Giant Cell Tumor of Bone

The role of enhanced fluorodeoxyglucose F 18 uptake of giant cell tumor of bone(GCTB) should be mentioned in an overview such as that reported by van der Heijden etal., with regard not only to the response to denosumab treatment for unresectableGCTB but also to the clinical implications for the diagnosis of this disease.In a recent article in The Oncologist, van der Heijden et al.[1] provided an overview of imaging,histopathology, genetics, and multidisciplinary treatment of giant cell tumor of bone(GCTB). The authors, however, do not mention the role of metabolic imaging withfluorodeoxyglucose F 18 (¹⁸F-FDG) positron emission tomography/computedtomography scans (PET/CT) in the diagnosis of this disease; they cite only the reduceduptake on ¹⁸F-FDG PET/CT after denosumab treatment [2]. In addition to conventional radiographs and contrast-enhancedmagnetic resonance imaging (MRI), ¹⁸F-FDG PET/CT may be helpful for gainingdiagnostic information by assessing tumor metabolism [3–6]. Recently we observed a55-year-old man with melanoma for which FDG-PET/CT performed as a staging procedurerevealed enhanced ¹⁸F-FDG uptake (a maximum SUV of 9.96) at the level of theproximal end of the right fibule (Fig. 1). This uptakewas interpreted as bone metastasis from the melanoma. Conventional radiograph CT scans ofthe right leg revealed an osteolytic lesion; MRI confirmed the lesion with a low signal onT1- and T2-weighted spin-echo invading and reinflating the cortical bone and surrounded bya sclerotic area. To allow a definite diagnosis, an open biopsy of the lesion wasperformed, and histopathology examination showed a giant cell tumor of the bone and notmetastatic melanoma, as suspected. As reported by van der Heijden et al. [1], GCTB is an intermediate, locally aggressive, butrarely metastasizing tumor. Despite their histopathology classification, giant cell tumorshave generally enhanced ¹⁸F-FDG uptake, attributable mainly to an enhancedvascular fraction and increased ¹⁸F-FDG transport [6]; other authors attribute this to overexpression of hexokinase-2, akey enzyme in the glycolytic pathway in tumor cells [7]. We believe that the role of enhanced ¹⁸F-FDG uptake of GCTBshould be mentioned in an overview such as that reported by van der Heijden et al. [1], with regard not only to the response to denosumabtreatment for unresectable GCTB [8] but also to theclinical implications for in the diagnosis of this disease [3, 9].Open in a separate windowFigure 1.Positron emission tomography/computed tomography showing enhanced F-18fluorodeoxy-D-glucose uptake at the level of the proximal end of the rightfibula.