Positron emission tomography/computed tomography imaging appearance of benign and classic “do not touch” osseous lesions

Abstract

BACKGROUND Classic “do not touch” and benign osseous lesions are sometimes detected on 18 -F-fluorodeoxyglucose ( 18 F-FDG) positron emission tomography/computed tomography (PET/CT) studies. These lesions are often referred for biopsy because the physician interpreting the PET/CT may not be familiar with the spectrum of 18 F-FDG uptake patterns that these lesions display. AIM To show that “do not touch” and benign osseous lesions can have increased 18 F-FDG uptake above blood-pool on PET/CT; therefore, the CT appearance of these lesions should dictate management rather than the standardized uptake values (SUV). METHODS This retrospective study evaluated 287 independent patients with 287 classic “do not touch” (benign cystic lesions, insufficiency fractures, bone islands, bone infarcts) or benign osseous lesions (hemangiomas, enchondromas, osteochondromas, fibrous dysplasia, Paget’s disease, osteomyelitis) who underwent 18 F-FDG positron emission tomography/computed tomography (PET/CT) at a tertiary academic healthcare institution between 01/01/2006 and 12/1/2018. The maximum and mean SUV, and the ratio of the maximum SUV to mean blood pool were calculated. Pearson’s correlations between lesion size and maximum SUV were calculated. RESULTS The ranges of the maximum SUV were as follows: For hemangiomas (0.95-2.99), bone infarcts (0.37-3.44), bone islands (0.26-3.29), enchondromas (0.46-2.69), fibrous dysplasia (0.78-18.63), osteochondromas (1.11-2.56), Paget’s disease of bone (0.93-5.65), insufficiency fractures (1.06-12.97) and for osteomyelitis (2.57-12.64). The range of the maximum SUV was lowest for osteochondromas (maximum SUV 2.56) and was highest for fibrous dysplasia (maximum SUV of 18.63). There was at least one lesion that demonstrated greater 18 F-FDG avidity than the blood pool amongst each lesion type, with the highest maximum SUV ranging from 9.34 times blood pool mean (osteomyelitis) to 1.42 times blood pool mean (hemangiomas). There was no correlation between the maximum SUV and the lesion size except for enchondromas. Larger enchondromas had higher maximum SUV ( r = 0.36, P = 0.02). CONCLUSION The classic “do not touch” lesions and classic benign lesions can be 18 F-FDG avid. The CT appearance of these lesions should dictate clinical management rather than the maximum SUV.

Differentiation of soft tissue and bone sarcomas from benign lesions utilizing 18F-FDG PET/CT-derived parameters

“…Moreover, a positive correlation between the FDG activity and the pathological grade of sarcoma has been established; however, the histological sub-types cannot be always distinguished accurately [ 21 ]. Specifically, some benign lesions may exhibit deceptively high FDG uptake, leading to indefinite diagnoses [ 22 ]. HF is another parameter obtained from PET images and was reported to reflect the intratumoral heterogeneity of 18 F-FDG affinity.…”

Cross-sectional evaluation of FGD-avid polyostotic fibrous dysplasia: MRI, CT and PET/MRI findings

“…Both malignant and benign bone tumours, as well as tumour-like lesions, can show increased FDG uptake depending on their biological activity. These include bone cysts, geodes, haemangiomas, bone infarcts, bone island, enchondromas, FD, osteochondroma, Paget’s disease and bone infections (Elangovan and Sebro 2019 ). Although increased glucose metabolism may be suspicious for malignancy, a correct differential diagnosis requires the pattern of FDG uptake to be always considered in the specific clinical context together with the radiological appearance of the lesion.…”

Bone Infarction Mimicking a Bone Metastasis on 18F–Prostate-Specific Membrane Antigen PET/CT

“…[3][4][5][6][7][8] Nonprostatic PSMA ligand expression has been described in various other solid benign and malignant lesions. [9][10][11][12][13] This illustrates an unusual case of 18 F-PSMA tracer uptake in a femoral bone infarct. Although PSMA uptake can be seen in benign bone disease, 14 an English literature search revealed no previous cases of PSMA ligand expression in a bone infarct.…”