The dentine pulp complex

The dental pulp is encased within the hard tissue structure consisting of the enamel and dentine. As the dental pulp and the dentine are so inter-related it is better to consider them together as the dentine–pulp complex and hence to consider dentine as a vital tissue.

The dentine is derived from complex cells, the odontoblasts, that form a layer at the periphery of the dental pulp (Figure 3.1). The dentine forms a tubular structure, each tubule filled with an odontoblastic process. The tubules are more highly concentrated at the pulp surface than at the enamel–dentine junction. There is a diffusion gradient across the dentine that is related to the number of tubules and the thickness of the dentine. The response of the pulp to progressive injury is by the deposition of dentine (reactionary or tertiary dentine) from the intact odontoblasts and also mineralization within the dentinal tubules (peritubular dentine), thereby reducing their diameter and their ability to allow diffusion through them (Figure 3.2). Thus, the tissue has modulating effects on restorative procedures and that, combined with inherent neutralizing capabilities of tissue fluids from the pulp for both acids and alkalis, means that the amount of residual dentine thickness, after tooth preparation, is inversely proportional to the damage that may occur to the pulp after chemical application to the dentine surface. This is important when considering the use of filling materials, including temporary dressings, and bonding techniques, where an acid is applied to the dentine surface.

Figure 3.1 Decalcified section showing normal dentine pulp complex.

Figure 3.2 A hemisected tooth showing a carious lesion and dentine–pulp complex reactions.

(Courtesy of Dr Chris Longbottom)

Dentine is laid down throughout the life of the tooth: primary dentine as the tooth develops, secondary dentine after eruption of the tooth and tertiary dentine as a result of some insult to the tooth which may result in invasion of the dentine by bacteria or their toxic products. The aetiology of the last is usually dental caries or tooth wear, but may be induced by a restorative procedure (Figures 3.2 and 3.3). Odontoblasts are post-mitotic cells and may easily be damaged during restorative procedures. If this occurs, they are replaced by stem cells from the pulp that differentiate into odontoblast-like cells and lay down mineralized tissue at the injury site. The quality of tertiary dentine is dependent upon the intensity of the insult to the pulp: in general terms, the greater the intensity of the insult (e.g. rapidly progressing caries), the more rapid the formation and the poorer the quality (Figure 3.3). Tertiary dentine is often porous, which makes it susceptible to invasion by micro-organisms and toxins. Therefore, once tertiary dentine is exposed by tooth wear or caries there is a greater risk of subsequent pulp pathology.

Figure 3.3 A decalcified section showing a carious lesion (top right corner) and tertiary dentine formation. The caries is likely to have been rapidly progressing as the tertiary dentine formation is less regular and has lost its tubular structure. Note the pulp is inflamed with an increased number of blood vessels and inflammatory cells.

Nerves in the pulp

The principal elements of the dental pulp consist of stromal cells, fibroblasts, and an extensive network of nerves, blood vessels and lymphatics (see Figure 3.1). The nerves of the pulp conduct pain sensation. They consist of two main types: myelinated Aδ-fibres that conduct rapid, sharp pain sensation, and unmyelinated C-fibres that transmit the dull aching sensation that is typical of ‘toothache’. In addition, nerves of the autonomic nervous system are also present. Various vasoactive neuropeptides are contained within these nerves. They are produced in the cell bodies of the trigeminal ganglion and are stored in the terminals of the nerves in the pulp. Release of these peptides causes a number of tissue reactions including changes in pulpal blood flow, blood vessel permeability and recruitment of immunocompetent cells as part of the inflammatory reaction. This is known as neurogenic inflammation, which may be damaging to the dental pulp. There are also effects on the growth of cells in the pulp, including fibroblasts and odontoblasts, where release of neuropeptides such as calcitonin gene-related peptide may cause the expression of bone morphogenetic protein-2 transcripts which results in more dentine formation. Recently it has been shown that fibroblasts in the pulp may also release these peptides, particularly substance P.

