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Disease Dynamics of the Dental Pulp


W. R. Hume
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W. L. K. Massey

n awareness of the events which occur in the pulp following insults enables the dentist to both protect the tissue and to provide appropriate treatment if it is damaged. Interceptive therapy may make the difference between pulp survival through healing and pulp death. Various therapies may also reduce or eliminate pulpal pain. In very general terms, the pulp responds to damage in ways similar to other connective tissues, i.e. it can undergo various forms of inflammation, it can heal, or it can die. However the pulp is unique among connective tissues in that it is entirely enclosed in dentine and it has processes which extend throughout the dentine so that the pulp and the dentine should be regarded as a single entity Any trauma or therapy applied to the dentine should be regarded as trauma or therapy applied to the pulp. Insults, such as the caries process and tooth restoration, are unlike those found elsewhere in the body and will challenge the pulp. It is not surprising, therefore, that some aspects of the pulpal response to insult are unique. Some therapies used to treat the dental pulp are also unique.

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Preservation and Restoration of Tooth Structure

Insults to the Pulp

he pulp can be damaged or die in a variety of ways. The cause can be caries, microleakage, mechanical, chemical or thermal trauma, either alone or in combination.

Dental caries
Most commonly, the dental pulp can become inflamed and may die as a consequence of the advance of the caries process through dentine.1 The process can be halted by effective treatment of the disease or through the application of preventive measures, either alone or in combination with tooth restoration.

by heat generated during tooth cutting by chemicals applied to dentine, particularly when freshly cut exposure of pulp tissue during cavity preparation It is rare for the entire pulp to be killed in this way and, although these events cause pain the pulp will usually heal in the weeks after the damage occurs, unless bacteria or their products can also reach the damaged tissue.

Defence Within Dentine

Microleakage in restored teeth


Although the restoration of a caries defect in tooth structure is usually in the interests of the patients health and well-being, the action of restoration may not in itself be sufficient to prevent the ultimate death of the pulp, over time, even when carried out in parallel with effective caries preventive measures. The principal reason for pulpal inflammation following restoration is microleakage, the existence of a gap between the restorative material and the dentine, in which bacteria can propagate. Evidence for this phenomenon, and the measures which can be taken to minimize it, are described in detail in Chapter
15.

entine has a limited capacity for its own defence. Dentinal tubules are a potential pathway for the diffusion of noxious chemicals from the external environment to the pulp and for the inward movement of micro-organisms. However, they can be reduced in diameter or totally closed by one or more of several processes. Dentinal sclerosis Dentinal sclerosis is the SUMMARY narrowing of dentinal Dentine can protect tubules by the formation itself through minerof peritubular dentine, al deposition from dense calcific material saliva laid down through an pulp active, odontoblastic, metabolic process. Scler-osis may progress relatively rapidly in dentine beneath the advancing carious lesion or in dentine which has been exposed to the oral environment through abrasion, attrition or erosion. Sclerosis also occurs more slowly as a natural part of aging.

Mechanical, thermal or chemical trauma


Direct mechanical trauma to a tooth can interrupt the blood supply by tearing the fine blood vessels at the root apex, leading to avascular necrosis of the tissue within the tooth. There is little that can be done, except to encourage those at risk of injury (e.g. contact sports players) to wear protective mouth guards. Some pulpal cells, in particular the odontoblasts, can be killed by direct trauma

Calcium phosphate deposition Crystals of calcium phosphate may also be deposited deep within dentinal tubules as a response to slowly advancing caries by a mechanism which is not understood, but which is presumably mediated by odontoblasts (Chapter 15).

