Plaque is a soft, sticky film that builds up on your teeth, made primarily of bacteria, the sugary polymers they produce, and proteins from your saliva. The word “plaque” also refers to fatty deposits inside artery walls, which have a completely different composition. Since both types affect millions of people and come up in routine health conversations, here’s what each one actually contains.
What Dental Plaque Is Made Of
Dental plaque is a living biofilm. It contains roughly 100 billion bacteria per gram, packed into a matrix of sticky molecules, water, and food debris. That matrix isn’t random gunk. It’s an organized structure that bacteria actively build and maintain on your tooth surfaces.
The process starts within minutes of brushing. Proteins from your saliva, particularly a group that binds strongly to the mineral surface of enamel, coat your teeth in a thin layer called the pellicle. This protein film forms in about 30 to 90 minutes and is fully established within two hours. It serves as both a protective coating and, unfortunately, a landing pad for bacteria.
Streptococci are among the first bacteria to attach to the pellicle. Once anchored, they begin recruiting other species, creating a layered community that grows more complex over time. The deeper layers become oxygen-starved, allowing anaerobic bacteria to thrive in pockets along the gumline. This shift in bacterial populations is what eventually drives gum disease.
How Sugar Builds the Biofilm Scaffold
Bacteria don’t just float in a film on your teeth. They construct a physical scaffold out of sugar, and sucrose (table sugar) is the key building material. One species in particular, Streptococcus mutans, converts sucrose into sticky glucose-based polymers called glucans using specialized enzymes. These glucans act like glue, anchoring bacteria to enamel and to each other.
The effect of sugar is measurable. In lab studies, bacterial attachment to surfaces increased from about 1% in sugar-free conditions to nearly 6% when sucrose was present at 1% concentration. That’s a sixfold jump in stickiness. The glucans don’t just hold the biofilm together. They also help it grow from a flat layer into a three-dimensional structure with internal pockets where acid accumulates, eating into enamel. This is the direct link between sugar consumption and cavities: sugar doesn’t damage teeth on its own, but bacteria convert it into both the acidic waste that dissolves enamel and the structural glue that keeps the acid-producing colony in place.
When Plaque Hardens Into Tartar
If dental plaque isn’t removed, minerals from your saliva gradually crystallize within it, turning it into a hardite deposit called tartar (or dental calculus). Tartar is roughly 77% mineral by weight. Its main components are calcium (34% of the mineral content) and phosphorus (19%), with smaller amounts of magnesium and fluoride. This mineral makeup is similar to bone, which is why tartar bonds so firmly to teeth that it can only be removed with professional scaling instruments.
Tartar tends to accumulate fastest near the openings of salivary glands, especially behind the lower front teeth and along the outer surfaces of upper molars. Deposits that form below the gumline contain slightly more magnesium and fluoride than those above it, and they’re particularly damaging because they trap bacteria against sensitive gum tissue.
What Arterial Plaque Is Made Of
Arterial plaque is an entirely different substance. It forms inside blood vessel walls, not on surfaces, and it’s driven by cholesterol rather than bacteria. The core ingredients are LDL cholesterol, immune cells, dead cell debris, connective tissue, and calcium deposits.
The process begins when LDL particles (the “bad” cholesterol) accumulate in the inner wall of an artery. Once trapped there, these particles become chemically modified through oxidation and clumping. The immune system treats them as a threat, sending white blood cells called macrophages to absorb them. But the macrophages can’t fully break down the modified cholesterol. Instead, they swell with fatty droplets and become what pathologists call foam cells. These bloated immune cells pile up, die, and leave behind a greasy core of lipids and cellular debris.
Over time, the artery wall responds by building a cap of connective tissue over this mess. Smooth muscle cells in the artery produce collagen, elastin, and other structural proteins that form a fibrous layer. In mature plaques, this collagen-rich tissue often becomes the largest component by volume, essentially walling off the fatty core from the bloodstream.
Stable vs. Dangerous Arterial Plaques
Not all arterial plaques are equally threatening. What determines the danger is the internal structure, not just the size.
Stable plaques have thick fibrous caps, extensive calcification, and relatively small fatty cores. They narrow the artery gradually and may cause symptoms like chest pain during exercise, but they’re less likely to trigger a sudden heart attack. Calcium deposits in stable plaques can become quite large, sometimes visible on CT scans. A coronary artery calcium score of zero means no detectable calcified plaque. Scores of 1 to 99 indicate mild buildup, 100 to 299 moderate, and 300 or above severe.
Vulnerable plaques are the ones that cause most heart attacks. They have a large core of dead cell material (averaging about 34% of the plaque’s cross-section in ruptured specimens), covered by a dangerously thin fibrous cap, often less than 65 micrometers thick. For reference, that’s thinner than a human hair. These thin caps are infiltrated with macrophages that release enzymes breaking down collagen, weakening the structure further. When the cap tears, blood contacts the fatty core, triggering a clot that can block the artery within minutes. The plaques most likely to rupture tend to have fewer smooth muscle cells maintaining the cap, more inflammatory immune cells degrading it, and only small, scattered calcium deposits rather than the large stabilizing sheets seen in safer plaques.
Amyloid Plaques in the Brain
There’s a third type of plaque worth knowing about: the amyloid plaques found in the brains of people with Alzheimer’s disease. These are made of protein, not fat or bacteria.
The building blocks are short protein fragments called amyloid-beta peptides, with the 42-amino-acid version (Aβ42) being the most common in plaques. In a healthy brain, these peptides are produced and cleared regularly. In Alzheimer’s, they accumulate and misfold, stacking into thread-like structures called protofilaments. Two protofilaments twist together to form filaments, and filaments clump into the dense, insoluble plaques that disrupt brain cell communication. Researchers have identified at least two distinct filament shapes: one where the protofilaments extend arm-like structures to lock together, and another where they connect without these extensions. These structural differences appear to correspond to different forms of Alzheimer’s, suggesting the shape of the plaque may matter as much as the amount.