Microinvasive Therapy: 17 Caries Infiltration
The microinvasive procedures for occlusal and approximal sealing described in the previous chapters use materials that are familiar from restorative therapy. According to the clinical procedure, the tooth surface is etched with phosphoric acid, then adhesive or fissure sealant is applied which is subsequently light cured.
In this chapter, a microinvasive treatment will be described that was introduced to general dentistry in 2009, namely caries infiltration. In this technique for arresting the progress of caries, a comparatively strong acid (hydrochloric acid 15%) is required to condition the carious tooth surface, and resins with a modified monomer composition, so-called infiltrants, are applied. In contrast to adhesives and fissure sealants, these highly liquid resins are able to penetrate the porous structures of the lesion body more deeply and thereby obstruct the diffusion pathways for cariogenic acids. In caries infiltration as opposed to the (occlusal) sealing of caries, the diffusion barrier is created not on but within the caries itself1–4 ( Fig. 17.1 ).
In detail this chapter will cover:
The development of caries infiltration
The biological and therapeutic backgrounds of caries infiltration
The use of caries infiltration to arrest caries progression
The use of caries infiltration for esthetic reasons
Development of Caries Infiltration
As described in Chapters 2 and 3, the early-to-intermediate stages of enamel caries manifest a pronounced demineralization of the tooth enamel (lesion body) below an apparently intact surface layer. The elevated mineral loss alters the refraction of light, which gives the lesions their white appearance (white spots). During remineralization, pigments can become incorporated, and the caries lesion assumes a darker color (brown spots). A major portion of these caries lesions that are clearly visible to the dentist (ICDAS 2) is not limited histologically to the enamel. The dentin underneath is also demineralized. Such caries lesions in approximal surfaces (histological extension around the enamel–dentin junction) will be visible in xray radiographs as being extended into the enamel only. Thus, the appearance of the caries in the x-ray image under-represents the actual histological extension (see Chapters 5 and 6). Such caries lesions that appear restricted to the enamel in the x-ray photo rarely show cavitated surfaces.
Radiographs of enamel lesions (E1 and E2) rarely reveal cavitation. Once the caries has advanced up to the first third of the dentin as shown in the x-ray (D1), cavitation is clinically detectable in approximately one-third of lesions.5,6
In contrast to cavitated lesions, noncavitated caries lesions only manifest a few bacteria in the area of the lesion body, and there is no established biofilm.7 Cavitated caries lesionsare more difficult to clean, which is why there is a greater probability that they will progress.8
Pioneering Work on Penetration of Resins in Caries Lesions
The possibility of penetrating caries with resins was first described in the 1970s, by using artificial enamel caries with a surface layer that was less mineralized than natural carious enamel. Natural lesions are difficult to penetrate with the adhesive that was employed.9 The progress of caries in artificial lesions was demonstrably halted by applying a low-viscosity resin. However, the material that was used in this study, resorcinol form-aldehyde, was highly unsuitable for clinical use due to its toxic properties.10 The observations of using adhesives for penetrating caries lesions were confirmed in a few subsequent investigations.11–17 These authors generally described a seal that essentially covers the surface using commercially available adhesives which leaves a surface layer of material. It was revealed that multiple applications of the sealant improved the penetration of the resins.16 This causes a comparatively strong reduction in the pore volume.10,15 Generally, in these studies any excess resin on the surface was left, it is assumed, to at least partially block the access of acids to any remaining pores in the lesion body.10,15 The positive association of penetration depth with application time was also demonstrated by removing the excess from the surface of artificial lesions.18 Furthermore, the employed adhesives and fissure sealants inhibited caries to different degrees depending on the application time and homogeneity of the created resin layer within the lesion body.19
Development of Caries Infiltration
Even after the tooth surface is etched for 2 minutes with phosphoric acid, the adhesives have difficulty penetrating natural caries lesions.20 This is due to the relatively low pore volume of the surface layer which prevents deeper penetration, and the inadequate physical properties of available adhesives.20 Etching the tooth surface for 2 minutes with hydrochloric acid gel (15%) specifically erodes the surface layer21 and enables the adhesive to penetrate at maximum ca. 100 µm into natural caries lesions20 ( Fig. 17.2 ). On the other hand, monomers of low viscosity may penetrate the demineralized enamel, which can be viewed as a system of minute capillaries much more easily. The penetrating properties of a liquid are described by the Washburn equation,22 where the term in parentheses represents the penetration coefficient (PC).23,24
First, the PCs of a few combinations of monomers were determined,26 and some of these materials were investigated with regard to their penetrating27 and cariesinhibiting28 properties using artificial caries lesions. The penetration depth of the monomers correlates with the root of the product of the PC and the application time. This means that the penetration coefficient of the monomer mixture is a good predictor of its penetrating and caries-inhibiting ability. Materials with a penetration coefficient above 50 cm/s were consequently termed infiltrants.27,28
Penetration experiments using the infiltrants on natural lesions revealed results comparable with those for artificial lesions. In an initial study, it was found that the penetration depth of an infiltrant was significantly higher than that of the adhesive used in previous experiments.29 In particular, infiltrants with a PC above 200 cm/s almost completely penetrated enamel lesions with an average depth of ca. 900 µm.30,31 The infiltrated lesions were then stored in a demineralization solution to induce the further progress of caries. In contrast to untreated controls, the progress of caries was almost completely stopped by the infiltrants after 400 days of storage in a demineralizing environment at pH 4.95.32 The relatively long application time of 5 minutes used in these experiments could apparently be shortened to 3minutes.31 Treating the tooth surface once with ethanol to dry it directly before applying the infiltrant was not inferior to using acetone.33
An initial study of the efficacy of preventing the progress of caries was performed in situ. Ten test subjects wore removable appliances in this experiment. Enamel samples containing artificial caries were placed in these. One part of the lesions was treated before the in situ phase with an infiltrant, and another part served as an untreated (negative) control. Enamel samples with artificial caries to which a layer of fissure sealant was applied served as a positive control. The infiltrated areas and positive controls manifested an insignificant amount of caries progression after being worn for 100 days, whereas the untreated areas progressed ca. 100%.34
These positive results served as a foundation for clinically testing the efficacy of infiltration.
