Asgeir Sigurdsson
7.1 Introduction
Correct pulpal diagnosis is the key to all endodontic treatments. It is paramount to have established a clinical diagnosis of the pulp and the periapical tissue prior cutting access into the pulp chamber or to do any other treatment to a tooth. This clinical diag- nosis has to be based on history of symptoms, presenting symptoms, diagnostic tests, and clinical findings. If it is not possible to establish the diagnosis or a differential diag- nosis cannot be ruled out, therapy should not be initiated until further evaluation has been done or second opinion gained.
Unfortunately, it has been reported that there is a poor correlation between clinical symptomatology and pulpal histopathology [5, 31, 42, 107]. In the past, attempts were made to accurately diagnose the condition of the pulp based only on clinical signs and symptom, on electric pulp or thermal tests and radiography however most of those failed to show much of any correlation [25, 31, 83]. Many of those attempts used variety of different pulpal diagnostic terms where at least some were elaborate and almost all these classifications had in common of being very descriptive of the assumed histological appearance of the pulp. [5, 105]. Due to obvious reasons the assessment of the histology is impossible with current technology without removing and microscopically evaluating the pulp. In more recent times the trend has been to move away from these elaborate classifications and to use a some- what modified version that Morse et al. sug- gested already in 1977 and later adopted with some minor simplification by the American Association of Endodontists [1, 82]. Even though this classification refers to some degree to histological status of the pulp, it helps the clinician to decide upon treatment because there is no crossover between categories in terms of treatment needs. More recently studies have been reported that using these more defined criteria for clinical and histologic classification of pulp conditions revealed a good agreement, especially for cases with no disease or reversible disease [101].
Since symptoms or test results can have somewhat limited predictor of pulpal and periapical status, as much information as possible should be collected about the presentation and history of symptoms and as many tests that are practical should be conducted prior to a formulation of final diagnosis [89]. Thus, clinical signs and symptoms, diagnostic tests in addition to a comprehensive knowl- edge of the reaction of the pulp to caries, operative manipulations, trauma, and periodontal disease, enable us to establish an empirical pulp diagnosis only.
7.2 Pulpal Diagnostic Terms
7.2.1 Healthy Pulp
According to the definition, a healthy pulp is vital, asymptomatic, and without any inflammation. This diagnostic term is only used if the pulp needs to be removed and the tooth root-filled for restorative reasons, e.g., need for a post space or when shortening an extruded tooth. Additionally this term is used in case of dental trauma when a crown of a tooth breaks off, exposing the pulp, but then is treated within the first 30 to 48 hours [49].
7.2.2 Reversible Pulpitis
This implies that the pulp is vital, but inflamed to some degree. Symptoms can be very misleading, ranging from none at all to very sharp sensation associated with a thermal stimuli. Through information gathered during testing (see below), it is predicted that the inflammation should heal and return to normal once the irritant, like deep caries, is removed, or when an exposed dentin surface is sealed again. The mild trauma with subsequent inflammation can cause small regions of neurogenic inflammation and sufficient mechanical damage to stimulate nerve sprouting reaction [20, 21] and thereby pos- sibly cause exaggerated response to vitality tests, indicating more severe inflammation than actually there is. As already stated, clinical signs or symptoms or diagnostic test do not always correlate with the histopathologic status of the pulp. There is, however, quite a high risk of diagnosing a pulp with mild symptoms as being reversibly inflamed, when actually it is irreversibly inflamed (see below). It is therefore very important to re-evaluate all patients with a diagnosis of reversible pulpitis few weeks after treatment and evaluate symptoms, including all possible changes in signs and symptoms as well as re-do appro- priate vitality tests. A telephone consultation is not enough in these cases, because the pulp may have become necrotic and thereby give the false impression to the patient that the problem has been resolved. The history of symptoms for the diagnosis of reversible pulpitis will mainly reveal provoked pain or sensation, and the tooth will only bother the patient when the tooth is exposed to a hot and/or cold or other excitatory stimuli.
7.2.3 Symptomatic Irreversible Pulpitis
This term implies that the pulp is still vital but so inflamed that it will not be able to heal again even if the irritant or cause of the symptoms are removed. Therefore, the pulp needs to be removed and root canal therapy done. In almost all cases, if this condition is left alone the pulp will eventually become necrotic, and then bacteria will have an easy access to the apex and periapical structures. This is a clinical diagnosis based on subjective and objective findings and the patient will complain, in addition to pain associated with direct stimuli, lingering thermal pain, spontaneous pain, and/or referred pain [34].
