There are number of possible mechanisms by which inflammation could lead to arterial stiffening. (1) Inflammation is associated with endothelial dysfunction and this can regulate arterial stiffness via changes in smooth muscle tone. (2) Inflammation leads to increased synthesis of matrix metalloproteinases, which can degrade elastin, resulting in stiffening. (3) Several mediators of inflammation may directly stimulate vascular calcification, whereas endogenous inhibitors of vascular calcification are downregulated during inflammation, both of which can lead to stiffening. (4) During inflammation arterial glycosaminoglycan (GAG) synthesis is upregulated. In animal models, an overproduction of certain GAGs in the aorta results in stiffening of the arterial wall by thinning of elastic lamellae. (5) Finally, direct vascular inflammation could lead to arterial stiffening by changing the composition of extracellular matrix. This review aims to discuss potential mechanisms by which inflammation could lead to aortic stiffening.