The term “plaque” in biology refers to an abnormal, localized accumulation of material that forms a distinct deposit or film in or on a tissue surface. This phenomenon represents a pathological process where a substance, whether a microbial community or a host-derived accumulation, adheres and builds up in a manner detrimental to surrounding biological function. Plaque is fundamentally an unwanted accumulation, but its specific composition, location, and consequences vary widely. The context of where this deposit forms determines whether it is a microbial matrix, a hardened fatty deposit, or an aggregate of misfolded proteins.
Plaque as an Oral Biofilm
Dental plaque is a colorless, sticky film that adheres to the surfaces of teeth, representing a classic example of a complex, structured microbial community known as a biofilm. This accumulation begins minutes after brushing with the formation of an acquired pellicle, a thin layer of salivary proteins that coats the tooth enamel. Initial colonizer bacteria, such as Streptococcus mutans, then adhere to this pellicle, establishing the foundation of the growing film.
As the biofilm matures, the bacteria consume dietary sugars, particularly sucrose, and produce sticky, extracellular polysaccharides called glucans. These compounds form the matrix that encases the diverse microbial population. The metabolic activity of these bacteria generates acids as a byproduct, which lowers the pH on the tooth surface. This acidic environment causes the demineralization of the enamel, a process that eventually leads to dental decay, or caries.
If the dental plaque is not regularly removed, it can absorb minerals from saliva, such as calcium and phosphate, leading to hardening. This calcified deposit is known as dental calculus, or tartar, which provides a rough surface for more plaque to accumulate. Plaque accumulation near the gum line initiates inflammation, known as gingivitis. If left untreated, the deeper infection can progress to periodontitis, which involves the destruction of the bone and ligaments supporting the teeth.
Plaque in Arterial Walls
Plaque that develops within the walls of arteries is known as atherosclerotic plaque, which drives the disease process called atherosclerosis. Formation begins with an injury or dysfunction of the endothelium, the thin layer of cells lining the artery, often due to factors like high blood pressure or high levels of low-density lipoprotein (LDL) cholesterol. LDL particles penetrate the arterial wall and become trapped within the inner layer, where they are oxidized and consumed by immune cells called macrophages.
These lipid-engorged macrophages transform into “foam cells,” which are a hallmark of the early-stage fatty streak lesion. This accumulation of foam cells, along with fatty substances, cholesterol, and cellular debris, forms a lipid core. A fibrous cap, composed of smooth muscle cells and connective tissue, then grows over this core, creating the mature atherosclerotic plaque. This slow buildup causes the artery wall to thicken and stiffen, narrowing the vessel lumen in a process called stenosis.
The danger of atherosclerotic plaque often lies in its instability, particularly in plaques with a thin fibrous cap and a large lipid core. If this unstable cap ruptures, the internal contents of the plaque are exposed to the bloodstream, immediately triggering the coagulation cascade. This leads to the formation of a blood clot, or thrombus, which can quickly block blood flow. Blockage in a coronary artery causes a heart attack, while obstruction in an artery leading to the brain results in an ischemic stroke.
Plaque in Neurological Function
In the brain, a distinct type of deposit called amyloid plaque is a defining pathological feature of Alzheimer’s disease and other neurodegenerative conditions. These plaques are abnormal, extracellular aggregates of misfolded protein fragments, specifically Beta-Amyloid (A\(\beta\)) peptides, which accumulate in the spaces between nerve cells. The A\(\beta\) peptide is generated when a larger protein, the Amyloid Precursor Protein (APP), is sequentially cleaved by two enzymes, beta-secretase and gamma-secretase.
The resulting A\(\beta\) fragments, particularly the A\(\beta_{42}\) variant, misfold and clump together into small, soluble assemblies called oligomers, which are toxic to neurons. These oligomers then aggregate further to form the larger, insoluble amyloid plaques, which often present as a dense core surrounded by damaged nerve cell processes. This accumulation is believed to disrupt the normal communication between neurons at the synapse, impairing the brain’s ability to process information and form memories.
The presence of these plaques contributes to chronic inflammation and eventual death of brain cells. Amyloid plaque accumulation typically begins years or decades before the onset of cognitive symptoms, first appearing in areas of the brain associated with memory and learning. These protein deposits, along with another type of protein aggregate called neurofibrillary tangles, represent the structural damage that underlies the progressive decline seen in Alzheimer’s disease.