Recently, inflammation has been recognised as an important co-requisite to orthodontic tooth movement. When such a reaction is initiated, the process of up-regulation of certain adhesion molecules may occur, resulting in the extravasation of leukocytes. This may stimulate progenitor/precursor pathways and signals that regulate the biological responses resulting in tooth movement. We propose that up-regulation of leukocyte adhesion molecules occurs in response to orthodontic forces, resulting in circulating monocyte attraction, extravasation and differentiation into osteoclasts, which are responsible for bone resorption that results in orthodontic tooth movement. To investigate this hypothesis, it is necessary to determine whether periodontal ligament (PDL) endothelium responds to inflammatory stimuli as other organs do. We studied the normal distribution of endothelial adhesion molecule ICAM-1 within PDL vessels, and then the following exposure to an inflammatory endotoxin. The rat PDL blood vessels expressed ICAM-1 in response to the inflammatory stimulus, similar to other organs, suggesting that the inflammatory responses are similar. Whether and where in the PDL microvascular bed orthodontic forces cause up-regulation of ICAM-1 needs to be established.