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Salivary precipitation Precipitation of salivary calcium and phosphate can occlude dentinal tubules exposed to saliva and effectively desensitise hyper-sensitive dentine. Remineralisation will not occur in the presence of actively advancing caries or in acid erosion because of the low pH which is integral to these processes. In the presence of active abrasion or attrition there is unlikely to be precipitation but it will start again if any of these processes are arrested (Chapter 5).

die, leaving substantial defects in the reparative tissue. Chronic injury In the chronically inflamed pulp diffuse calcification may occur, presumably because of activation, differentiation and calcific matrix secretion by mesenchymally-derived cells. Relatively well organised dentine may also be laid down within a chronically inflamed pulp to form pulp stones. On rare occasions pulp stones will form in an otherwise normal pulp for no apparent reason.

Reparative dentine
Dentine is formed by odontoblasts and, as long as they remain alive, these cells will retain the capacity to make additional dentine in response to injury. There are other cells in the pulp which can form new dentinogenic cells if odontoblasts die, providing the rest of the pulp remains vital. The hard tissue which they form has all the constituents of dentine, but may vary in form. Mild injury If the injury to dentine is mild, such as attrition or the preparation of a shallow cavity, most odontoblasts beneath the damaged area survive. Regular reparative dentine, which contains relatively normal tubules, will be laid down at the pulp-dentine interface in relation to the area of damage as a continuation of the main body of dentine. Moderate to severe injury If more odontoblasts die because the injury is more severe, in either degree or duration, the pulpal cells can produce reparative hard tissue of widely varying types. The form will depend on the nature and the stage of differentiation of the cells which effect the primary calcific repair process. Secondary dentinogenic cells are derived by mitotic activity from the cell-rich sub-odontoblastic layer. This layer contains a high proportion of both fibroblasts and more primitive mesenchymal cells, either of which may be precursors of the replacement cells. The reparative dentine laid down in this way may be totally atubular, or may be poorly mineralised. In some cases cells in the area of calcification may become entrapped and

Pulpal inflammation in response to bacteria


Inflammation is a series of events in vascular connective tissue which, ideally, neutralise or eliminate damaging factors and initiate tissue repair.2 Inflammatory response in the pulp to bacterial insult can be identified through degenerative changes in the tissue which are not very different from changes seen in other tissues. Early changes include fibrosis and thickening of the basement membrane in associated small vessels. Frustrated repair will often induce calcific foci associated with amorphous, partially mineralised connective tissue matrix with degenerate cells and tissue. Chronic inflammation Whatever the microbial mix and its pathogenic vectors it is likely that the first response to caries or microleakage within pulpal tissue will be a low grade, chronic inflammation, characterised by the presence of greatly increased numbers of T-lymphocytes in the extra-vascular space. Mild chronic inflammation is usually symptomless, since the lymphocytes do not cause the release of factors which change the sensitivity of the pulps sensory nerves. An infiltrate will form with varying numbers of lymphocytes, monocytes/macrophages and plasma cells within the pulpal connective tissue. The capillaries may become engorged and increase in number and many small vessels in the area may display features resembling high endothelial venules which are specialised for the exchange of inflammatory and immune cells. As the inflammation progresses there may be haemorrhagic changes in relation to extensive

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Preservation and Restoration of Tooth Structure

leukocyte infiltration. There may be extravascular haemorrhage, complete loss of connective tissue architecture and scattered chronic inflammatory infiltrate as well. It is likely that the level BE AWARE of response depends to a There can be large degree on the parconsiderable ticular bacteria involved. variation in response In one individual there between patients. may be a small zone of dentinal caries, well removed from the pulp, which evokes a vigorous response because either the lesion contains particularly pathogenic micro-organisms or the pulpal response includes a specific immune component related to prior challenge. On the other hand, the microbial mix may be particularly benign in another patient and there may be little or no response until the lesion is large and close to the odontoblast layer. Similarly, a relatively small number of bacteria beneath a leaking restoration may evoke a chronic inflammatory response in one patient but not in another.

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ly that the pulpal tissue, after such a cycle of inflammation and repair, will be less vascular, less cellular and more fibrous than before, and may therefore be less able to withstand subsequent insults.