7.2.4 Asymptomatic Irreversible Pulpitis
Symptoms can be rather misleading. It has been well documented that in many cases an apparent irreversible pulpitis is asymptomatic. Studies have reported that dental pulps can progress to necrosis without pain in 26 to 60% of all cases [4, 79]. It is of interest to note that neither gender nor tooth type seems to matter such cases of asymptomatic pulpitis [80].
This clinical diagnosis is therefore based on subjective and objective findings, indicating that the vital, but inflamed pulp, is incapable of healing because of long-standing exposure to bacteria and bacterial by-products, as in case of indirect/direct caries exposure or trauma [12].
7.2.5 Necrotic Pulp
When the pulp necroses, the necrotic part of the pulpal space is filled with sterile debris at best but no vital structures [11].
The distinction between partial and total necrosis can be very important in cases of immature teeth, where the presence of intact pulp tissue apically may allow con- tinued root development. The only way to confirm vitality in those cases is to enter the pulp chamber and remove the necrotic debris down to a vital pulp stub because vitality test are not reliable in those cases even in healthy state [40].
7.2.6 Infected Pulp/Infected Pulpal Space
Infection of the pulp may affect only part of the pulp canal, such as in a recent pulpal exposure by trauma or caries, or when just one or two roots in multi-rooted teeth are involved. The space that is left once the pulp has become completely necrotic can be sterile in case of trauma where the blood supply to the tooth was cut off, but where there is no ingrowth of bacteria from the coronal part of the tooth [11]. In most cases, though, the pulp has become necrotic secondary to bacterial invasion through caries or crack/fracture in the crown and there fore the space is infected. It has been shown that all teeth with periapical lesions have infected pulp spaces [11]. Teeth that do not a have detectable periapical lesion may or may not be infected, as it is well known that there has to be a significant loss of bone structure before it becomes radiographically apparent [9, 10].
7.3 Symptomatology of Pulpal Disease
The dental training focuses primarily on diagnosing a problem by visual means, like assessing restorations, clinical signs of oral health or disease, and radiographs. However, when diagnosing origins of pain, most of the diagnosis is done by collecting anamnestic information, i.e., what we hear, and not what we can see [91]. In fact visual clues may throw us off track and lead to an incorrect diagnosis. Therefore, it is important to carefully listen to the patient and to systematically review all his/her present symptoms as well as the history of the symptoms prior to coming to a conclusion about the cause.
7.3.1 Presenting Symptoms
Presenting symptoms are, by definition, symptoms that are recognizable during the consultation. The presenting symptoms, while suggestive, cannot be used alone to make the final diagnosis.
Pain-free
It is a well-established fact that pulpitis can be painless [7, 31, 49, 79]. Lack of pain is therefore not a good indicator of the pres- ence, severity, or reversibility of pulpitis. The reasons, however, for the variability of pain symptoms in pulpitis are not well known. At least in some cases the progression of the inflammation may either be so rapid that there is no pain, or so slow that the classical inflammatory mediators participating in the pain process never reach a critical level [79]. A more likely explanation would be that there is effective modification by local as well as centrally mediated systems. There are sev- eral local regulatory factors and systems in the pulp. Endogenous opioid, adrenergic sympathetic, and nitric oxide systems exist in the pulp [20, 55, 92], and there is a good indi- cation that, for example, somatostatin may inhibit pulpal pain activation under certain conditions [23, 113, 114]. And more recently it has been shown in a study of pulps from patients diagnosed with irreversible pulpitis that several genes known to modulate pain and inflammation had different expression in asymptomatic and mild pain patients compared with those with moderate to severe pain; key inflammatory response like IL8, TNFA, and ILIB, which are all potent mediators of pain, were expressed at relatively lower levels in pulp samples from asymptomatic to mild pain patient compared to those who reported higher pain [41].
Sharp Pain
If the pain is short and only associated with a stimulus, like cold air or drink, it is likely to be mediated only by the A-delta neurofibers that are normally active throughout the dentin-pulp complex [7, 85]. Complaints of only provoked pain may therefore possibly indicate only mild (reversible) inflammation. Vital pulp therapy may be sufficient to treat the condition, e.g. by removing a shallow caries lesion, replacing a leaky restoration, or covering up exposed root surfaces.
