The progression of atherosclerosis is currently believed to involve the interaction of monocytes with the vascular endothelium. Within the last decade, the cell-surface proteins thought to control these interactions have been investigated. This review seeks to describe the nature of these interactions through what are known as adhesion molecules and their role in atherogenesis. It begins with the stages of atherogenesis from the movement of the monocyte to the endothelium, followed by the migration of smooth muscle cells from the media to the intima, and subsequently to the later stages of fibrofatty plaque formation and potential complications due to thrombosis and/or plaque fissure and embolism. The different structural classifications of the adhesion molecules, such as integrins, cadherins, selectins, and members of the immunoglobulin gene superfamily, are outlined, and interaction of binding domains are highlighted. The vascular endothelium and the basic role of adhesion molecules in dysfunction are considered. Discussion of the role of adhesion molcules in atherogenesis focuses on interactions of the endothelium, monocytes, and leukocytes, as well as the influences of cytokines, oxidized low-density lipoproteins, and genetic determinants. Finally, epidemiological risk factors associated with atherosclerosis such as hypertension and dyslipidemia are considered in light of their effects on adhesion molecule expression.