Pulp vasculature

The pulp shows a complex vascularity with a capillary bed adjacent to the odontoblast layer. The coronal part of the pulp has a more concentrated distribution of blood vessels than the radicular pulp. The pulp has a positive pressure compared with the outer surface of the tooth and this allows movement of fluid into the dentinal tubules. When the tubules are cut, and the tubule is patent, the outer cut surface of the dentine becomes wet as tissue fluid wells out. This provides a defensive mechanism, diluting toxic products that may enter the tubule and delivering immunocompetent cells and immunoglobulins to the surface. Unfortunately, this mechanism is usually insufficient to prevent penetration by micro-organisms, especially if the surface is heavily contaminated.

The dental pulp is often referred to as a low compliant tissue. This means that any increases in tissue pressure in the pulp – for example, by vasodilation of blood vessels during acute inflammation – may have devastating effects on the tissue because it is encased within a rigid hard tissue framework. It is essential that pathophysiological mechanisms are present to minimize such damaging effects on the pulp. Specific arteriovenous shunts may be opened to reduce damage to the capillary network and it is believed that lymphatic drainage has an important role in the reduction of tissue pressure.

Pulpal blood flow is higher than for other tissues in the oral region and is controlled by neuropeptide release and also the action of the autonomic nervous system. A transient increase in pulpal blood flow can be produced by various noxious stimuli when applied not just to the tooth in question but also adjacent teeth and adjacent tissues. This demonstrates the complexity of the nerve distribution in the oral cavity.

Pulpal defence mechanisms

The dental pulp is a complex structure that demonstrates various strategies to protect itself from injury. It has been shown to have good powers of healing through the deposition of tertiary dentine and mineralization of the peritubular dentine, even in the presence of bacterial contamination. The peritubular sclerosis gives rise to the histological appearance of translucent dentine (seen in ground sections; Figure 3.2) and the dentine in this region becomes more resistant to diffusion of bacteria and their noxious products. If, however, the damage is so severe that odontoblasts adjacent to the region of irritation die, then the tubules are left empty and are much less resistant to ingress of toxins and bacteria. These tubules are known as dead tracts.

Restorative intervention may cause damage to the pulp and it is important that the clinician is aware of this when undertaking operative procedures on the teeth and knows how best to minimize these effects.

Health of the pulp

Clinically it is difficult to tell the health of the dental pulp, especially if there are no outward clinical signs and symptoms. Previously restored teeth that require further clinical intervention may be at risk. Abou-Rass, in 1982, coined the term ‘the stressed pulp’. This was a pulp that was neither healthy nor diseased but one that might be compromised to such an extent that further operative intervention would lead to irreversible damage. Taking a careful history from the patient regarding previous symptoms from, and treatment to, the tooth should be taken.

Nevertheless, the dental pulp may be injured during operative procedures on the tooth.

Preparation of the tooth

The most common method of tooth preparation is using rotating instruments in either an airotor, rotating at speeds up to 450 000 rpm, or in a slow speed handpiece that can be varied in speed from 1000 rpm to over 100 000 rpm. Cutting tooth tissue produces a smear layer, an amorphous mixture of inorganic and organic debris that blocks the cut dentinal tubules. Although the smear layer is inconsistent in thickness and distribution, it provides a barrier to bacteria, certainly in the short term. Many restorative procedures involve the removal of the smear layer, leaving open dentinal tubules which may make the pulp more vulnerable to damage by penetration of toxins and bacteria. Odontoblastic processes may also be cut during the preparation which may lead to subsequent irreversible damage to the pulp.

Frictional heat

The heat generated during tooth preparation for a restoration may cause irreversible damage to the pulp. The trauma damages the adjacent odontoblast layer and these cells can be sucked into their respective tubules. This is termed odontoblast aspiration and results in death of the cells and formation of a dead tract. These tracts are more susceptible to bacterial invasion as there is no protective outflow of tissue fluid or ability of the pulp tissue adjacent to the damaged area to form tertiary dentine quickly enough to prevent further damage to the pulp from the bacterial invasion. The microvasculature of the pulp is severely affected with plasma extravasation and a reduction in pulpal blood flow. In some cases the preparation may be so traumatic that haemorrhage occurs into the dental tubules and the pulp is irreversibly damaged immediately adjacent to the affected cut surface. If the tooth does not become non-vital then there may be an increased likelihood of internal root resorption taking place because of the local severe trauma.

Frictional heat occurs more readily with the following conditions: