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Nuclear Medicine |
1 From the Departments of Diagnostic Radiology (J.A., H.I., N.O., N.S., K.E.), Orthopedic Surgery (H.W., T.S., K.T.), and Nuclear Medicine (T.I., K.E.), Gunma University School of Medicine, 3-39-22 Showa-machi, Maebashi 371-8511, Japan. From the 2000 RSNA scientific assembly. Received May 11, 2000; revision requested June 19; revision received August 4; accepted September 12. Address correspondence to J.A. (e-mail: junaoki@showa.gunma-u.ac.jp).
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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MATERIALS AND METHODS: Fifty-two (19 malignant, 33 benign) primary bone lesions were examined with FDG PET prior to tissue diagnosis. The SUVs were calculated and compared between benign and malignant lesions and among histologic subgroups that included more than four cases.
RESULTS: There was a statistically significant difference in SUV between benign (2.18 ± 1.52 [SD]) and malignant (4.34 ± 3.19) lesions in total (P = .002). However, giant cell tumors (n = 5; SUV, 4.64 ± 1.05) showed significantly higher SUV than chondrosarcomas (n = 7; SUV, 2.23 ± 0.74) (P = .036, adjusted for multiple comparisons) and had no statistically significant difference in SUV compared with osteosarcomas (n = 6; SUV, 3.07 ± 0.96) (P = .171). There was no statistically significant difference in SUV between fibrous dysplasias (n = 6; SUV, 2.05 ± 0.98) and osteosarcoma (P = .127) or chondrosarcomas (P = .667). Although the number of cases was small, three chondroblastomas, one sarcoidosis, and one Langerhans cell histiocytosis showed levels of FDG accumulation as high as that of osteosarcomas.
CONCLUSION: Radiologists should be aware of the high accumulation of FDG in some benign bone lesions, especially histiocytic or giant cell–containing lesions. Consideration of histologic subtypes should be included in analysis of SUV at FDG PET of primary bone tumors.
Index terms: Bone neoplasms, diagnosis, 40.31, 40.32 • Bone neoplasms, PET, 40.12163 • Bone neoplasms, radionuclide studies, 40.12163 • Fluorine, radioactive
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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The PET examinations were performed prior to tissue diagnosis, and final diagnoses of all the lesions were pathologically proved. All benign lesions were examined at biopsy or were operated on because of clinical symptoms, pathologic fractures, or indeterminate radiologic appearances. No patient had received any treatment prior to PET. Nineteen malignant primary bone tumors and 33 benign bone lesions were included. The malignant tumors were seven chondrosarcomas (one grade I, five grade II, one grade III), six osteosarcomas (one low-grade surface type, five high-grade conventional type), four primary bone lymphomas, and two Ewing sarcomas. Various histologic types were included among the benign lesions, which were six fibrous dysplasias, five giant cell tumors, five bone cysts, four enchondromas, three chondroblastomas, three nonossifying fibromas, two osteoid osteomas, two osteochondromas, one sarcoidosis, one Langerhans cell histiocytosis, and one hemangioma. Maximum diameter of the lesions measured on radiographs ranged from 1.0 to 19.5 cm (6.31 cm ± 4.38).
PET studies were performed by using a whole-body positron camera (SET 2400W; Shimadzu, Kyoto, Japan). Transverse fields of view were 59.5 and 20 cm. Transverse spatial resolution was 4.2 mm full width at half maximum at the center of the field of view, and transverse spatial resolution was 5.0 mm full width at half maximum. FDG was synthesized by using a method modified from that of Hamacher et al (11). The patients fasted for at least 4 hours and received injections of 185–250 MBq of FDG (5 MBq per kilogram of body weight). None of the patients were diabetic. One 8-minute simultaneous emission-transmission scan per bed position was obtained at 40–50 minutes after the injection of FDG. Images were acquired in only one bed position that allowed depiction of a lesion. Attenuation-corrected images were reconstructed by using the ordered-subsets expectation maximization method. By using the attenuation-corrected images, injection doses of FDG, patient’s body weight, and cross-calibration factors between PET and the dose calibrator, functional images of the SUV were produced. SUV was defined as follows (1,12): SUV equals the radioactive concentration in tissue (in becquerels per gram) divided by the (injected dose [in becquerels] divided by the patient’s body weight [in grams]).
