Summary

The main cause of pathological pulp, root canal, and periapical conditions is the presence of bacteria in the tooth. Bacteria can enter the dentine-pulp complex via various pathways such as through caries, cracks, fractures, and broken-down restoration margins. The pulp initially attempts to wall off the invading bacteria and their endotoxins with reparative or reactionary dentine. However, if the invasion continues (i.e. no treatment is provided), the pulp becomes inflamed (pulpitis). Reversible pulpitis is the first stage and if not treated, it progresses to irreversible pulpitis, followed by a brief ‘necrobiosis’ stage while the pulp is progressively necrosing, so there is both irreversible pulpitis and necrotic, infected pulp tissue present. The pulp necrosis and infection progresses to involve the entire pulp, and within a few months, the root canal system becomes pulpless and infected. In conjunction with this progression of disease in the root canal system, the periapical tissues become inflamed (apical periodontitis). This inflammatory process is dynamic with various phases of acute or chronic inflammation. It can also progress to develop acute or chronic abscesses and sometimes facial cellulitis. In some cases, if epithelium is present in the periapical tissues, a pocket cyst may develop and this may progress to become a true cyst. Following appropriate endodontic treatment, the periapical tissues usually heal and return to a clinically normal state although in some cases there may be some scar tissue present.

4.1 Introduction

The dental pulp is an important structure within the tooth and it has several functions. Initially, the pulp is involved with formation of the tooth root through its ability to form dentine. The pulp maintains this ability throughout its life, which enables it to form secondary dentine. This forms circumferentially and at a slow rate throughout the normal life of a healthy tooth. The pulp can also form reactionary dentine and reparative dentine in response to adverse stimuli such as caries, the presence of bacteria, operative dental procedures, or trauma to the tooth. The dentine tubules in reactionary dentine are continuous with the primary dentine, and they include the odontoblastic processes. Reparative dentine is localised to the site of irritation and it has irregular, and often missing, dentinal tubules [1].

The pulp itself is a soft tissue that is mainly connective tissue with many different cells and a rich neuro-vascular network [1, 2]. The pulp is surrounded by the hard dental tissues – dentine, enamel, and cementum – all of which help to protect the pulp from external stimuli. However, this protective function can only occur if these hard tissues remain intact. The most important of these protective tissues is the enamel because it is the outermost layer and it is exposed to the oral cavity, which contains many bacteria. Hence, once the enamel loses its integrity, and especially if the dentine is exposed, there is the potential for pulp irritation as a result of bacterial ingress through the defect. If the bacteria reach the dentine, then the dentinal tubules provide direct pathways to the pulp for bacteria and/or their endotoxins to irritate the pulp [3].

There is a direct relationship with several pathways of communication between the pulp and the periradicular tissues [4, 5]. The main pathway is via the apical foramen. Other pathways include the dentinal tubules, accessory canals (including lateral and chamber canals and apical delta), radicular grooves, invaginations, developmental defects, cracks, and fractures of the tooth [4]. Hence, the state of the pulp (or root canal system) directly affects the periradicular tissues. As outlined next, both inflammation of the pulp and infection of the root canal system initially cause inflammation of the periapical tissues. This response can then progress to other conditions such as periapical infections, abscesses, or cysts. Such periapical conditions cannot, and do not, develop in isolation or in the absence of pulp or root canal disease (except following trauma to the tooth). Therefore, the various pulp, root canal, and periradicular conditions must be considered together and not in isolation [6–8]. As an example, it is inappropriate to diagnose ‘chronic apical periodontitis’ alone as this condition is usually a direct result of an infected root canal system. In order to manage the entire disease process within and around a tooth, it is essential to diagnose and understand the conditions in the pulp, in the root canal system, and within the periradicular tissues as well as diagnosing and understanding what has caused these conditions [6].

4.2 What Causes Pulp, Root Canal, and Periradicular Conditions?

Bacteria are the most common cause of pulp, root canal, and periradicular diseases. The role of bacteria in pulp disease was clearly demonstrated many years ago using a ‘germ-free’ rat model [9, 10]. When there were no bacteria present in the ‘germ-free’ rats, the pulps that had been mechanically exposed and left open to the oral cavity healed, whereas the pulps exposed in normal rats (i.e. with bacteria in their mouths) necrosed and became infected, and their periapical tissues were inflamed.

