A dental cavity (dental caries) begins when acid produced by oral bacteria erodes the hard structures of a tooth. Bacteria feed on sugary and starchy debris, converting them into corrosive acids that dissolve the mineral content of the tooth surface. An untreated cavity is a progressive infection that travels deeper through the tooth’s layers, transforming from a minor issue into a severe health threat. Ignoring this bacterial invasion leads to a destructive sequence, moving from the outer shell to the inner nerve, and eventually to the surrounding bone.
The Initial Advance Through Enamel and Dentin
The initial stage of decay affects the enamel, the tooth’s outermost and hardest protective layer. Decay often presents as a small white spot, indicating localized demineralization, and is typically asymptomatic because enamel contains no nerves. If caught early, this process can sometimes be reversed with fluoride treatments. If left alone, the acid dissolves the enamel, creating an opening that allows bacteria access to the next layer, the dentin.
Dentin lies directly beneath the enamel and makes up the bulk of the tooth structure. Unlike enamel, dentin is softer and more porous, composed of millions of microscopic tubules that radiate outward from the central pulp chamber. These tubules act as a direct pathway to the tooth’s nerve, causing decay to accelerate rapidly once the infection reaches this layer.
Decay in the dentin introduces the first noticeable symptoms, primarily sensitivity to stimuli like hot or cold temperatures, or sweet foods. This occurs because thermal and chemical changes are transmitted through the dentinal tubules directly to the pulp tissue. At this stage, the pain is usually intermittent, sharp, and quickly subsides once the stimulus is removed, signaling that the infection is close to the nerve but has not yet caused irreversible damage.
Pulp Involvement and Nerve Damage
When decay continues its inward path, it reaches the pulp chamber—the soft, innermost compartment containing the nerves, blood vessels, and connective tissue. The invasion of bacteria and their toxins triggers a severe inflammatory response known as pulpitis. Because the pulp is encased within the rigid walls of the dentin, swelling has nowhere to expand, leading to increased internal pressure that compresses the nerve and blood vessels.
Initially, pulpitis may be reversible, meaning the pulp can recover if the decay is promptly removed and the tooth is sealed. As the infection deepens, however, the inflammation becomes irreversible, leading to constant, intense, throbbing pain that can spontaneously occur or wake a person from sleep. This lingering pain indicates that the nerve tissue is dying, a process called pulp necrosis.
The pain may suddenly disappear, which is not a sign of healing but indicates that the pulp tissue has died and nerve signals have ceased. The infection remains, and the dead tissue provides a breeding ground for bacteria to multiply unchecked. At this irreversible stage, a simple filling is insufficient; the only options to save the tooth are root canal therapy to remove the infected pulp, or extraction.
Development of a Dental Abscess and Bone Loss
Once the infection has killed the pulp, bacteria travel through the root canal system and exit the tip of the tooth root, invading the surrounding jawbone. This results in the formation of a periapical abscess—a localized pocket of pus composed of dead cells, bacteria, and tissue debris. An abscess is accompanied by swelling in the face or jaw, a persistent bad taste, and sometimes a fever.
The abscess exerts pressure on surrounding structures, leading to a constant, dull ache or sharp pain when biting down. The body attempts to relieve this pressure, sometimes resulting in the formation of a fistula—a small channel that opens onto the gum tissue, allowing pus to drain. While draining may temporarily relieve pain, the underlying infection remains active and continues to cause damage.
A consequence of this localized infection is the destruction of the alveolar bone, the specialized bone that supports the tooth. The chronic bacterial infection triggers an inflammatory response that dissolves the surrounding jawbone tissue, resulting in bone loss. This erosion weakens the tooth’s foundation, making the infection difficult to manage and potentially leading to the tooth becoming loose.
Systemic Risks and Complex Treatment Needs
If the abscess is not treated, the infection can break out of the jawbone and spread to adjacent tissues in the head and neck. This spread can result in complications such as cellulitis (a rapidly spreading bacterial infection of the soft tissues) or the life-threatening condition known as Ludwig’s angina, which can obstruct the airway.
In severe cases, bacteria from the dental infection can enter the bloodstream, leading to a systemic infection known as sepsis. Sepsis is a medical emergency where the body’s response damages its own tissues and organs, potentially resulting in organ failure or death. These systemic risks underscore the importance of treating dental infections before they progress beyond the oral cavity.
By the time decay reaches the stage of an advanced abscess, the tooth is often non-salvageable and requires extraction. Tooth removal necessitates subsequent complex and costly interventions, such as a dental bridge or implant, to restore function and prevent shifting of surrounding teeth. These procedures are more invasive and expensive than the simple filling that would have resolved the problem earlier.