dentin is exposed to oral fluids because of enamel wear, or enamel caries, bacterial products may diffuse down the dentinal tubules and cause a hypersensitive response from the odontoblast to normal stimuli. Cutting or grinding procedures on exposed dentin to remove dental caries is painful and usually requires anesthesia. It has been suggested that a normally cooled preparation of a completely caries-free tooth would not be particularly painful as the dental pulp is not hypersensitive. For obvious reasons this is not routine. The most common clinical sign of dentin hypersensitivity is a painful response of the pulp–dentin to hot and cold foods.
When odontoblasts are subjected to chemical or physical irritants, they increase in size and start laying down new peritubular dentin. They also lay down dentin in the roof of the pulp chamber, called secondary dentin, and retreat from the irritation behind this layer.
2.2.5 Secondary Dentin
Secondary dentin may entirely fill the original pulp chamber in an old and worn tooth. It is a normal physiological process related to tooth wear and aging of the tooth. With age, secondary dentin reduces the diameter of the root canal, causing difficulty in performing endodontic therapy for elderly patients. When secondary dentin is gradually formed, the microscopic appearance differs little from primary dentin. The dentin tubules are less regularly arranged, but they are continuous with the primary dentin. If the progression of tooth wear or dental caries is more rapid, the secondary dentin tubules are quite irregular and not continuous with the primary tubules. So, the new dentin acts like an impermeable barrier wall. This irregular secondary dentin has been referred to as reactionary or reparative dentin. The barrier formed by reparative dentin reduces not only dentin sensitivity but also the responsiveness of the odontoblast to further irritation (▶ Fig. 2.12).
Fig. 2.11 A SEM image of dentin which has been cracked in preparation so as to reveal dentin tubules. This dentin in this image was close to the dental pulp. (Magnification × 300, window × 1,500). There are many open tubules and no peritubular dentin. This zone of the pulp–dentin would have a high fluid permeability.
2.2.6 Dental Pulp Hyperemia
If the progress of an advancing carious lesion is rapid, there is insufficient time for secondary dentin to form, and odontoblasts are damaged by bacterial products. Their damage invokes an inflammatory response, with hyperemia, the arrival of inflammatory cells, and the potential for a localized abscess in that part of the pulp closest to the caries lesion. This is a critical point in the progress of pulp damage. If the irritation can be removed by removing the carious dentin and sealing the cavity, pulpal hyperemia may subside. If, however, the hyperemia is extensive and severe, the damage is irreversible and the pulp tissue must be removed by endodontic treatment.
From a clinical point of view, it is difficult to determine whether pulp hyperemia is reversible or irreversible, but there are some guidelines. Firstly, it is suggested that if the sensitivity to stimulation with hot or cold is short-lived, and the pain disappears soon after the stimulus is removed, the situation is hopeful for retaining the pulp tissue. Continual pain after stimulation suggests that the outlook for the pulp tissue is poor and that the pulp damage is widespread. Recall that the pulp is encased in a rigid shell and has a small opening for blood vessels. It is therefore highly vulnerable to vascular congestion and increased tissue pressure. The age of the tooth has a bearing on the outlook for a hyperemic tooth. Younger teeth with open apical foramina allow optimum vascular flow through the pulp, less venous congestion, and therefore greater healing potential than older teeth with narrow apical foramina.
Fig. 2.12 A histological section through the pulp–dentin of a tooth affected by dental caries. (a) Normal odontoblast cells in an area of the tooth crown unaffected by caries (magnification × 200). (b) In another part of the same tooth, bacteria (B) in the dentinal tubules seen as fine black stains are advancing toward the pulp. In response to the irritation caused by bacteria, the odontoblasts (OB) and other pulp cells have increased in size and number and there is a greater vascular supply to the tissue (BV). A layer of predentin which will become reparative dentin (RD) has been formed to protect the pulp.
If infected pulp tissue is not removed, further spread may occur into the periodontal ligament through the apex of the tooth and may also communicate with the periodontium via accessory root canals (▶ Fig. 2.9). These routes of communication with the periodontium are responsible for periapical abscess formation and further spread of infection into the alveolar bone. Infected pulp tissue must be removed and the empty spaces of the pulp chamber and root canal sealed up. This process, known as endodontic therapy, requires an intimate knowledge of the anatomy of pulp chambers and root canals. A brief and simplified version is presented below.
2.2.7 The Pulp Chamber and Root Canal
The pulp chamber is largest in the deciduous tooth, so the pulp is rapidly reached by advancing caries. It is also readily exposed during cavity preparation for a restoration, particularly if the operator is determined to remove all softened dentin.
In the permanent tooth, the pulp chamber is largest when the tooth has just been formed, that is before any secondary dentin has been laid down.
Pulp chambers generally follow the shape of the tooth crown. It would be more accurate to say that during tooth formation, the crown shape follows that of the pulp chamber. Thus, the pulp chamber is fan shaped in the incisor teeth, being flattened in a labial–lingual direction. In the canines it is flame shaped, and in the premolars and molar teeth the pulp chamber has peaks, known as horns, which lie under each tooth cusp (▶ Fig. 2.13).
Fig. 2.13 A maxillary second premolar, sectioned down its long axis in a buccal–lingual plane. The shape of the pulp chamber follows that of the tooth crown, with a pulp horn under each cusp. The pulp chamber is flattened mesiodistally.
During tooth wear, and aging, it is in these pulp horns that the first secondary dentin appears. In the floor of the pulp chamber, narrow canals lead along the center of each root. So, there are at least as many canals as there are roots and sometimes more. For example, the mesial root of the mandibular first molar is a fusion of two roots. This root, which appears to be single, actually has two root canals, one buccal and the other lingual. A buccal and a lingual canal should also be expected in the maxillary second premolar, even though this root may be appearing to be single. There are other examples of additional canals. The endodontist needs to be familiar with them all.
In the developing root, the root canals are quite wide and funnel shaped at the apex (▶ Fig. 2.14). The apical foramen of the root becomes progressively narrower as the root forms. As we have noted, sometimes there are extra accessory canals in the root, which are difficult to locate, clean out, and fill during endodontic procedures. The apex of the root may also have accessory canals, forming a sort of delta of canals emerging from the root. The apex of the tooth