The bacteria that cause pulp and root canal diseases originate from within the mouth so they need to have a pathway by which they can enter the tooth and reach the pulp/root canal system. Such pathways develop once the enamel loses its integrity or when restorations break down at the tooth:restoration interface (Figure 4.1). The integrity of the enamel is most commonly lost as a result of dental caries or due to the effects of chemicals (such as acids) and mechanical events (such as cracks and fractures) [2, 11]. If the tooth has been restored previously, then the tooth/restoration interface is critical as any gaps that develop at this interface will provide a potential pathway for bacteria to enter the dentine and subsequently reach the pulp space [2, 12, 13].

Dental caries in the permanent dentition is the most prevalent disease in humans [14]. Caries should be considered as a bacterial disease, which results in loss of the tooth’s mineralised content. If dental caries is not treated in a timely and adequate manner, then it can have serious consequences because the bacteria within the carious lesion can progress through the dentine to then involve the pulp, the root canal system, and eventually the periradicular tissues [1, 2, 6].

Caries is a progressive disease process, which is helped by the nature of the disease itself. The cavitation of the tooth that develops early in the process has a somewhat protective effect on the bacterial plaque that develops within the cavity because the deeper parts of the cavity will be harder to clean. The lesion then progressively becomes deeper. Once the cavity reaches the dentine, there are tens of thousands of dentinal tubules per square millimetre [3], through which the bacteria and their by-products can progress towards the pulp.

Infractions, cracks, and fractures are defects in the tooth structure [15]. There is some confusion within the dental profession regarding these terms with practitioners often using them interchangeably. Each is a different defect (Figure 4.2) with potentially very different consequences for the tooth; hence, it is important to differentiate between them. The defects may involve the enamel only, in which case they are known as infractions or craze lines, and these do not normally cause any pulp irritation [15]. However, they may propagate over time or with trauma to the tooth. Such trauma could be due to an accident or it may be a result of normal function such as chewing, biting, etc. A crack is a defect that extends into the dentine but the fragments on either side of the defect cannot be separated [15]. Cracks can also extend into the pulp and/or cementum, depending on the location, direction, and extent of the crack. If there are fragments of the tooth that can be separated, or a fragment has already dislodged and been lost, then the defect is a fracture [15]. Fractures may involve enamel, dentine, pulp and/or cementum depending on the location, direction, and extent of the defect. Cracks and fractures that involve dentine provide direct pathways for bacteria to enter the tooth and progress towards the pulp. The resultant pulp disease is similar to that caused by caries [15].

Once a tooth has been restored, it will always be compromised to some extent. The degree of compromise will depend on many factors – in particular, the extent of lost tooth substance, the restorative materials used, and the time since restoration. Unfortunately, all restorations have a finite life and they may break down, fracture, dislodge, and so forth over time [12]. Restorations have several functions, which include restoring teeth to provide function and aesthetics. However, the most important function of a restoration is to protect the pulp by preventing bacterial entry into the tooth. Unfortunately, the dental profession has yet to develop a material that can provide this protection on a permanent or long-term basis in the harsh environment of the oral cavity. Hence, it is inevitable that most restorations will break down at some stage and when this occurs, the critical factors are whether the gaps under the restoration can be cleaned by the patient, whether bacteria can enter these gaps, and whether caries develops. In many teeth, caries will not be evident clinically, but bacteria can still enter the dentine tubules via the marginal gaps. Once this occurs, pulp disease can develop and progress in the same manner as when there is caries present [12].

Periradicular conditions are a direct result of pulp and root canal diseases [2, 7, 8]. That is, whenever there is inflammation or infection within the root canal system, the periapical tissues become inflamed. This should be considered as a reaction or a response, and not as a disease. The inflammation can then progress and other conditions can develop, such as infections and cysts, as outlined next. Hence, periradicular conditions are indirectly caused by bacteria from the oral cavity that enter the tooth and, subsequently, the pulp and root canal system through the same pathways mentioned previously – that is, caries, cracks, fractures, and breakdown of restoration margins.

4.3 The Development and Progression of Pulp and Root Canal Conditions

Whenever any tissue in the body is injured, irritated, or stimulated, the first reaction will be inflammation (Figure 4.3). If there is no treatment provided to remove the stimulus or irritating factor, the tissue will typically necrose and then it will become infected. Over time, there will be loss of the necrotic tissue as the bacteria digest and remove it. Gangrene in the extremities of the body, such as the toes and fingers, is an example of this progressive reaction to injury and bacterial invasion.

