goal in cavity preparation was to remove all soft dentin until hard dry dentin was reached. In the 1970s, Massler and Pawlak promoted the idea that this was unnecessarily destructive and could often lead to exposure of the pulp in deep cavities.4 They maintained that soft dentin was not necessarily infected but could be merely affected by plaque acids. They proposed a more conservative cavity preparation, which required the removal of infected dentin only, leaving behind soft but not infected, so-called affected dentin. Affected dentin could be remineralized if the acid production was halted. These suggestions were at the time supported by little experimental data, but there is now convincing evidence that the pulp–dentin has a significant ability to repair by the formation of reactionary dentin, provided that the heavily infected dentin is removed and the cavity is well sealed from the oral environment. The formation of reactionary dentin is the result of a cellular process involving the mineralization of a supportive extracellular matrix produced by the odontoblast. Demineralized (affected) dentin or enamel may also remineralize by a simple precipitation of mineral salts. The process may take place on the surface of an enamel or dentin cavity which is relatively free of bacteria but at some distance from the odontoblast.
2.3.4 Arrested Caries in Dentin
Arrested caries in dentin is clinically defined by hardness of the dentin surface and a yellow to dark brown color. Arrested carious lesions are found most commonly on lingual and labial aspects of teeth and less commonly in caries which has become arrested, the dentinal tubules in the area between the soft and hard dentin have been shown to be obstructed by large crystals. It has been suggested that this process appears to occur in a number of stages5 (▶ Fig. 2.18).
Fig. 2.18 A diagrammatic representation of the stages in the formation of an arrested lesion in dentin. (a) The dentin tubule contains a high concentration of acid and dissolved mineral salts. (b) If bacterial acid production is reduced, and the pH increases, the salts precipitate into large crystals of tricalcium phosphate which temporally block the tubule. (c) If further bacterial activity is suppressed, the odontoblast process secretes collagen and calcium salts. Crystals of hydroxyapatite (HA) then form and block the tubule more effectively and permanently. (Adapted from Daculsi et al 1987.5)
First stage: The acids produced by advancing bacteria have dissolved the mineral in the surrounding intertubular dentin. The tubular fluid becomes saturated with calcium, magnesium, and phosphate ions. The lesion progresses unless the level of metabolic activity of the bacteria is reduced. If acid production is reduced, then the second stage may occur.
Second stage: When the acid levels drop, the saturated solution precipitates, producing large crystals of tricalcium phosphate. These crystals are comparatively soluble but nevertheless block the tubule.
Third stage: The odontoblast process, protected by the large crystals blocking the tubule, secretes collagen into the dentin tubule. Small plate-like crystals of hydroxyapatite accumulate, which are less soluble than tricalcium phosphate and therefore block the tubule more effectively. At the same time, crystal growth occurs in the intertubular dentin. Zavgorodniy and coworkers conclude that the growth of crystals in arrested caries is both a biomineralization process and a dissolution/precipitation mechanism.6 The dissolution/precipitation mechanism is dependent on the level of acid production by bacteria and the availability of salivary buffers and minerals. These factors determine whether precipitation of minerals or further dissolution will occur. The biomineralization process is dependent on the secretion of collagen by the odontoblastic process, which acts as a scaffold for the precipitation of insoluble apatite crystals.
2.3.5 Regeneration after Pulpal Exposure
A breach in the dentin, which causes exposure of the pulp, may be repaired by a bridge of new dentin provided that the pulp was not inflamed, the exposure was surgical and not carious, and that suitable stimulation was given to the pulpal cells. The stimulation which has been widely used is calcium hydroxide; a more recent material, mineral trioxide aggregate (MTA) has also proved to be successful. The calcium hydroxide is applied as a paste, which applied to the pulpal exposure causes local necrosis and a bridge of scar tissue to form. Calcium is deposited into the scar tissue, and this is followed by the secretion of dentin against the calcified bridge by odontoblasts. The degree of inflammation, the time of irritation and infection, and the location of the exposure must be regarded as decisive factors for the healing of the inflamed pulp rather than the effect of calcium hydroxide as such.7 This conclusion indicates that the use of calcium hydroxide to induce bridge formation in a carious exposure will have to be a carefully considered clinical decision. Unfortunately, the degree of inflammation of the pulp is difficult to assess as there is a poor correlation between signs and symptoms and the histological state of the pulp. If the pulp tissue stops bleeding without the presence of a blood clot, it does suggest that the hyperemia associated with inflammation is not advanced. The rapid formation of a clot may indicate that a dentin bridge could not form under any circumstances. In view of the considerable time required to perform endodontic treatment on a molar tooth, the possibility of inducing a dentin bridge after removing infected dentin and pulp tissue should be considered (see Chapter 5.3.3 Healing of a Pulp Exposure).
2.3.6 The Origin of Replacement Odontoblasts
The odontoblast-like cells which form the dentin-like bridge appear to come from stem cells in the pulp tissue. These cells migrate, divide, and reveal changes which are characteristic of secreting cells, such as an increase in the size of the cytoplasm and nucleus, and the orientation of their cytoskeletal elements (actin and vimentin) toward one side of the cell. They also secrete fibronectin and type II collagen. The cells, which have a terminal process like an odontoblast, secrete a matrix against the wound tissue which becomes calcified. These cells differentiate without the inductive influence of the enamel epithelium, a prerequisite during tooth development. It is thought that the stem cells which remain in the pulp have already been influenced by ectoderm and may be at an intermediate stage of differentiation, between primitive mesenchymal cells and odontoblasts. They are thus responsive to signals in the environment which stimulate their last stage of differentiation.
Key Notes
The aggressive removal during cavity preparation, of all soft dentin, until a hard cavity floor is reached, is the first step in a downward cycle of overtreatment. It increases the risk of pulpal exposure, followed by endodontic therapy, reduction of the tooth crown, which may require pin- or post-retention, and the risk of root fracture, and extraction. The principles of conservation are preferable.
Review Questions
1. How would you account for the hardness of enamel and its resistance to acid attack?
2. What evidence supports the view that enamel caries is a dynamic process, and not simply a progressive demineralization of enamel?
3.