Severe Pain that Lingers
There is building evidence that the classical inflammatory mediators that cause pain are released in the pulp in direct proportion to the insult. Serotonin (5-TH) can sensitize intradental A fibers, resulting in increased responsiveness [60, 92], and bradykinin has been shown to be in significant higher con- centration in irreversibly inflamed human pulps [67]. It is not only the inflammatory mediators that are associated with pulpal pain. Recent studies have also demonstrated that neuropeptides from the nociceptive nerve fibers present in the pulp (calcitonin gene-related peptide (CGRP), neurokinin A (NKA), and substance P) are in significantly higher concentrations in symptomatic compared to asymptomatic pulps [17, 48, 86]. Initially these mediators and peptides will primarily affect the more peripheral A-delta fibers, but when the inflammation reaches deeper structures, the C fibers will be affected as well. This will cause their firing threshold to be lower and make the receptive field larger. Therefore, it is important when the patient is questioned about lingering pain after the stimulus has been removed to not only ask about the time it took the pain to go away, but also about the quality of the lingering sensation. A dull, throbbing, pain compo- nent of the lingering pain indicates that more C fibers are involved and that there is an increased likelihood of severe inflammation. This can be used, with caution, to predict if the pulp is likely to be irreversibly inflamed or not.
Pain to Hot, Relived by Cold
It is interesting and generally accepted that there are not nearly as much complaints about heat in normal pulp compared to cold sensitiv- ity. However, when there is severe inflammation in the pulp there seems to be a strong tendency for heat sensitivity, especially in latter stages of the disease. Studies on this are scarce but clinical experience indicate that when a patient complains about severe heat sensitivity there is almost a certainty that the pulp is irre- versibly inflamed. In the past it was theorized that this was due to increased intrapulpal pressure when heat was applied to the tooth and the increased pressure caused increased neural activity [14]. The same activity was not seen by similar degree of cooling [53] and therefore it was though that this was related to a pressure increase. It has become clear that this is an incomplete explanation at best. It is more likely that clinical heat sensitivity is due to a reaction of the heat-sensitive pulpal nerves. Heat-sensitive C fibers are not easily stimulated under normal circumstances, but they become more active with more extensive inflammation [20]. When the pulp becomes inflamed the nerves respond due to the influx of inflammatory mediators into the inflamed area as well as due to secretion of neuropeptides. This response will cause the nerves to undergo both local and centrally mediated changes, changes which are likely to explain the alterations in pulpal sensitivity seen in pulpitis. An example: symptoms of throbbing pain associated with pulpitis [20] could be allodynia in pressure-sensitive fibers. The same would hold for a tooth with heat sensitivity alleviated by cold. The firing threshold of heat-sensitive fibers may be lowered so much by the inflammatory mediators that in extreme cases the nor- mal body temperature would activate the pulpal nerves, and cause pain: the only relief to the pain is then to cool the tooth down below ambient temperature [62].
Pain on Biting, When the Pulp has been Confirmed to be Vital
This may be indicative of a severe inflammation involving the pulp and periodontium, and differential diagnosis to non-pulp-related conditions must be carefully considered. If the pulp is involved, the clinical finding suggests at least some necrosis within the pulp and an irreversible pulpitis of the vital tissue [10].
Referred Pain
As the inflammation progresses in the pulp there is an increased tendency for the pain to be referred to a site remote from the tooth. It has been shown that pain from one tooth can be referred to another adjacent tooth or even to the opposite arch as well as to remote areas like the ear, clavicle and temple. In a classical study on referral patterns from teeth with pulpitis, Glick [44] showed that there were certain tendencies in the referral patterns. Upper teeth tended to refer the pain to the zygomatic or temporal areas. Mandibular molars were more likely to refer the pain back to the ear or even to the occipital area. Pain from a tooth may be referred between the arches but never across the midline of the face. The mechanisms for referred pain is not fully understood but it is clear that both peripheral and central mechanisms are responsible [110]. It is inter- esting to note that soft tissue structures, like temporal and masseter muscles, can refer pain in similar fashion from the tissue to the teeth [115]. Therefore, it is important to pal- pate any area of pain that patient reports away from the teeth in the head and neck area. If the palpation of a muscles of the face and/or neck increases the pain response, then there is a strong possibility that the patient is suffering from muscular pain rather than dental pain (see later 7.10).
