Caries is formed after tooth eruption by dissolution of enamel induced by cariogenic acids being produced by cariogenic bacteria during fermentation of carbohydrates. In the past, caries was often regarded as a transmittable disease caused by an infection with bacteria like Streptococcus mutans (Keyes 1960). Today, caries is rather seen as a process triggered by the frequent intake of fermentable carbohydrates (sugars) and characterized by an ecological shift in the oral microbiology toward acidogenic and aciduric bacteria (Marsh 2003). Moreover, it is emphasized that multiple (mostly protective) factors such as oral hygiene, access to fluorides, or amount and composition of saliva influence the caries process (Paris and Meyer-Lückel 2012).

The cariogenic bacteria produce organic acids (e.g., lactic acid), which diffuse into the tiny pores of enamel and there dissolve the enamel apatite. This causes an increasing porosity within the enamel. Thus, in the initial stages of the disease the caries lesion is characterized by porous enamel. The word “initial” may be somewhat misleading because lesions that appear as white spots are often several hundred micrometer deep, often extending up the enamel dentin junction or even deeper. It may take weeks to months and years until a caries lesion reaches a stage where so much mineral is lost that the lesion collapses and a cavity forms. Nevertheless, caries is a dynamic process. If the interplay of multiple etiological factors shifts toward less cariogenic conditions, lesions can take up mineral from the saliva again and start to remineralize. Usually de- and remineralization cycles alternate several times a day, but if over time remineralization overweighs demineralization, the lesion does not progress but arrests. This remineralization is usually confined to the outer surface of the lesion where over time a so-called pseudo-intact surface layer is formed. This surface layer has usually a thickness of approximately 20–40 μm (but sometimes even more then 100 μm) and is considerably less porous than the underlying lesion body (Meyer-Lueckel et al. 2007). Thus, arrested or remineralized lesions look very similar to active progressing caries lesions except the higher mineralized surface. For this reason, it is a challenge to differentiate inactive lesions (enamel scars) from active progressing caries.

When white spot lesions arrest, along with the minerals also organic components such as food pigments can be incorporated into the surface layer. This is why some lesions may get a brownish discoloration and thus are called “brown spots” (Fig. 10.2).

Caries lesions usually develop in tooth sites where plaque formation is fostered such as in the fissure system or interproximal. On oral or buccal smooth surfaces plaque formation is usually increased at the cervical margin. Quite frequently, buccal caries lesions are observed after treatment with fixed orthodontic brackets. These appliances hamper the natural cleaning as well as oral hygiene and thus promote plaque formation. After removal of the brackets, these surfaces may be easily cleaned again. This improvement in oral hygiene leads to an arrest of many buccal white spot lesions. These lesions do not need any further treatment, as they are not signs of active disease, but enamel scars. From an aesthetic point of view, however, both active and inactive caries lesions are unattractive and may need intervention.

Buccal early caries lesions can be easily differentiated from developmental defects (see below) as caries only forms in plaque stagnation areas and thus caries on buccal surfaces is confined to cervical areas or the areas around the bracket base (Lovrov et al. 2007; Mitchell 1992).

Developmental defects are caused by a disturbance during enamel formation. Multiple factors such as toxic agents, infections, trauma, or irradiation have been elucidated. The resulting defects can be quantitative (with a lack of enamel volume) or qualitative (with a deficiency of enamel structure) or a combination of both. Here we concentrate on qualitative defects, which are characterized by increased enamel porosity.

The technique of resin infiltration was originally developed to arrest noncavitated caries lesions. The mineral loss of early caries lesions results in the formation and growth of porosities in the enamel matrix. These pores act as diffusion pathways for acids into the enamel and dissolved minerals out of the enamel. Caries infiltration aims to penetrate these pores with low viscosity light curing resins – so called infiltrants – that infiltrate the porous enamel driven by capillary forces (Paris et al. 2010). When the resin is light cured, it blocks the diffusion pathways and protects the remaining apatite crystals (Meyer-Lueckel and Paris 2008).

One positive side effect of resin infiltration is an immediate color change of the whitish lesion once it is infiltrated. The infiltrant resin has a refractive index of 1.52, which is close to that of enamel (1.62). Therefore, light scattering between the enamel pores and the surrounding enamel is significantly reduced when the pores are filled with resin instead of water or air (Fig. 10.5). Under best conditions, the resin-infiltrated lesions are optically masked and “disappear” (Paris and Meyer-Lueckel 2009; Eckstein et al. 2015).

To achieve resin infiltration of porous enamel, the lesions need to be conditioned. As the pseudo-intact surface layer has a much lower porosity compared with the underlying lesion body, it hampers penetration of the infiltrant resin and thus must be removed. This can be achieved by etching the lesion with 15 % hydrochloric acid (HCl) gel for 2 min.

In the next step, the lesion must be properly desiccated. As the penetration of the infiltrant resin infiltration is based on capillary action, any other liquid within the porous enamel network would inhibit any infiltration. Usually, the desiccation is achieved by a combination of air-blowing, an application of ethanol and another air-blowing subsequently. Finally, the infiltrant resin is applied for 3 min. Although infiltrants are chemically similar to many commercial bonding agents, it is strongly recommended not to misemploy adhesives or bonding agents for caries infiltration but to use the commercially available infiltrant kit. Infiltrant resins show a much higher penetrability compared with bonding agents and thus ensure a deeper infiltration. But even with an infiltrant the relatively long application time of 3 min is recommended to ensure a preferably complete infiltration of the lesion body (Fig. 10.6).