The mean and maximum CT attenuations can differentiate between enostoses and sclerotic metastases; however, the accuracy of both metrics decreases after treatment.

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.

Aggrecan is a proteoglycan within the physeal and articular cartilage. Aggrecan deficiency, due to heterozygous mutations in the ACAN gene, causes dominantly inherited short stature and, in many patients, early‐onset osteoarthritis and degenerative disc disease. We aimed to further characterize this phenotypic spectrum with an emphasis on musculoskeletal health. Twenty‐two individuals from nine families were enrolled. Histories and examinations focused on joint health, gait analysis, joint specific patient reported outcomes, and imaging studies were performed. All patients had dominantly inherited short stature, with the exception of a de novo mutation. Short stature was worse in adults versus children (median height −3.05 SD vs. −2.25 SD). ACAN mutations were not always associated with bone age advancement (median advancement +1.1 years, range 0 to +2 years). Children had subtle disproportionality and clinically silent joint disease—25% with osteochondritis dissecans (OD). Adults had a high prevalence of joint symptomatology–decline in knee function, disability from spinal complaints, and lower physical activity on outcome measures. Osteoarthritis (OA) and OD was detected in 90% of adults, and orthopedic surgeries were reported in 60%. Aggrecan deficiency leads to short stature with progressive decline in height SD, mild skeletal dysplasia, and increasing prevalence of joint pathology over time. Optimal musculoskeletal health and quality of life can be attained with timely identification of pathology and intervention.

No abstract