 Recent research recognizes inflammation as a necessary cofactor for orthodontic tooth movement, which may stimulate progenitor slash precursor pathways and signals that regulate biological responses resulting in tooth movement. Upregulation of leukocyte adhesion molecules occurs in response to orthodontic forces, resulting in circulating monocyte attraction, extravasation and differentiation into osteoclasts responsible for bone resorption. To investigate this hypothesis, it is necessary to determine whether periodontal ligament, PDL, endothelium response to inflammatory stimuli like other organs do, and whether orthodontic forces cause upregulation of ICM1 in the PDL microvascular bed. This article was authored by Tom's Andrew, Gannon Brand, and Karate Collin.