Traditionally, before placing a restoration, excavation of tissues affected by caries was recommended. The goal was to have all walls of the cavity on sound, hard dentin, even when at risk of pulpal exposure. Current understanding of the caries process indicates that preserving tooth structure can lead to better long-term outcomes. Selective caries excavation refers to preserving tooth structure by delineating excavation in the pulpal and axial wall according to lesion severity and depth as well as pulpal health while keeping all cavity margins on sound tooth structure. Compounding evidence indicates that when a good marginal seal is present, the lesion will arrest.
Selective caries removal preserves tooth structure.
Presence of bacteria underneath as well-sealed restoration does not preclude lesion arrest.
Understanding dentin demineralization process is crucial to understanding the new paradigm of surgical management of caries lesions.
For centuries, the understanding of dental caries has focused on excising the problem (caries) and restoring the teeth. In fact, restoration of teeth can be found from ancient writings of many populations including Egyptians, Mesopotamians, Israelites, Indians, Chinese, Greeks, Romans, Aztecs, Mayans, Incas, and Arabs. The first full description of restoration of teeth is attributed to Pierre Fauchard in 1728. Although the understanding of dental caries as a disease has come a long way since then, the approach to dental caries management has not changed significantly.
It is well established that dental caries is a biofilm-mediated disease modulated by diet. A cariogenic diet can cause dysbiosis in the oral biofilm, over time leading to demineralization of exposed hard tooth surfaces. This ongoing process of repeated demineralization at the enamel subsurface level can eventually progress to a collapse of the surface, causing a cavitation in the enamel surface. As the process continues, demineralization of the inorganic phase of the dentin and denaturation and degradation of the organic phase (primarily dentin collagen) result in dentin cavitation. Severe demineralization of dentin results in the exposure of the protein matrix, which is denatured initially by host matrix metalloproteinases (MMPs) and subsequently degraded by MMPs and other bacterial proteases.
Once cavitation occurs, the biofilm has a protected, highly acidic and anaerobic environment ideal for cariogenic bacteria. Thus progression can occur at a faster rate. Although theoretically any caries lesion given the right conditions can be arrested and have progression to larger lesions forestalled, once cavitation occurs, removal of the biofilm is more difficult, and sealing off the cavity by a restorative intervention is usually needed to stop disease progression. Restorative intervention is also often needed to restore tooth to function and aesthetics and support tooth structure integrity independent of the activity status of the carious lesion.
The caries process in dentin
The effects of the caries process in dentin have conventionally labeled dentin as affected and infected. These terms are not accurate, as bacteria have been found in even sound dentin; they also are not helpful to the clinician, as it is difficult to distinguish what is affected from infected. Traditionally, it was thought that all tissue affected by the dental caries process should be removed, and all surfaces of the cavity should be left in sound, hard dentin, even if that meant placing the pulp at risk of exposure. Current knowledge indicates that carious tissue should be removed selectively with the goal of preserving tooth structure. Understating the processes that occur in dentin because of the dental caries process is important to appreciate the recommended selective caries excavation guidelines. In a vital pulp, with adequate blood supply, the pulp–dentin complex reacts to caries activity by attempting to initiate remineralization and blocking off the open tubules. These reactions, which occur even before the lesion has reached the dentin, result from odontoblastic activity and the physical process of demineralization and remineralization. The pulp does not need to be directly exposed to the biofilm to elicit an inflammatory response, as toxins and other metabolic byproducts can penetrate via the dentinal tubules to the pulp. Even when the lesion is limited to enamel, the pulp can be shown to respond with inflammatory cells.
Demineralization in dentin occurs at first via weak organic acids which demineralize dentin and expose its organic matrix; the organic matrix, particularly collagen, is then denatured and degraded, eventually losing its structural integrity and being invaded by bacteria.
