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. Why is there a high concentrated fluoride at the periphery of a carious lesion?
4. Why is it useful to consider the pulp and dentin as one biological unit?
5. What is the clinical significance of the high concentration of dentinal tubules in root dentin?
6. What factors alter the permeability of dentin?
7. What zones of caries have been described in dentin, and how can you account for them?
8. What is the clinical significance of discriminating between infected and affected dentin?
9. How does the pulp–dentin develop a mineral barrier to caries?
10. What is the likely consequence of some bacteria remaining in a sealed cavity?
11. Why does the rate of caries progression in dentin differ from enamel?
12. What is the difference between biomineralization and dissolution/precipitation?
References
[1] Kidd EA, Joyston-Bechal S, Beighton D. The use of a caries detector dye during cavity preparation: a microbiological assessment. Br Dent J 1993; 174(7):245–248
[2] Kidd EA. How ‘clean’ must a cavity be before restoration? Caries Res 2004; 38(3):305–313
[3] Ricketts D. Deep or partial caries removal: which is best? Evid Based Dent 2008; 9(3):71–72
[4] Massler M, Pawlak J. The affected and infected pulp. Oral Surg Oral Med Oral Pathol 1977; 43(6):929–947
[5] Daculsi G, LeGeros RZ, Jean A, Kerebel B. Possible physico-chemical processes in human dentin caries. J Dent Res 1987; 66(8):1356–1359
[6] Zavgorodniy AV, Rohanizadeh R, Bulcock S, Swain MV. Ultrastructural observations and growth of occluding crystals in carious dentine. Acta Biomater 2008; 4(5):1427–1439
[7] Schröder U. Effects of calcium hydroxide-containing pulp-capping agents on pulp cell migration, proliferation, and differentiation. J Dent Res 1985; 64 (Spec No):541–548
Suggested Readings
Berkowitz BWK, Moxham BJ, Linden RWA, Sloan AJ. Oral biology; oral anatomy histology,