Irritation of the pulp commences once bacteria or their endotoxins reach the dentine. The pulp reacts in a similar manner to other soft tissues but with one very important exception (Figure 4.4). The pulp is a unique tissue in that it is the only soft tissue in the body that has the ability to form hard tissue (i.e. the various forms of dentine) and this function becomes the pulp’s first response to irritation. If the bacteria are not removed and the pathway for their entry remains (i.e. no dental treatment is done), the pulp will eventually become inflamed (i.e. pulpitis) and, over time (if still untreated), the pulp will necrose as the bacteria and/or the caries spread closer to the pulp chamber [10].

The formation of reactionary or reparative dentine is the pulp’s attempt to wall itself off from the irritant bacteria and/or their by-products. However, the pulp is not able to maintain this function indefinitely, and at some stage, it will succumb to the bacterial invasion. From this time point onwards, the pulp is similar to all other soft tissues in the body in the way it reacts to the constant presence of bacteria; that is, it initially becomes inflamed and then subsequently it dies (necroses) and becomes infected. The processes of pulp necrosis and infection occur simultaneously in teeth with the ‘bacterial front’ progressively moving through the pulp, from the coronal pulp chamber through the root canal(s), and towards the apical foramen. Apical to the ‘bacterial front,’ the pulp tissue will be irreversibly inflamed whilst coronal to this ‘front,’ the tissue will be necrotic and infected. Once the entire pulp is necrotic and infected, and within a relatively short period of time, the necrotic tissue will be removed by the bacteria and the root canal system becomes pulpless and infected. This was very clearly demonstrated in the study by Jansson et al. [16] where monkey premolar pulps were exposed and severed at the apical foramen. The pulp tissue was left in the canals and it was infected with oral bacteria from the animal’s plaque. The cavities were left open (i.e. unrestored) for 10–14 days to ensure the root canal systems became infected. Then, zinc oxide-eugenol (ZO-E) temporary restorations were placed in one group of teeth while the teeth in the other group were left open until the animals were sacrificed at various time intervals from 1 month up to 10 months. Histological examination revealed that the root canals in the ‘closed’ teeth (i.e. those with the ZO-E temporary restorations) had become pulpless within 1 month whilst the root canals in the teeth left ‘open’ took 2 months to become pulpless. This process of the root canal system becoming pulpless when infected is similar to the development of gangrene in extremities of the body, such as the toes and fingers, following bacterial infection.

Although the pulp’s first response to irritation is to form reparative or reactionary dentine, this cannot be assessed clinically. Hence, from a clinical diagnostic perspective, the first stage of pulp disease is inflammation, which is known as pulpitis. There are four stages of pulpitis; they are reversible and irreversible pulpitis and each of these can be chronic or acute. Reversible pulpitis is considered to be a milder form of inflammation, with relatively mild symptoms, and the clinical judgement leads the clinician to believe that conservative treatment (i.e. not root canal treatment) will resolve the inflammation [5, 8]. Such treatment typically involves removing the cause of the pulp irritation – such as caries, a crack, or a restoration that is breaking down – and then either restoring the tooth again or placing a sedative lining and an interim restoration to allow time for pulp healing, plus time to reassess the pulp status. Ideally, 3–4 months is required for a pulp to heal, at which time pulp sensibility tests would indicate whether the pulp has returned to a clinically normal state or it has necrosed [15].

If a tooth with reversible pulpitis is not treated, then the inflammation will continue to develop and spread throughout the pulp to become irreversible pulpitis. It is likely that chronic irreversible pulpitis will be present for some time. It will then become acute irreversible pulpitis when the irritation increases or reaches a specific threshold level.

Some patients with irreversible pulpitis may not seek treatment as the pain may not be severe, or the pain may subside in a short period of time. This occurs when the pulp starts to necrose. The necrosis will initially only involve that part of the pulp that communicates with the irritant, such as within a pulp horn. However, it will spread apically to involve the entire pulp. During the period when there is necrotic and infected pulp tissue coronal to the bacterial front (as mentioned previously) and irreversible pulpitis apical to this front, the tooth can be classified as having ‘pulp necrobiosis.’ This term was originally proposed by Grossman [17] and is an excellent descriptor as it implies that there is a mixture of necrotic (necro-) and live (bio-) tissue. This stage of the disease process is usually relatively short – perhaps only for several hours or a few days – as the bacterial front moves apically so the entire pulp becomes necrotic. Depending on the conditions within the particular tooth and root canal system, the tooth will become pulpless and infected within 1–2 months [16]. This progression of the pulp and root canal system through the various stages of the disease process is illustrated in Figure 4.5.

