摘要： 18F-sodium fluoride (18F-NaF) was introduced as a tracer for imaging skeletal diseases in 1962 and was approved by the Food and Drug Administration in 1972.1 Recently, with the increased availability of positron emission tomography (PET) scanners there has been a surge in clinical utilization of 18F-NaF imaging for oncological applications. The incidental observation, nearly a decade ago, of 18F-NaF uptake in the vasculature in patients undergoing PET imaging for cancer has led to a growing number of investigations exploring the potential role of this tracer in atherosclerosis.2–4 However, the biological correlates of 18F-NaF imaging in the vasculature, and its potential role in risk stratification of patients and prospective identification of vulnerable plaques remain incompletely characterized. In this issue of the Journal, Creager et al5 address some of these gaps by exploring the relationship between 18F-NaF binding and the size of microcalcifications using a 3-dimensional hydrogel platform.6 In agreement with a previous publication,2 their study finds that smaller and more numerous microcalcifications (ie, higher surface areas of calcifications) are associated with higher 18F-NaF binding when compared with fewer larger calcifications.5 The study also provides ex vivo proof-of-concept evidence for the correlation between 18F-NaF binding and foci of ongoing calcification in mouse and human atherosclerotic plaques.5