Age-related changes in vessel wall structure that enhance susceptibility to vasculitis. The vessel wall is prone to age-related changes that accumulate over a lifetime. Vascular stiffening results from biochemical changes of the cellular and extracellular components comprising the wall. Aged vessels typically lose elasticity and pliability. Elastic fibers/membranes show fatigue and fracture and matrix proteins accumulate biochemical modififications. Cell numbers and cell mobility through the wall layers change. The overall effect is a thinning of the medial layer, luminal widening and expansion of the intimal layer. Calcium deposition in the wall occurs frequently and may indicate foci of tissue injury. The 'old' artery provides a distinct microenvironment that potentially increases the risk for the homing and the persistence of pro-inflammatory immune cells and supplies a novel spectrum of neoantigens.