Teeth that have had previous endodontic treatment can become infected again and this will lead to a range of periradicular conditions, as outlined below. The new infection of such teeth will be a result of breakdown of the restoration in the tooth, further caries, a crack, or a fracture – that is, the same pathways through which bacteria enter teeth to cause pulp disease in the first instance [18]. Previous endodontic treatment could include pulp capping, partial pulpotomy, pulpotomy, partial pulpectomy, or root canal treatment. The important thing to assess when examining such teeth is whether there are any signs of the root canal system being infected [5]. Such signs usually manifest as one of the periradicular conditions discussed next. The periradicular responses to infections of teeth that have had previous endodontic treatment are the same as those that occur with teeth infected for the first time – that is, apical periodontitis which can be followed by an apical abscess, extra-radicular infection, periapical cyst, and so forth [5, 7].

Over time, the pulp can show degenerative changes – these include pulp atrophy, pulp canal calcification, pulp hyperplasia (pulp polyp), and various forms of internal resorption (note: internal resorption will be discussed in detail in chapter 5) [5, 8]. These degenerative conditions are a result of ageing (i.e. atrophy, pulp canal calcification), irritation from caries, cracks, fractures, or restorations breaking down (i.e. pulp canal calcification, pulp hyperplasia, internal surface resorption, internal inflammatory resorption), or sometimes specific events such as trauma to the tooth (i.e. calcification, internal inflammatory resorption). Internal replacement resorption is rare and no specific aetiology has been reported. These degenerative conditions are usually only noted through radiographic examination of the teeth and therefore some clinicians may consider them to be observations rather than diagnoses. In any case, it is essential to also assess the state of the pulp or root canal system when these degenerative conditions are noted [5, 8]. For example, a tooth with pulp canal calcification can have a pulp or root canal in any of the stages of the pulp disease process; that is, it may have irreversible pulpitis, may be pulpless and infected, or may have another condition.

4.4 The Development and Progression of Periradicular Conditions

As discussed previously, periapical conditions are a direct result of pulp and root canal conditions [5, 7]. The periradicular tissues are similar to other tissues in the body in that their first response to irritation will be inflammation (Figure 4.6). The most common irritants will be bacteria located within an infected root canal system.

The relationship between an infected root canal system and the periapical tissue response is demonstrated in Figure 4.7. It is important to understand that the bacteria are not usually in the periapical tissues unless there is an abscess or extra-radicular infection. In some cases, when there is no treatment, some of the bacteria in the root canal system may enter the periapical tissues via the apical foramen or other pathways (e.g. lateral canals, dentinal tubules with cementum defects caused by inflammatory resorption), and then the periapical tissues can become infected. This leads to the formation of an apical abscess or extra-radicular infection [5, 7, 19, 20]. The inflammation will continue and progress so that, over time, there will be a larger periapical radiolucency evident on radiographs. In some cases, a periapical cyst may form but this can only occur if there is epithelium present within the periapical tissues. Nair et al. [19] have shown that only about 50% of teeth have such epithelium and therefore these teeth are the only ones that have the potential to form periapical cysts, although only a very small number do actually form cysts. Nair et al. [19] also reported two forms of cysts, with the periapical pocket cyst likely forming first and then progressing to become a periapical true cyst. A pocket cyst has an opening which communicates with the infected root canal system (Figure 4.8), whereas a true cyst has no such opening and the cyst is completely lined by epithelium (Figure 4.9). True cysts are self-propagating lesions that will not respond to root canal treatment and require surgical removal, whereas it is believed that a pocket cyst is likely to heal following disinfection of the root canal system through root canal treatment [5, 7, 20].

Between the mid-1960s and early 1980s, several studies [21–26] reported that periapical inflammation only occurred once the root canal system was infected. However, it is now believed that the inflammatory response can develop earlier – that is, when the pulp is inflamed, in which case it could be considered as an extension of the pulp’s inflammatory response because there is only one direction in which the inflammation can spread – that is, apically and out into the periapical tissues [27]. Hence, teeth with reversible or irreversible pulpitis may have clinical or radiographic signs of apical periodontitis such as tenderness to percussion, widened periodontal ligament spaces, or condensing osteitis [6–8, 28, 29].

