Ultrastructural alteration of the tunica intima consists of extracellular lipid accumulation; an increase in the presence of collagen fibrils, elastic fibers, and glycosaminoglycans; foam cells derived from macrophages or smooth muscle cells; and calcium deposits.
2,20) These observations are in contrast to what is known about the mechanism of atherosclerosis in other species and the current, widely accepted theory that atherosclerosis is initiated by endothelial dysfunction and the accumulation of oxidized lipoproteins in the tunica intima, which results in a chronic inflammatory response.
Our case presents similarities to atherosclerosis described in humans and other avian species in that lesions were primarily found in the tunica intima and the luminal side of the tunica media, and the lesions were composed, as demonstrated by histology and electron microscopy, primarily of extracellular lipids and foamy macrophages.
Histologically, a 'Normal' aorta was characterised as having a tunica intima that was relatively thin and loose, with regularly arranged smooth-muscle cells and elastin fibres in the tunica media, and a loosely organised tunica adventitia.
Thickening of the tunica intima, disruption of the smooth muscle cells in the tunica media and branching and 'splitting' of elastic fibres with deposits of collagen in the region between the two layers can be seen in Fig.