The term “plaque” in a biological context refers to a distinct, abnormal accumulation of material that develops on a surface within the body. When found in arteries, this structure is specifically known as an atheroma and represents the fundamental lesion of atherosclerosis, a chronic inflammatory disease. The formation and progression of this structure can compromise the function of the affected organ or tissue.
Defining the Biological Structure
Atherosclerotic plaque is a complex, raised deposit that forms within the tunica intima, the innermost layer of an artery wall. It is a three-dimensional structure embedded beneath the endothelial lining, primarily composed of an extracellular matrix, various cells, and accumulated fatty substances.
The plaque features a core rich in lipids, including cholesterol crystals and fatty acids, surrounded by debris from dead cells. This lipid-rich center is covered by a protective layer known as the fibrous cap, which consists mainly of smooth muscle cells and dense connective tissue, such as collagen.
The overall composition of a mature plaque also includes calcium deposits and white blood cells, particularly macrophages. The presence of calcium contributes to the hardening and stiffening of the arterial wall, a process known as arteriosclerosis.
The Step-by-Step Formation Process
Atherogenesis is initiated by damage to the endothelial cells lining the artery. Factors like high blood pressure, high cholesterol, and smoking can cause chronic injury and dysfunction to this lining. This damage allows low-density lipoprotein (LDL) cholesterol particles to seep into the arterial wall’s sub-endothelial space.
Once inside the intima, trapped LDL particles become chemically modified, primarily through oxidation, making them highly inflammatory. The immune system responds by sending monocytes from the bloodstream into the arterial wall. These monocytes differentiate into macrophages, which then begin to engulf the modified LDL particles.
The macrophages become engorged with fat, transforming into characteristic “foam cells,” which are the earliest visible sign of plaque formation, often called a fatty streak. As these foam cells accumulate and eventually die, they release their lipid contents, contributing to the formation of a growing pool of fat and debris known as the necrotic core. This core is the engine of plaque instability.
In response to the growing lesion, smooth muscle cells migrate from the middle layer of the artery wall and proliferate. These cells lay down a new extracellular matrix, primarily collagen, creating the fibrous cap that attempts to wall off the lipid core from the flowing blood. This encapsulation stabilizes the plaque, but chronic inflammation continues to remodel the structure.
Categorizing Different Manifestations
Atherosclerotic plaques are categorized based on structural characteristics that determine their clinical significance and risk. The primary classification distinguishes between stable and unstable, or vulnerable, plaques. This distinction is based primarily on the thickness of the fibrous cap and the size of the necrotic core.
A stable plaque is characterized by a thick, dense fibrous cap that effectively separates the lipid core from the arterial lumen. They contain a small necrotic core and are rich in smooth muscle cells and dense collagen, making them structurally sound. While a stable plaque may cause gradual narrowing of the artery, leading to predictable symptoms like chest pain during exertion, it is less likely to rupture unexpectedly.
In contrast, an unstable or vulnerable plaque possesses a thin fibrous cap and a large, soft, lipid-rich necrotic core. Vulnerable plaques are also characterized by intense inflammation, with active macrophages that secrete enzymes degrading the collagen structure of the cap. This combination of a thin, weakened cap over a large core makes the structure highly susceptible to mechanical rupture.
When a vulnerable plaque ruptures, the highly thrombogenic material of the necrotic core is exposed to the bloodstream, triggering the rapid formation of a blood clot. This sudden clot can completely block the artery, leading to acute events such as a heart attack or stroke. Another manifestation is the fibrocalcific plaque, which is heavily calcified with dense calcium deposits that make the structure hard and rigid, indicating a more stable, chronic lesion.