The periapical tissues can also be damaged as a result of trauma to a tooth. Injuries such as concussion, subluxation, lateral luxation, extrusion, intrusion, and avulsion can all damage the periodontal ligament and/or cementum [30, 31]. If the injury is mild (e.g. concussion, subluxation) and appropriate treatment is provided, then the tissues will usually heal [31]. These injuries can be considered as a ‘short-term insult’ to the periradicular tissues, and healing is expected once the injury has been appropriately managed (Figure 4.10). However, the more severe injuries (such as avulsion, intrusion, lateral luxation, and extrusion) cause more damage and can result in various forms of root resorption [31]. These will be discussed in other chapters of this book.

Traumatic occlusion is a further instance where there may be apical periodontitis without infection of the root canal system [32, 33]. The premature contact or occlusal interferences associated with traumatic occlusion are continuous and constant irritations to the periodontal ligament, which result in periradicular inflammation.

The periapical region is the interface between the root canal system (or the pulp, if it is present) and the body’s defence (or immune) system [5, 6, 34, 35]. Periapical conditions will continue as long as the root canal system remains infected. In turn, the root canal system will remain infected as long as the coronal entry point for the bacteria (and nutrients) remains open to the mouth. Hence, the basis for effective management of periapical conditions is to first remove the coronal pathway(s) of entry for the bacteria and nutrients – that is, remove the cause of the disease(s) [12] – and then to do root canal treatment in order to disinfect the root canal system.

The periapical response is dynamic with several possibilities that may be present at times, but not at all times [5, 6, 34, 35]. That is, the response can change, and this depends on the interaction between the bacteria in the root canal system and the host’s defence system [5, 6, 34, 35]. The former is largely dependent on the type of bacteria present, their virulence, the conditions (anaerobic versus aerobic), and the availability of nutrients. The host’s response is dependent on many factors including the patient’s general state of health and how effective their immune system is. All of these factors can change and thus the nature of the periradicular response can change. Figure 4.11 demonstrates the potential interactions that can occur between the different periapical conditions [5, 6, 34, 35].

Figure 4.10 demonstrates how the periapical conditions progress if there is no treatment provided [7, 8, 34, 35]. Patients may present for treatment at any stage of this disease process, but the most common times will be when there is an acute condition present as these will usually be painful. However, some patients may not present immediately and the pain may subside as the acute inflammation becomes chronic. This allows time for further progression of the disease process. A common scenario would be for a patient to have a short episode of pain with primary acute apical periodontitis and this progresses to chronic apical periodontitis, during which time a periapical radiolucency develops. The patient may then have occasional episodes of pain when bacteria exit the root canal and enter the periapical tissues to cause secondary acute apical periodontitis, but the body’s defence system may control this and it returns to chronic apical periodontitis. This cycle may occur several times before the pain eventually increases to the point where the patient seeks treatment. Other scenarios are also possible, such as when a chronic apical abscess develops and the patient notices the draining sinus, which leads him/her to seek treatment.

4.5 Classifications of Conditions and/or Diseases

In order to diagnose any condition or disease, it is necessary to have a classification of the various conditions/diseases that can occur [8]. The terms used for diagnosis are essentially a few words that summarise a set of symptoms, clinical signs, radiographic observations, and the results of various diagnostic tests [8]. It is implied that the diagnosing clinician and any other clinician involved in treating the patient will know what is meant by the diagnosis.

Hence, in developing a classification, it is necessary to understand the changes that occur in the tissues over time. It is also important to know the symptoms that occur plus the clinical and radiographic signs that can be seen when a patient is examined. Some conditions may have similar presentations, and in such situations, it is important to be able to differentiate between them in order to provide the appropriate management for the tooth and for the patient [8].

Classifications of dental and medical conditions ideally need to satisfy several criteria [6, 8]:

1) Possible to use in a clinical setting

• The diagnosis can be made based on information gained from the symptoms, clinical signs, tests, radiographs, and so forth.

2) Meaningful

• The various conditions reflect what is happening, or has already happened, in the tissues.

3) Useful

• The diagnosis directs the clinician to the management options.

4) Clear

• The diagnosis and terminology used is understood by all clinicians.

5) Universal

• The classification should be used throughout the world to standardise terminology and to allow effective communication amongst clinicians, educators, and students.

Unfortunately, this is not the case in the endodontic literature. Many classifications have been used over the years but with little consistency between them or with the terminology used [6].