The injected dose of radioactivity of FDG was measured by using a dose calibrator (IGS-3; Aloka, Tokyo, Japan). The cross-calibration factor between the dose calibrator and PET was measured with a cylindrical phantom containing a germanium 68–gallium solution (13). One of the authors (T.I.) manually placed a circular region of interest of 1 cm in diameter on the SUV image over the area corresponding to the lesion. This size of the region of interest was used because the diameter of the smallest lesions (two osteoid osteomas) was 1 cm and because it was more than two full widths at half maximum of the spacial resolution of our PET system (14). All other lesions were larger than 1.6 cm, and the region of interest was placed to include the site of maximum FDG accumulation in a lesion. The mean SUV in each region of interest was determined for data analysis.
The significance of the difference in SUV, age of the patients, and size of the lesions between benign and malignant primary bone tumors was statistically analyzed by means of the nonparametric Mann-Whitney U test. A P value less than .05 was regarded to indicate a significant difference. The same statistical analysis was performed among different histologic subgroups that included more than four cases, with adjustment for multiple comparisons where indicated.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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SUVs of each histologic tumor type are shown in Figure 1. A considerable overlap in SUV was observed between some benign and malignant tumors. Malignant lymphomas and Ewing sarcomas showed an extremely high accumulation of FDG. Osteosarcomas and chondrosarcomas demonstrated relatively high SUVs. The types of benign lesions that showed a high accumulation of FDG were giant cell tumor (Fig 2), chondroblastoma (Fig 3), Langerhans cell histiocytosis, fibrous dysplasia (Fig 4), and sarcoidosis. Giant cell tumors (n = 5; SUV, 4.64 ± 1.05) showed significantly higher accumulation of FDG than chondrosarcomas (n = 7; SUV, 2.23 ± 0.74) (P = .036, adjusted for multiple comparisons). There was no statistically significant difference (P = .171) in SUV between giant cell tumors and osteosarcomas (n = 6; SUV, 3.07 ± 0.96). There was no statistically significant difference in SUV between fibrous dysplasias (n = 6; SUV, 2.05 ± 0.98) and osteosarcomas (P = .127) or between fibrous dysplasias and chondrosarcomas (P = .667). Although the number of cases was small, three chondroblastomas, one sarcoidosis, and one Langerhans cell histiocytosis showed levels of FDG accumulation as high as those of osteosarcomas. All enchondromas, all osteochondromas, all bone cysts, all osteoid osteomas, one hemangioma, two of three nonossifying fibromas, and three of six fibrous dysplasias showed SUVs lower than 2.0.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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It may be reasonable to consider that glucose is consumed by the main proliferating cells of each bone tumor. However, the cellular composition of primary bone tumors is frequently heterogeneous, and many tumors are known to contain histiocytic cells and giant cells. Interestingly, all our benign cases that showed high FDG uptake (SUV > 2.0), except fibrous dysplasias, can be categorized as histiocytic or giant cell–containing lesions (15,16). Histiocytes and giant cells in a tissue are in monocyte-macrophage lineage (15,16). Macrophages play a central role in the host response to injury and infection, and their energy is predominantly supplied by means of intracellular glucose metabolism (17,18). High uptake of FDG in inflammatory cells has already been reported (9,10,19) in patients with chronic osteomyelitis and rheumatoid arthritis, and in an animal experiment on chemically induced cellulitis. Findings of a microautoradiographic study of inoculated FM3A tumor cells in C3H/He mice showed higher accumulation of FDG in infiltrating macrophages and granulation tissues than in the tumor cells (20). High accumulation of FDG has been reported (21,22) in sarcoidosis, which has characteristics of inflammatory reaction with activated lymphocyte and macrophage infiltration followed by formation of granulomas. Although it is still controversial whether histiocytic cells and giant cells in primary bone tumors are reactive or neoplastic, these cells might partially contribute to the high uptake of FDG in the benign bone lesions. Intratumoral distribution of FDG in bone lesions with a heterogeneous cellular composition should be investigated in the future.