Initial Stages of Dentin Demineralization
During the initial stages of caries lesions or mild caries activity, as found in slowly advancing caries lesions, a long-term, low-level acid demineralization of dentin occurs. Dentin responds to the stimulus of its first caries demineralization episode by deposition of crystalline material from the intertubular dentin in the lumen of the tubules in the advanced demineralization front (formally called affected dentin). The refractive index of the dentin changes, and the intertubular dentin with more mineral content than normal dentin is termed sclerotic dentin ( Fig. 1 ). The apparent function of the sclerotic dentin is to wall off a lesion by blocking (sealing) the tubules. The permeability of sclerotic dentin is greatly reduced compared with that of normal dentin because of the decrease in the tubule lumen diameter. Hypermineralized areas may be seen on radiographs as zones of increased radiopacity (often S-shaped following the course of the tubules) ahead of the advancing, remove portion of the lesion. Sclerotic dentin formation may also be seen under an old restoration. Sclerotic dentin is usually shiny and darker in color but feels hard to the explorer tip ( Fig. 2 ). Hard dentin represents the deepest zone of a caries lesion, – assuming the lesion has not yet reached the pulp, and may include tertiary dentin, sclerotic dentin, and normal (or sound) dentin . Clinically this dentin is hard, cannot be easily penetrated with a blunt explorer, and can only be removed by a bur or a sharp cutting instrument. By contrast, normal, freshly cut dentin lacks a shiny, reflective surface and allows some penetration from a sharp explorer tip. When these affected tubules become completely occluded by the mineral precipitate, they appear clear when a histologic section of the tooth is evaluated. This portion of dentin has been termed translucent dentin and is the result of mineral loss in the intertubular dentin and precipitation of this mineral in the tubule lumen. Consequently, translucent dentin is softer than normal dentin and is called firm dentin, in contrast to sound dentin (ie, hard) dentin. Although organic acids attack the mineral and organic contents of dentin, the collagen cross-linking remains intact in this zone and can serve as a template for remineralization of intertubular dentin. Therefore, provided that the pulp remains vital, firm (affected) dentin is remineralizable. Clinically, firm dentin is resistant to hand excavation and can only be removed by exerting pressure. The transition between soft and firm dentin can have a leathery texture, particularly in slowly advancing lesions, and has been called leathery dentin. Clinically, leathery dentin does not deform upon pressure from an instrument but can be excavated with hand instruments such as spoons and curette without much pressure.
Advanced Stages of Dentin Demineralization
More intense caries activity results in bacterial invasion of dentin. The most superficial (closer to the tooth surface) zone of the carious dentin is the necrotic zone. This soft (formerly infected) dentin is primarily characterized by bacterial contamination and contains a wide variety of pathogenic materials or irritants, including high acid levels, hydrolytic enzymes, bacteria, and bacterial cellular debris. These products can cause the degeneration and death of odontoblasts and their tubular extensions below the lesion and a mild inflammation of the pulp. The pulp may be irritated sufficiently from high acid levels or bacterial enzyme production to cause the formation (from undifferentiated mesenchymal cells) of replacement odontoblasts (secondary odontoblasts). These cells produce reparative dentin (reactionary or tertiary dentin) on the affected portion of the pulp chamber wall. This dentin is different from the normal dentinal apposition that occurs throughout the life of the tooth by primary (original) odontoblasts. The structure of reparative dentin varies from well-organized tubular dentin (less often) to irregular atubular dentin (more often), depending on the severity of the stimulus. Reparative dentin is an effective barrier, allowing limited diffusion of material through the tubules, and is an important step in the repair of dentin. This carious soft dentin closer to the tooth surface has low mineral content, and irreversibly denatured collagen. Histologically, this zone may be referred to as necrotic and contaminated. Although soft dentin typically does not self-repair, the advance front of the soft dentin zone (near firm dentin) is characterized by superficial bacterial invasion, and the caries process can still be stalled when a good restorative seal is obtained. Clinically, soft dentin lacks structure and can be easily excavated with hand and rotary instrumentation ( Fig. 3 ).