In the past, many textbooks and journal articles have only referred to ‘pulp diseases,’ rather than ‘pulp and root canal conditions.’ However, it is important to distinguish between conditions and diseases because not all conditions are diseases [8]. A ‘disease’ is defined as a disordered or incorrectly functioning organ or system of the body resulting from (amongst other causes) the effect of infection, toxicity, or unfavourable environmental factors. It is considered as an illness or ailment [36]. As many pulp conditions do not fit this definition, it is inappropriate to group them all together as ‘diseases.’ Clinically normal pulps, pulp atrophy, and pulp canal calcification are examples of conditions that are not ‘diseases.’ Likewise, it is also important to distinguish between pulp conditions and root canal conditions because not all teeth have pulps. Examples are teeth with pulpless, infected root canal systems and teeth with previous root canal treatment. Hence, the general heading ‘pulp and root canal conditions’ is more appropriate.

The term ‘periradicular conditions’ is also more appropriate than ‘periapical diseases’ for two main reasons. First, not all such conditions are ‘diseases’ according to the definition, such as clinically normal periapical/periradicular tissues, apical periodontitis (this is a response, not a disease, as explained previously), and periapical scars. Second, not all of the conditions occur in the periapical region, such as the various types of external resorption that can occur anywhere along the tooth root. Many of the other conditions can occur in other locations along the root if associated with an infected lateral root canal or a crack extending into the tooth root.

Many pulp, root canal, and periradicular conditions are chronic in nature, whereas others are acute. When the term ‘chronic’ is used as part of a clinical diagnosis, it implies that there are no symptoms, or only occasional mild symptoms present [7, 8]. Typically, the problem has been present for a long time (e.g. weeks, months, or even years) and the patient may only mention it ‘in passing’ when they attend for a routine dental examination. In contrast, when the term ‘acute’ is used as part of a clinical diagnosis, it implies that there is some urgency about the matter. The patient typically has moderate or severe pain and this pain may only have been present for a short time (e.g. several hours or a few days) [7, 8]. These clinically defined terms are commonly used in medicine and dentistry. They should not be confused with the same terms when used as descriptors for the histological assessment of inflamed tissues [7, 8].

Other terms that have become popular in recent years are ‘symptomatic’ and ‘asymptomatic’ to replace ‘acute’ and ‘chronic,’ respectively, even though these terms are not used elsewhere in the dental or medical literature [7, 8]. Such terms tend to over-simplify the situation. As stated by Gutmann et al. [37], there is ‘little, if any, support in the historic or contemporary peer-reviewed literature for the use of these terms,’ and they ‘have slowly crept into usage with little scientific basis for their applications or meanings.’ A study by Bestall et al. [38] has shown that dentists were significantly less likely to treat pulp and periapical conditions labelled as ‘asymptomatic’ compared to when the same condition was labelled as ‘chronic’ (for example ‘asymptomatic apical periodontitis’ compared to ‘chronic apical periodontitis’). There were also differences when ‘acute’ was used rather than ‘symptomatic.’ The implications of this study are that many teeth with potentially serious pulp and periradicular conditions would be left untreated by many dentists because there were no symptoms rather than treating the tooth to resolve the condition or to remove the disease and improve the patient’s health. The authors concluded that ‘diagnostic terminology is important in directing appropriate management of diseases rather than just managing symptoms.’ This study clearly indicates that ‘words do matter’ and appropriate terminology should be used [38].

4.6 Classification and Description of Pulp and Root Canal Conditions

Table 4.1 outlines the classification of the status of the pulp and root canal conditions that has been adapted from Abbott and Yu [6] and Abbott [8]. The concept behind this classification is to follow the general stages of disease progression that can occur in any tissue (Figure 4.3) with the terminology adapted to suit pulp and root canal conditions (Figure 4.4). The conditions are grouped according to the general nature of the conditions – namely, healthy tissue (no signs of disease), inflammation (pulpitis), tissue necrosis and infection (pulp necrosis), tissue destruction (pulpless teeth), and degenerative changes.

Tables 4.2–4.9 outline the typical symptoms, clinical signs, radiographic findings, and associated periapical/periradicular conditions for teeth with the various pulp and root canal conditions listed in Table 4.1. When reading and using these tables, if any clinical or radiographic finding is not mentioned, then the reader should assume that the results for that particular test are normal (for example, if periodontal probing depths are not mentioned, then there are no deep periodontal pockets). A comprehensive examination incorporating a thorough history, all clinical tests, and appropriate radiographs or other imaging should still be performed to assess whether any aspect that is not mentioned is normal.