**2. 18F-FDG**

Cellular uptake of fluorodeoxyglucose, which is a structural analog of 2-deoxyglucose, is governed by three mechanisms: passive diffusion, active transport by a Na1 dependent glucose transporter (GLUT), and *via* GLUT-1 through GLUT-13 transporters. Once inside the cell, it is phosphorylated to 2'-FDG-6 phosphate by the hexokinase enzyme. Unlike glucose-6-phosphate, 2'-FDG-6 phosphate is not a substrate for the enzymes of the glycolytic pathway or the pentose–phosphate shunt. It is trapped intracellularly but is not metabolized, and does not diffuse back into the extracellular space [3].

The normal distribution of 18F-FDG includes the brain, myocardium, and urinary tract. Thymic uptake, particularly in children, has been observed. Gastric and bowel activity are variable. Liver, spleen, and bone marrow uptake generally are low-grade (**Figure 1**) [4]. The small 18F-FDG molecule enters poorly perfused areas rapidly, so imaging can be performed within 1–2 hours after administration. Skeletal uptake usually normalizes within 3–4 months after trauma or surgery, and degenerative bone

#### **Figure 1.**

*Normal 18F-FDG maximum intensity projection image. There is brain, myocardial, liver, spleen, and urinary tract activity. Faint bone marrow uptake is present.*

## *PET Imaging of Infection DOI: http://dx.doi.org/10.5772/intechopen.110633*

changes ordinarily show only mildly increased uptake, which are advantageous when musculoskeletal infection is a concern [5]. Over the past two decades, 18F-FDG has assumed an increasingly important role in molecular imaging of infection.
