Dental caries, commonly known as cavities or tooth decay, is a widespread infectious disease affecting the hard tissues of the teeth. It results from a dynamic imbalance within the mouth’s ecosystem. Decay is not simply a hole; it is a process of mineral loss driven by biological and environmental interactions. Understanding this science reveals that decay is a preventable cycle of destruction and attempted repair.
The Acid Attack: How Demineralization Occurs
The primary driver of decay is specific oral bacteria, particularly Streptococcus mutans, which colonize the tooth surface within a sticky biofilm called plaque. These microorganisms consume fermentable carbohydrates, such as glucose and sucrose, introduced through the diet. The metabolic byproduct is a sustained production of organic acids, primarily lactic acid, right against the tooth structure. This localized acid concentration initiates the destructive process.
The outer layer of the tooth, the enamel, is composed almost entirely of hydroxyapatite crystals. When the pH level in the plaque drops below approximately 5.5, demineralization begins. The acidic environment dissolves calcium and phosphate ions out of the enamel structure, weakening its integrity. This attack often leaves the surface looking opaque or chalky, signaling the earliest stage of decay.
Saliva acts as the mouth’s natural defense system, serving multiple protective functions. It mechanically washes away food debris and bacteria, helping to dilute the acid. Crucially, saliva is supersaturated with calcium and phosphate ions, which aids in remineralization—the repair of early demineralized lesions. Bicarbonate ions in saliva also function as a natural buffer, neutralizing bacterial acids and raising the local pH level.
Fueling the Process: Dietary and Environmental Factors
The frequency of carbohydrate exposure is often a greater risk factor than the total quantity consumed. Every time sugar or starch is eaten, plaque bacteria begin an acid-producing cycle that lasts for about 20 to 40 minutes. Frequent snacking or sipping on acidic or sugary drinks keeps the oral environment continuously acidic, preventing necessary periods of remineralization.
Inadequate oral hygiene allows the bacterial biofilm, or plaque, to mature and thicken undisturbed. This thick layer acts as a physical barrier, trapping acid against the enamel and preventing saliva from neutralizing the area. Mechanical removal through consistent brushing and flossing is required to disrupt this colonization and prevent acid concentration.
A primary environmental factor is reduced salivary flow, known as xerostomia or dry mouth. Many common medications, including those for allergies or depression, can suppress salivary gland function. Without the natural rinsing, buffering, and remineralizing effects of saliva, the decay process accelerates drastically.
The physical architecture of the teeth also plays a role in decay susceptibility. Deep pits and fissures on molars are difficult for toothbrush bristles to reach effectively. Similarly, crowded or misaligned teeth create tight spaces where plaque can accumulate and become sheltered from cleaning efforts. Genetic predispositions, such as variations in enamel structure or saliva composition, also influence resistance to decay.
From Surface Spot to Deep Cavity: Understanding Decay Stages
The initial clinical sign of decay is the white spot lesion, representing the first stage of mineral loss within the enamel. At this point, the decay is confined to the outer shell and may be halted or reversed through improved hygiene and fluoride application. If the acidic environment persists, the lesion penetrates further into the enamel, sometimes appearing as a darkening or brownish discoloration.
Once the decay breaches the enamel-dentin junction, progression accelerates significantly. Dentin is softer and less mineralized than enamel, making it more vulnerable to acid dissolution. This layer contains microscopic tubules that provide a rapid pathway toward the center of the tooth, allowing the decay to spread laterally and quickly deepen the lesion.
The continued destruction eventually reaches the pulp chamber, the innermost part of the tooth containing nerves, blood vessels, and connective tissue. When bacteria invade the pulp, it causes inflammation and infection, often resulting in severe pain. This advanced stage can lead to a periapical abscess at the root tip if left untreated, signaling a deep-seated infection in the jawbone.