BE AWARE

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Bacterial insults are the most damaging Each insult will lead to reduced response Accumulated insults may lead to pulp death

Acute inflammation Foci of acute inflammation can develop within the chronically inflamed tissue if microbially-derived toxins damage pulpal cells, bringing about the local synthesis of histamine, bradykinin or prostaglandins. Alternatively, humorally-mediated hypersensitivity reactions to microbial components or products themselves may cause tissue damage. If such acute foci develop, the pulpal nerves may become sensitised to normal stimuli and the patient may report sensitivity of short duration to hot or cold food or drink, to cold air, or to osmotic change while eating. The pulp will not necessarily die under these circumstances and the institution of appropriate therapy may well lead to healing. Reversible pulpitis If, at the stage of simple, chronic inflammation or chronic inflammation with small, acute foci, the aetiologic factors are removed by debridement, or denied substrate by the creation of an effective seal, the inflammation may resolve. That is to say, the inflammation is reversible. However, it is like-

Irreversible pulpitis If the injury is more severe or there is a major immune-mediated response to the microbial challenge the tissue changes may become irreversible. The pulp may then die painlessly over time, or alternatively total necrosis may take place quite rapidly and cause considerable discomfort. If the level of stimulus remains relatively constant, such as under a leaking but otherwise stable restoration, the ability of the tissue to resist bacterial toxins will decline over time and a reversible inflammatory process may become irreversible. Some form of surgical ablation of the pulp tissue, such as pulpotomy or pulpectomy, will then be required if the tooth is to be retained. The boundary between reversible and irreversible pulpitis is impossible to define. Remove the cause and a pulp in a healthy young patient may heal from a state of chronic, suppurative inflammation such as a pulp micro-abscess. On

Fig. 2.1. Following symptoms of pain on temperature change the restoration was removed and the pulp chamber exposed revealing a suppurating pulp. The pulp tissue is beyond recovery and endodontics is indicated.

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the other hand, in older individuals or in teeth which have been subjected to previous episodes of inflammation, a pulp micro-abscess is more likely to spread because the tissue is less able to elaborate repair. In such circumstances toxic products of cell lysis may kill adjacent cells. Prediction of outcome Clinically it is important to develop the ability to discriminate between a pulp which might heal following conservative therapy and one which will not.3 In an adult, irreversible inflammation is characterised by symptoms of severe pain of long duration in response to hot or cold, or spontaneous unstimulated pain particularly at night. The patient may not be able to accurately identify which tooth is causing the pain, or whether it is in the maxilla or mandible. Histological examination NOTE of the tooth responsible will Total isolation of generally reveal at least one the lesion with an pulpal micro-abscess, often adhesive provisionin the area of a pulp horn. A al restoration is the micro-abscess is an accuonly treatment for mulation of polymorphonuan inflamed pulp. clear leucocytes and dead and dying pulp cells in the form of pus. The area of pus formation will be surrounded by fibrous connective tissue infiltrated with polymorphonuclear leucocytes and, slightly

further away, chronic inflammatory cells. A diagnosis can be made on whether the inflammation is reversible or not by removing the infected layer of carious dentine or the leaking restoration and totally sealing the lesion from the oral environment with a glass-ionomer or zinc oxide/ eugenol temporary restoration. If the inflammation is reversible the pain will cease almost immediately and, after a delay of at least three weeks to allow healing in the pulp, a definitive restoration can be placed.

Open-form chronic pulpitis


In the presence of a more advanced necrosis of the pulp tissue drainage may occur from the pulp chamber through the overlying carious dentine (Figure 2.1). The pulpitis is then regarded as ulcerative or open-form, and may not be painful. Drainage allows the development of chronic pulpitis, with the inflammatory response being confined to the superficial area (Figures 2.2 and 2.3). This may persist for a considerable period of time, even years, because of the development of a balance between the injurious agents and tissue resistance. At this point the elimination of drainage by the placement of a temporary or permanent restoration by a dentist can lead to severe pain, total pulp necrosis and progression to a periapical lesion.

