesion extends to the proximal end of the phalanx. There is a large area of cortical disruption along the volar aspect of the lesion.

MRI shows an expansile, lobulated medullary lesion that is moderately hyperintense on STIR, with low signal internal septations. The lesion is slightly hyperintense to muscle on T1 and shows diffuse heterogeneous enhancement. Despite the volar cortical disruption, the mass does not invade the surrounding soft tissues.

Image from US-guided biopsy shows the biopsy needle within a uniform intermediate-echogenicity mass.

Histopathology images demonstrate numerous multinucleated osteoclast-like giant cells, surrounded by mononuclear neoplastic cells.

Giant cell tumour (GCT) of bone is a locally aggressive, rarely metastasizing benign osseous neoplasm. Histologically, GCTs are characterized by osteoclast-like giant cells and neoplastic mononuclear stromal cells [1]. At least 95% of GCTs demonstrate an H3F3A gene mutation. Malignant transformation occurs in <10% of giant cell tumours.

The majority of GCTs occur in patients 20-45 years old, with a slight female predominance. Pain and swelling are the most common presenting symptoms. GCTs are most common at the ends of the larger long bones of the extremities (femur, tibia, humerus, radius). GCT of the hand accounts for <5% of all GCTs [2] and <5% of all primary tumors of the hand [3].

Because of the osteoclastic nature of the giant cells, GCTs appear radiographically as lytic lesions, with expansion and disruption of the cortex. Endosteal ridging may result in internal septation/trabeculation.  There is often a notable lack of sclerosis along the periphery of a GCT due to osteoclastic activity. Periosteal reaction is unusual in the absence of a pathological fracture.

On MRI, the appearance of GCT is non-specific. T1 and T2 signal intensity are variable, based on the presence of hemosiderin from prior hemorrhage or fibrosis. Fluid-fluid levels may be present in areas of aneurysmal change. With contrast, there is enhancement of the solid portions of the tumor.

GCT can be treated with surgical curettage, as in this case. Placement of cement impregnated with zoledronate helps to prevent local recurrence. Between 15% and 50% of GCTs develop local recurrence after curettage.

Written informed patient consent for publication has been obtained.