Principle of Caries Infiltration
The relatively strongly mineralized surface layer of caries prevents resins from penetrating the lesion body.20 Consequently, the surface should first be specifically eroded with a hydrochloric acid gel. This cannot be achieved with a phosphoric acid gel even after a long exposure time21,35 ( Fig. 17.3 ). After the surface has been sufficiently etched and is fully dry, the infiltrant is able to penetrate natural caries lesions up to a few hundred micrometers29,30 ( Fig. 17.4 ). After it hardens, the resin seals the caries internally to prevent the further progression of caries.32,34,36
The principle of caries infiltration is based on the penetration of a low-viscosity resin (infiltrant) into the lesion body of the caries. After it hardens, the infiltrant seals the pores of the lesion and therefore offers a diffusion barrier to acids and fermentable carbohydrates.
As a positive side-effect, the enamel areas of caries lesions lose their whitish appearance after infiltration. These carious areas are therefore visually similar to healthy enamel. This masking effect is based on a modification of the light refraction within the enamel lesion. Healthy enamel has a refractive index (RI) of 1.62. The microporosity within enamel caries is either filled with an aqueous medium (RI: 1.33) or air (RI: 1.0). The different refraction indices cause light to scatter at the boundary surfaces which gives these lesions a whitish opaque appearance, particularly when dry.37 The micropores of the infiltrated lesions are in contrast filled with resin (RI: 1.52) which cannot evaporate like the aqueous medium. Due to the relatively slight difference between the refraction indices of the infiltrated pores and that of the surrounding healthy enamel, the caries appears much less white than before infiltration38 ( Fig. 17.5 ).
The masking of caries by means of infiltration is based on the change in the refraction index of the caries lesion.
Infiltration to Prevent Caries Progression
Due to the strong epidemiological relevance of approximal caries(see Chapter 8) and the few the rapeutic options available (either surveillance plus use of fluorides, or filling), caries infiltration was chiefly developed to prevent the progression of caries in these surfaces. Other smooth surfaces (especially of the anterior and buccal teeth) can be infiltrated to stop the progression of caries, especially in patients with a high risk of caries. However, one should avoid overtreating, and microinvasive treatments have to be balanced against noninvasive forms of intervention. In most patients with low or moderate risk for caries, buccal lesions remineralize as a result of enhanced oral hygiene or altered nutritional habits. Consequently, caries infiltration is rarely indicated for these smooth surfaces, which are easily accessible to oral hygiene (Chapter 20).
Clinical Efficacy of Infiltrating Approximal Surfaces
In a clinical study of 20–34-year-olds in Germany, caries lesions in approximal surfaces of posterior teeth were treated. In the radiographs, the lesions extended at a minimum into the inner half of the enamel (E2), and at a maximum into the first third of the dentin (D1). Each patient was assigned one test lesion (infiltration) and one control caries (split-mouth design). Using digital subtraction radiography, it was found that 37% of the control lesions and only 7% of the infiltrated lesions had progressed after 18 months of observation.36 After 3 years of observation, 46% of the control lesions and 4% of the infiltrated caries lesions had progressed39 ( Fig. 17.6 ). Another clinical study of caries infiltration was performed on deciduous molars in 5–8-year-olds with relatively high caries risk. In addition to infiltration treatment, fluoride varnish was applied to the control and infiltrated lesions every 6 months. The radiographs revealed that 62% of the control lesions and 23% of infiltrated lesions (both mainly D1 at baseline) had progressed after 12 months40 ( Fig. 17.6 ).
The infiltration technique as it is used today has certain limits. Particularly for patients with a high caries risk, lesions that have progressed radiographically into the first third of the dentin should only be referred to caries infiltration with caution. The probability that these caries lesions already show microcavitations that cannot be completely filled with the infiltrant might be increased, which sets the lesion at a higher risk for progression. However, in general the clinical data on sealing approximal caries lesions support the thesis that tightly sealing caries enamel and dentin halts the advance of caries (“seal and heal,” see Chapters 15 and 20).
At present, there are no clinical studies on the progression of post-infiltrated caries in other smooth surfaces besides approximal smooth surfaces. Up to now, existing infiltrants have not been optimized to treat fissure caries efficaciously.