Our results may suggest that other giant cell–containing lesions may also show a high accumulation of FDG with PET studies. Such lesions include osteoblastoma, chondromyxoid fibroma, aneurysmal bone cyst, giant cell reparative granuloma, brown tumor, and malignant fibrous histiocytoma (15,16). High accumulation of FDG with PET studies has been emphasized in several cases of malignant fibrous histiocytoma in bone (SUV ranged from 2.69 to 7.57), as well as one osteoblastoma (mean SUV, 3.28) and one aneurysmal bone cyst (mean SUV, 2.69) (8). In this regard, it is interesting that two of 16 cases of Paget disease, in which a large number of osteoclasts are activated, were reported (23) to show a high accumulation of FDG. Osteoclasts are large multinucleated cells that are responsible for bone resorption and that are most likely derived from migrating monocytes of the macrophage type (24).
It may be difficult to attribute the high FDG uptake in some fibrous dysplasias to osteoclast-like giant cells, which are frequently observed around degenerative foci within this lesion (25). Because fibroblasts, which are the predominant proliferating cells of this lesion, are known to show a relatively high accumulation of FDG (26), the difference in SUV among fibrous dysplasias may be due to a difference in the amount of actively proliferating fibroblasts. The same speculation may be applicable to other types of fibrous lesions, such as a cortical desmoid, desmoplastic fibroma, nonossifying fibroma, and osteofibrous dysplasia. Further data are necessary to elucidate the importance of FDG uptake in these benign fibrous lesions, though most of them can easily be diagnosed as benign on radiographs.
In our study, a practical cutoff value of SUV could not be set to distinguish between benign and malignant primary bone tumors. When a previously suggested (7) cutoff point (SUV = 2.0) was applied, only 19 benign lesions and 15 malignant tumors (64% of the total cases) could be accurately differentiated. Other previously suggested (4,5) cutoff values, such as 2.5 and 3.0, could not provide better accuracy in our cases. More specific uses of FDG PET, such as grading and monitoring of musculoskeletal sarcomas with respect to each tumor of a different histologic subtype, should be considered in the future. It is also recommended that FDG PET be used for selected cases after careful evaluation of clinical and other radiologic findings.
In conclusion, radiologists should be aware of a high accumulation of FDG in some benign bone tumors and tumorlike lesions, especially histiocytic or giant cell–containing lesions. These lesions cannot be distinguished from malignant bone tumors by using SUV with FDG PET. It is hoped this information will be of practical value, particularly given the increasing clinical use of FDG PET in a variety of settings.
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FOOTNOTES |
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Author contributions: Guarantor of integrity of entire study, J.A.; study concepts, J.A., H.W., T.S.; study design, J.A., H.W., T.I.; literature research, J.A., H.I., N.O.; clinical studies, J.A., H.W., T.S.; data acquisition and analysis/interpretation, J.A., H.W., T.S.; statistical analysis, J.A., N.S.; manuscript preparation and definition of intellectual content, J.A., T.I.; manuscript editing, J.A., H.I., N.O.; manuscript revision/review, J.A., T.I.; manuscript final version approval, K.T., K.E.
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REFERENCES |
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= benign lesions, 
= malignant tumors, and * = histiocytic or giant cell-containing lesions. SUVs were 3.52 ± 1.42 for histiocytic lesions, 1.31 ± 0.76 for nonhistiocytic benign lesions, and 4.34 ± 3.19 for malignant tumors. BC = bone cyst, CB = chondroblastoma, CS = chondrosarcoma, EC = enchondroma, ES = Ewing sarcoma, FD = fibrous dysplasia, GCT = giant cell tumor, HA = hemangioma, LCH = Langerhans cell histiocytosis, ML = malignant lymphoma, NOF = nonossifying fibroma, OC = osteochondroma, OO = osteoid osteoma, OS = osteosarcoma, SA = sarcoidosis.
