Dental caries is a bacterially based disease that progresses when acid produced by bacterial action on dietary fermentable carbohydrates diffuses into the tooth and dissolves the mineral, that is, demineralization. Pathological factors including acidogenic bacteria (mutans streptococci and lactobacilli), salivary dysfunction, and dietary carbohydrates are related to caries progression. Protective factors which include salivary calcium, phosphate and proteins, salivary flow, and fluoride in saliva can balance, prevent or reverse dental caries. Fluoride works primarily via topical mechanisms which include (1) inhibition of demineralization at the crystal surfaces inside the tooth, (2) enhancement of remineralization at the crystal surfaces (the resulting remineralized layer is very resistant to acid attack), and (3) inhibition of bacterial enzymes. Fluoride in drinking water and in fluoride-containing products reduces tooth decay via these mechanisms. Low but slightly elevated levels of fluoride in saliva and plaque provided from these sources help prevent and reverse caries by inhibiting demineralization and enhancing remineralization. The level of fluoride incorporated into dental mineral by systemic ingestion is insufficient to play a significant role in caries prevention. The effect of systemically ingested fluoride on caries is minimal. Fluoride "supplements" can be best used as a topical delivery system by sucking or chewing tablets or lozenges prior to ingestion.

No abstract

The eventual outcome of dental caries is determined by the dynamic balance between pathological factors that lead to demineralization and protective factors that lead to remineralization. Pathological factors include acidogenic bacteria, inhibition of salivary function, and frequency of ingestion of fermentable carbohydrates. Protective factors include salivary flow, numerous salivary components, antibacterials (both natural and applied), fluoride from extrinsic sources, and selected dietary components. Intervention in the caries process can occur at any stage, either naturally or by the insertion of some procedure or treatment. Dental caries covers the continuum from the first atomic level of demineralization, through the initial enamel or root lesion, through dentinal involvement, to eventual cavitation. The dynamic balance between demineralization and remineralization determines the end result. The disease is reversible, if detected early enough. Since demineralization can be quantified at early stages, before frank cavitation, intervention methods can be tested by short-term clinical trials.

Dental caries is a transmissible bacterial disease process caused by acids from bacterial metabolism diffusing into enamel and dentine and dissolving the mineral. The bacteria responsible produce organic acids as a by-product of their metabolism of fermentable carbohydrates. The caries process is a continuum resulting from many cycles of demineralization and remineralization. Demineralization begins at the atomic level at the crystal surface inside the enamel or dentine and can continue unless halted with the end-point being cavitation. There are many possibilities to intervene in this continuing process to arrest or reverse the progress of the lesion. Remineralization is the natural repair process for non-cavitated lesions, and relies on calcium and phosphate ions assisted by fluoride to rebuild a new surface on existing crystal remnants in subsurface lesions remaining after demineralization. These remineralized crystals are acid resistant, being much less soluble than the original mineral.

A direct comparison of quantitative microradiography and microhardness profiles was made using artificial caries-like lesions in human enamel. Tooth crowns with lesions were cut in half through the center of the lesions and opposing halves were assessed by one of the techniques, from the anatomical surface, across the lesion, and into the underlying enamel. A linear relationship was found between volume percent mineral determined by microradiography and the square root of the Knoop Hardness Number assessed by microhardness testing in the mineral range of 40–90 volume percent. The relationship also holds for sound dentine. It is concluded that either technique can be used to measure mineral profiles through carious lesions as a result of demineralization and presumably remineralization.