Children have both macrophages and macrophages that are filled with lipid droplets (foam cells) at susceptible sites of arteries. Such changes are minimal and may not develop further. However, in some adolescents, small pools of dead foam cell remnants and lipid droplets (extracellular lipid) are added to the foam-cell accumulations at the susceptible sites. The pools are the precursor of a much larger confluent accumulation of extracellular lipids (the lipid core)-the hallmark of the atheromas of young adults. As soon as a lesion with a lipid core is present, calcium granules of microscopic size are found among the packed extracellular particles and droplets and in smooth-muscle cells isolated among them. Disintegration of arterial structure at the core facilitates tears at the surface, hematoma, and thrombosis. As a response, layers of reparative fibromuscular tissue are added and may predominate in a lesion. Over time, calcium lumps and plates form through accretion of adjacent extracellular calcium granules. In adults past the fourth decade of life, the greater part of the former lipid core of a lesion may be calcified and there may be osseous metaplasia. The effect of therapeutic reduction of high levels of blood cholesterol on lesions was studied in rhesus monkeys. Drastic reduction of blood cholesterol levels for 312 years resulted in the disappearance of macrophages, macrophage foam cells and lymphocytes, and reduction of extracellular lipid from advanced lesions. Calcium deposits remained in the arterial wall and were not visibly changed.