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Figure 15.5 Mechanism of foam cell formation. CHAPTER 15

2. MONOCLONAL HYPOTHESIS. This hypothesis is
based on the postulate that proliferation of smooth muscle
cells is the primary event and that this proliferation is
monoclonal in origin similar to cellular proliferation in
neoplasms (e.g. in uterine leiomyoma, Chapter 8). The
evidence cited in support of monoclonal hypothesis is the
observation on proliferated smooth muscle cells in
atheromatous plaques which have only one of the two forms The Blood Vessels and Lymphatics
of glucose-6-phosphate dehydrogenase (G6PD) isoenzymes,
suggesting monoclonality in origin. The monoclonal
proliferation of smooth muscle cells in atherosclerosis may
be initiated by mutation caused by exogenous chemicals (e.g.
cigarette smoke), endogenous metabolites (e.g. lipoproteins)
and some viruses (e.g. Marek’s disease virus in chickens,
herpesvirus).

MORPHOLOGIC FEATURES
Early lesions in the form of diffuse intimal thickening, fatty
streaks and gelatinous lesions are often the forerunners
in the evolution of atherosclerotic lesions. However, the
clinical disease states due to luminal narrowing in
atherosclerosis are caused by fully developed atheroma- Figure 15.6 Schematic evolution of lesions in atherosclerosis.
tous plaques and complicated plaques (Fig. 15.6).

1. FATTY STREAKS AND DOTS. Fatty streaks and the first year of life. However, they are uncommon in older
dots on the intima by themselves are harmless but may persons and are probably absorbed. They are especially
be the precursor lesions of atheromatous plaques. They prominent in the aorta and other major arteries, more often
are seen in all races of the world and begin to appear in on the posterior wall than the anterior wall.