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Fig. 2.2. This tooth also showed symptoms following change of temperature so the situation was investigated. The pulp was exposed and immediately showed signs of positive haemorrhage.

Fig. 2.3. The tooth shown in Figure 2.2. The cavity was blotted dry but the cavity immediately filled with blood once more showing that the pulp was positively and irreversibly inflamed.

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Preservation and Restoration of Tooth Structure

Pulp polyp In young people with untreated, gross carious lesions exposing the body of the pulp, chronic ulcerative pulpitis may lead to proliferation of hyperplastic granulation tissue into the carious cavity. The hyperplastic tissue, known as a pulp polyp, may have a relatively thin pedicle connecting it to the remainder of the pulp, and may be covered with a well developed epithelial layer, presumably seeded from desquamated oral epithelial cells via saliva (Figure 2.4).

Diffuse calcification Chronic pulpal inflammation may also induce the secretion of ectopic dentinal matrix by fibroblasts or undifferentiated mesenchymal cells, causing either diffuse or well organised calcification, often leading to narrowing or obstruction of the root canal.

Ideopathic resorption
In a small percentage of BE AWARE cases, for reasons which Ideopathic resorption are not fully understood, can be osteoclasts may prolifer internal ate instead and cause external resorption of dentine identify one lesion and from the internal surseek others in the face of the pulp chamsame patient. 4,5,6 ber (Figures 2.5 and 2.6). Parallel with the resorption there will be a disorganised calcification occurring so that there is a continuing destruction and rebuilding of dentine at the same time and progress will be intermittent and irregular. The resorption can commence internally within the pulp tissue or externally at the cemento-enamel junction. In both cases it is difficult to recognise in the early stages. Ideopathic internal resorption begins within the pulp tissue, probably at the interface between the

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Fig. 2.4. The pulp in this tooth was exposed by rampant caries that had progressed so fast that the pulp was exposed before it could die. The inflammatory response resulted in proliferation of the tissue into a pulp polyp.

Fig. 2.5. A bitewing radiograph reveals an area of vigorous ideopathic resorption on the distal of the upper first molar beneath the restoration. As it was considered to be beyond treatment the tooth was extracted.

Fig. 2.6. The tooth similar to the one shown in Figure 2.9 was sectioned following extraction to reveal the resorbed area. It would appear that the resorption commenced in relation to the cemento-enamel junction on the lingual surface so it was then classified as ideopathic external resorption.

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Fig. 2.7. The upper lateral incisor shows the typical pink tooth syndrome. There is an area of indeopathic internal resorption within the crown that shows first as a translucent area close to the gingival margin.

Fig. 2.8. A lesion similar to the one shown in Figure 2.7 has been opened and curetted in an attempt to arrest the resorption. It will be cauterised with trichloracetic acid and restored with glass-ionomer.

pulp and the dentine and, if it is not diagnosed early, can lead to the loss of a tooth. It is generally associated with trauma, including cavity preparation, or an external blow to a tooth. It will remain asymptomatic and the earliest signs will show radiographically as an ill-defined radiolucency in relation to the pulp chamber. Ultimately it will show as a pink blush through the enamel which, on careful examination will be revealed as the pulp tissue occupying a large area of the crown (Figures 2.7 and 2.8). An external lesion may be found at this time at the cemento-enamel junction, often disguised within the gingival crevice. In the early stages, pulpectomy is the only available treatment but if it is allowed to progress until it reaches the external surface the tooth will probably be lost. The alternative form of resorption commences on the external root surface and is known as ideopathic external resorption. It is sometimes associated with trauma or with orthodontic movement of a tooth and generally commences in the region of the cemento-enamel junction. In the early stages it may be successfully treated by careful debridement of the lesion and cauterising with trichloracetic acid followed by placement of a glass-ionomer restoration. However, this lesion is very prone to recurrence along the gingival margin in relation to inflammation in the gingival tissue (Figures 2.9).

