Dental Caries

Dental caries is a multifactorial infectious disease resulting in the localized destruction of susceptible dental hard tissues by acidic by-products from bacterial fermentation of dietary carbohydrates. It is the single most common chronic disease worldwide, affecting individuals across all age groups and socioeconomic strata.

The carious process begins with the dissolution of the mineral phase of enamel when the local pH drops below the critical threshold of 5.5 due to acid produced by cariogenic bacteria — primarily Streptococcus mutans and Lactobacillus species. Untreated, the lesion progresses through enamel into dentin and ultimately the pulp, leading to infection, abscess, and tooth loss.

Modern understanding frames caries as a disease of dysbiosis — a shift in the normally symbiotic oral biofilm toward an acid-tolerant, acid-producing community driven by frequent fermentable carbohydrate exposure and inadequate oral hygiene. Restoration of ecological balance, rather than mere surgical removal of decay, defines contemporary preventive and minimally invasive approaches.

Dental caries requires the simultaneous presence of three primary factors — a susceptible host (tooth), cariogenic microorganisms (plaque biofilm), and a fermentable substrate (dietary sugars) — interacting over sufficient time. This classic Keyes triad was expanded by Newbrun to include time as a fourth dimension.

Streptococcus mutans is the principal cariogen: it adheres to enamel via glucan-mediated mechanisms, metabolizes sucrose to lactic acid with extraordinary efficiency, tolerates low pH environments, and produces extracellular polysaccharides that fortify biofilm architecture. Lactobacillus acidophilus and Lactobacillus casei predominate in established dentinal lesions, sustaining progression.

Dietary sucrose is the preferred substrate. Frequency of sugar exposure is more damaging than total quantity — each acidogenic episode drops plaque pH below 5.5 for 20–40 minutes. Sweetened beverages, snacks, and hidden sugars in processed foods create repeated acid challenges throughout the day.

Host factors modulating susceptibility include: enamel crystallinity and fluoride content, tooth morphology (deep pits and fissures concentrate plaque), salivary flow rate and buffering capacity, genetic polymorphisms in enamel proteins, and the composition of the inherited and acquired oral microbiome.

Systemic risk factors — xerostomia from medications or radiotherapy, systemic diseases reducing salivary function, eating disorders causing acid exposure, and socioeconomic barriers to dental care — compound individual biological vulnerability.