Posterior_Direct_Restorations Salvatore_compressed

FIG 3-7 Where cariogenic biofilm is present, demineralization continues until the enamel structure collapses and dentinal infection results. Note that brown spots are present on the enamel of the mandibular right first premolar despite the greater tendency of this surface to demineralize.

Narrowing of the pulp chamber (Fig 3-8)

FIG 3-8 (left) Narrowing of the distal pulp horn of the mandibular right first molar resulting from the progression of a preexisting caries lesion.

Pulpitis

Loss of pulp vitality

Partial or total crown fracture

Tooth loss (usually by extraction; Fig 3-9)

FIG 3-9 (right) Edentulous space at the site of the maxillary right first molar, which was extracted because of sequelae of caries-related disease.

Caries or caries-related disease can therefore be defined as an “infectious and communicable process, where a cariogenic biofilm causes demineralization of the tooth’s hard tissues in the presence of oral conditions that are more pathologic than protective.”8 Protective oral conditions are those that promote a remineralizing oral environment, ie, one that is favorable to molecules attaching to the tooth rather than detaching from it (demineralization). These factors can be schematically represented9 as shown in Fig 3-10. A preponderance of pathologic conditions will make certain tooth surfaces (where the cariogenic biofilm can proliferate undisturbed) more inclined to demineralization than to remineralization.

FIG 3-10 Balanced model of caries, indicating protective and pathologic factors and disease indicators. Upstream determinants such as low socioeconomic status or presence of systemic disease also play an important role in disease predisposition. (Modified from Featherstone.9)

Caries is also currently interpreted as a behavioral condition with a bacterial component, where the host behavior is identified as the primary factor responsible for creating an ideal environment for the cariogenic biofilm to become established. Transmission of cariogenic bacterial strains (typically by parents or other children) is most significant during the first months or years of the patient’s life; therefore, the main aim of caries prevention should be to prevent, render unlikely, or postpone this event as long as possible through behavioral and dietary guidance given to children by their parents.

As with many diseases, the mere presence of risk factors (pathologic in this case) does not necessarily indicate that the disease is present and active. Caries-related disease can only be considered present if cavitated or noncavitated active lesions are found. A patient can be considered cured of disease 3 years after the latest treatment of an outcome of caries (eg, one or more restorations or attempts to remineralize an active white spot). Lastly, some outcomes of caries can still be detectable long after recovery even when disease is absent (examples include pulp

chamber narrowing or pulpitis that is revealed or occurs long after restoration has been performed). Though not directly related to the oral environment, factors referred to as upstream determinants have also been shown to be related to an increased probability of incurring cariesrelated disease. These conditions include low socioeconomic status, low level of education, presence of conditions or diseases that are debilitating or have an oral impact, the need to use certain drugs, and inaccessibility of treatment centers.10

Lesion Dynamics and Activity

The dynamics of a caries lesion in a tooth can be summarized as follows11,12:

1.Acidogenic bacterial plaque ferments carbohydrates introduced with the diet, thus producing acids (lactic, formic, acetic, and propionic) (Fig 3-11).

FIG 3-11 (left) Large buildup of bacterial plaque, potentially responsible for caries and/or periodontal disease.

2.The acids spread into exposed tooth tissues, partially dissolving their constituent mineral crystals (hydroxyapatite carbonate).

3.Detachment of mineral salts from tooth surfaces leads firstly to roughening, subsurface demineralization, and ultimately cavitation (Fig 3-12).

FIG 3-12 (above) Polarized photo of a WS in the cervical region of the tooth, showing early signs of cavitation.

4.The demineralization process can be reversed by calcium, phosphate, and fluoride, which spread inside the tooth tissues and deposit a new mineralized layer on the remaining crystals in noncavitated lesions (remineralization) (Fig 3-13).

FIG 3-13 WS with areas of partial surface remineralization. The remineralized surface feels the same as unaffected tissue when an instrument is passed over the surface.

5.When fluoride is present, the new surface is much more resistant to acid attack.

6.The demineralization-remineralization process takes place several times a day and can give rise to cavitation, repair, or maintenance of the status quo.

7.The prevalence of demineralization processes leads to the spread of infection with progressive loss of tooth tissue, pulp disease, and tooth loss (Figs 3-14 and 3-15).

FIG 3-14 Structural failure of the enamel and exposure of dentin.

FIG 3-15 Extreme outcomes of caries-related disease. The first molar will have to be extracted.

In the case of initial, ie, noncavitated, lesions the International Caries Detection and Assessment System (ICDAS II), which guides the visual diagnosis process for cleaned tooth surfaces, identifies two levels:

ICDAS 1: First visual change on enamel surface due to demineralization seen after 5 seconds of air drying

ICDAS 2: Distinct visual change in enamel seen whether the surface is wet or dry (see Fig 3-5)

The reader is referred to the ICDAS II Criteria Manual13 for details regarding the remaining categories, ranging from a sound surface (ICDAS 0) to cavitated lesions (ICDAS 3 to 6).

Noncavitated lesions (ICDAS 1 and 2) can also be classified based on their activity. According to the Nyvad et al criteria,14 a noncavitated lesion can be defined as:

Active: When the likelihood of lesion progression is greater than the likelihood of nonprogression. The lesion has a rough surface and a chalky, opaque appearance (active WS). Often found at the site of plaque deposits, and the nearby periodontium is often inflamed and bleeds on light probing; the enamel surface is porous and allows acids to pass through to subsurface layers. Feels rough to the touch (see Fig 3-12).

Inactive: When the likelihood of lesion nonprogression is greater than that of progression. The surface of the lesion is smooth and shiny; it is generally not located near plaque deposits, and the surrounding gingiva is free of inflammation. The enamel surface has been remineralized through a change in local and general circumstances; white areas often persist in subsurface layers (inactive WS), given that the remineralized surface acts as a strong barrier that prevents minerals from penetrating to greater depth. The surface feels like the sound surrounding surface (see Fig 3-13).

Inactive lesions may still feature persistent whitish areas in subsurface layers or brown pigmented areas during the remineralization