Fig. 2.9. A lower molar showing a proliferation of soft tissue in relation to an area of ideopathic resorption. It is not clear if the tissue arose from the pulp or the gingival tissue.

Inflammation in Response to Mechanical, Thermal and Chemical Insults


Reversible acute inflammation

on-bacterial, traumatic stimuli of short duration may kill or damage a few odontoblasts only. The action of cutting dentine or over-heating it during cavity preparation, or the placement directly onto dentine of restorative materials which release toxic chemicals, such as composite

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Preservation and Restoration of Tooth Structure

resin, may cause a simple, acute inflammatory response. The effect may be direct sensitisation of sensory nerve endings, short-term vasodilatation, a reversible increase in vessel wall permeability, followed by increased local tissue fluid pressure and, possibly, increased lymphatic flow. These effects will be mediated by the release of lysosomal proteins from damaged cells into the extracellular space. Later there may be release of histamine from mast cells and the synthesis of lysylbradykinin from kininogen and of cell membrane fractions following the synthesis of prostaglandins. The sensory nerve effects may include increased responses to otherwise sub-threshold stimuli such as hot or cold foods and represent the bodys attempt to remove debris and initiate repair. The pain thus generated may serve no apparent physiological function. Similarly, a mild, acute BE AWARE inflammatory process Aging of pulp tissue may be reversible if the without bacterial aetiologic factors do not involvement persist. The absence of repeated low level bacteria or their byprodchronic insult ucts means the likely isolated acute course of events may be episodes relatively simple and leads ultimately to predictable. The imporpulp death tant variables will be the degree of cell damage and the capacity of the host tissues to elaborate inflammation and repair. Histamine and bradykinin both have a short half life, in the order of minutes only, and prostaglandin synthesis ceases when the cell membrane fractions are cleared away by phagocytes, usually within a few days. Repair involves the return to normal tissue fluid dynamics, the redifferentiation of odontoblasts and, subsequently, the deposition of reparative dentine may occur. Although the inflammatory events described above can be regarded as reversible, the pulpal tissue will subsequently be less cellular, less vascular and more fibrous. That is, it will have aged, in a manner similar to pulp tissue after chronic inflammation, and will also be less able to withstand subsequent insult in any form.

Acute inflammation leading to pulp death


More severe, non-bacterial insults causing a greater degree of cell damage or death may bring about more marked vasodilatation and the movement of substantial amounts of blood fluid and protein into the injured tissues. In the young individual healing may occur through the sequence of events described above despite the severity of the injury and the initial response. However, in an older patient or where a pulp has been compromised by previous episodes of inflammation and repair, such damage may lead to the death of the entire pulp. Cell death and disintegration may release lysosomal enzymes into the extracellular environment causing the death of more cells. The process of cell death almost always ends just short of the root apex. The periapical tissues are more able to resist damage than those of the aged or compromised pulp because they have a rich collateral circulation. Direct pressure measurements in various areas of normal and inflamed pulps have shown that the tissue behaves as a gel, not a fluid, and that local pressure increases will not spread. The assumption that a pulp is destined to die if it suffers an episode of acute inflammation is therefore not warranted, particularly if bacteria are not involved. Treatment of the dead pulp Once blood supply and vitality have been lost the only predictable therapy which will allow tooth retention, in the long term, is the removal of necrotic tissue debris from the pulp space and its replacement with an inert filling material. Unfortunately, if this is not done, the tissue debris is likely to become infected at some later time, resulting in periapical infection, inflammation and pain. The anticipated mode of infection is by anachoresis, the lodgment of bacteria from adjacent tissues, or the blood supply, into the pulp chamber where they can survive and multiply.

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Periapical inflammation
There is continuity between the pulp and the periodontal ligament through either the apical foramina or the lateral accessory canals. Therefore,

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inflammatory processes within the pulp tend to affect the periapical or periradicular regions and induce what are generally termed periapical lesions. Most commonly, chronic apical periodontitis develops as a consequence of, and concomitantly with, chronic pulpitis of bacterial origin. Depending on the nature and number of the micro-organisms invading the dentine and pulp, this apical response can become well established while all or most of the pulp tissue is still alive.

Pulpal pain and sensation


The pulp is richly supplied with sensory nerves, many of which end close to the odontoblastic cell bodies, and will respond to stimuli such as change of temperature. Application of stimuli may also cause pain through movement of the odontoblast cells through fluid in the dentinal tubules. Finally cell damage and inflammation within the body of the pulp may fire the sensory nerves and also cause pain. Complete loss of sensibility of the dentine and pulp usually indicates that the entire pulpal tissue is dead. However there is not an absolute link between sensibility and vitality, since patients may report apparently normal sensory responses in teeth which, on histological examination, show

no evidence of vital pulp, while others have no sensibility in teeth which are otherwise normal. The periodontal ligament at the root apex is also well innervated. Sensory nerves within the ligament normally provide information to the brainstem nuclei on pressure or mechanical load and tooth displacement. Such sensory information subconsciously contributes to masticatory control and may also be noted consciously as touch, pressure and pain. Inflammation in the periapical tissues decreases the critical firing threshold of the sensory nerves of the region and allows the initiation of pain by relatively minor tooth movement. Palpation through gentle movement of the tooth with finger pressure or alternatively percussion by gently tapping with a solid instrument may well elicit pain under these circumstances.

Tests of pulpal and periapical status


No one test alone can give an accurate picture of the state of the dental pulp or periapex. It is only by the correlation of all available information that the clinician can arrive at a diagnosis. A careful visual examination, using good illumination and magnification, plus a radiographic examination should be used in conjunction with the tests described below.

TABLE 2.1: Methods for testing pulpal and periapical status


Heat Cold Percussion Palpation Electrical Sensibility to heat may be tested by the selective application of hot water from a syringe, heated gutta percha sticks or thermostatically controlled heat applicators Selective application can be carried out using cold water in a syringe, a stick of water-ice, solid carbon dioxide (dry ice), or ethyl chloride on a cotton pellet. Tap the tooth gently, vertically then laterally, with a suitable solid instrument such as the handle of a mouth mirror. Sharp pain may be elicited which may then persist for a brief time. Digital pressure on the tooth itself, then on the soft tissues adjacent to the root apices may elicit pain or may reveal soft or hard tissue swelling. Electric pulp testers may indicate the presence of viable pulp nerves but they do not give a reliable indication of the state of pulpal tissue. They should not be used in individuals with cardiac pacemakers. Despite using all of these tests it may necessary to use either sub-periosteal infiltration or intraligamentary local anaesthesia for individual teeth to help reach a decision on which tooth is causing pain.

Differential anaesthesia

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Preservation and Restoration of Tooth Structure

Further Reading
1. 2. 3. Kim S, Trowbridge H. Pulpal reactions to caries and dentine procedures. in: Pathways of the pulp. 6th Edition. Cohen S and Burns RC, editors, St Louis: Mosby, 1994. Smulson MH, Hagen JC, Ellenz SJ. Histopathology and diseases of the dental pulp. in: Endodontic therapy, 5th Edition, Weine FS, editor, St Louis: Mosby, 1996. Smulson MH, Hagen JC, Ellenz SJ. Pulpo-periapical pathology and immunological considerations. in: Endodontic therapy, 5th Edition, Weine FS, editor, St Louis: Mosby, 1996. 4. Heithersay GS. Treatment of invasive cervical resorption: an analysis of results using topical application of trichloracetic acid, curettage, and restoration. Quint Int 1999 Feb; 30(2):96-110. Heithersay GS. Invasive cervical resorption: an analysis of potential predisposing factors. Quint Int 1999 Feb; 30(2):8395. Heithersay GS. Clinical, radiologic and histopathologic features of invasive cervical resorption. Quint Int 1999; 30:2737.

5. 6.