7.3.2 History of the Presenting Symptoms
A number of factors related to a history of the patient's chief complaint are important to predicting irreversibility of pulpal inflammation. These include the following:
Character of the Pain; Dental Versus Pulpal Pain
In dentinal pain, the sharp rapid pain in response to external stimuli is a reaction of the fast-conducting A-delta fibers. They extend 150 pm into the dentin and are normally active throughout the dentin-pulp com- plex [47, 74, 76]. The deeper-seated, slower, and unmyelinated C fibers are for the most part unresponsive to all but very intense stimulus in normal, uninflamed pulp [20, 86]. When a long and intense enough stimulus is placed on a healthy pulp, there is first sharp pain, mediated by the A-delta fibers, followed by second, poorly localized, dull pain sensation [58, 59]. Complaints of only provoked pain indicate therefore possibly only mild (reversible) inflammation that a vital pulp therapy would be sufficient to treat, like removing a shallow caries lesion, replacing a leaky restoration, or covering up exposed root surfaces. However, when bacteria or bacterial products start to affect the pulp, inflammatory mediators will affect nerve fibers, resulting in a lower threshold to firing especially the C fibers [48, 67]. The history of the pain can be very revealing if it follows the pattern of starting as primarily temperature sensitivity, with sharp defined pain episodes, and then changing to a more dull, throbbing ache that is increasing in severity. This is important for two reasons; first, it indicates a shift in pain consistent with more activation of the C fibers that would then indicate increased inflammation; second, it has been shown that selfreports of intensity and quality of dental pain are a valid predictor of whether or not the pulpal inflammation is reversible or not [109].
Severe Pain
Self-reports on the intensity and quality of toothache pain seem to be valid predictors of whether the pulpal inflammation is reversible or not [46]. It has also been shown that the more severe the pain is and the longer it has been symptomatic, the more likely it is that irreversible inflammation is present. [7]. However, the reported severity of pain can be misleading due to the subjectivity of the sen- sation. The fear of dentists, for example, has been shown to result in an exaggerated per- ception of pain and response to diagnostic stimuli [63].
Spontaneous (Unprovoked) Pulpal Pain
Probably though the clearest sign of an irreversibly inflamed pulp is the history of spon- taneous pain, which will hit the patient without any thermal stimulation to the teeth, and may even wake the patient up from sound sleep [108]. Inflammation can cause spontaneous pain sensations in the affected area, and may at times prolong sensitivity to innocuous stimuli, which in the absence of inflammation would not cause any pain sensation (allodynia). This spontaneous activity is thought to be, at least in part, caused by the effects of inflammatory mediators on peripheral nociceptive nerve endings, primarily C fibers. [88]. These effects on the nerve endings will activate and/or sensitize them and cause local as well as central release of sub- stance P and calcitonin gene-related peptide (CGRP) [30, 48, 117] These neuropeptides can then further increase the release of inflammatory mediators, creating a positive feedback loop or a vicious cycle. This vicious cycle is sometimes referred to as neurogenic inflammation.
7.4 Clinical Findings
The findings of the clinical examination, in addition to an extensive knowledge of the pulpal reaction to external irritants, are important for arriving at a correct diagnosis. A clinical examination is critical since pulpitis is frequently painless and also because of the lack of correlation between symptoma- tology, diagnostic tests and the histopathologic state of the pulp.
7.4.1 Carious Pulpal Exposure
Scientific evidence indicates that when the pulp is exposed directly to caries, bacteria have already penetrated the pulp ahead of the caries lesion and formed micro abscesses [65, 72, 102]. Therefore the pulp should be considered irreversibly inflamed if it has a carious exposure. It has been recommended that in cases where root development is incom- plete an attempt should be made to estimate the level at which the pulp is inflamed or infected, that portion removed and apexog- enesis attempted. With the advent of calcium silicate materials as capping agents a reasonable successes has been reported, especially in cases that did not have presenting pain indicating irreversible pulpitis [19]. Recently there has been a quite a bit of interest in pulp capping of carious exposures in teeth with fully formed apex using these new materials [68]. Overall the success seems to be good, especially if the patient reported no pain, the pulp did respond normally to sensibility testing and frank caries exposure was avoided [16] (see further Chapter 9).
7.4.2 Age-related Changes
With age, the pulp is reduced in size and volume due to continued dentin formation. Its content of cellular components decreases relative to the number and thickness of collagen fibers [29]. There is also a decrease in the number of blood vessels and nerves, and an increased incidence of calcification and pulp stones [51]. Although it has not been shown experimentally, these changes have been assumed to result in a pulp which is less likely to reverse an inflammatory response compared to a young pulp. On the other hand, the pulp may remain vital for indefinite time periods following extensive degenerative changes.
7.4.3 Periodontal Disease
It has been reported that a moderate to severe periodontal disease will result in a pulp which is “prematurely” aged [13, 66, 103, 107]. Thus, a pulp in a periodontally involved tooth is also thought to be less resistant to inflammation than that in a tooth with a healthy pulp. However, this view is not universally accepted since Mazur and Massler [75] found no dif- ference in the pulp status of teeth with or without periodontal disease.
7.4.4 Previous Pulpal Insults
Previous pulpal insults such as caries, caries removal, and restorative procedures can all result in tubule sclerosis, reparative dentin formation, and fibrosis of the pulp. It has been hypothesized that this “premature” aging of the pulp may render it less likely to heal than an unstressed pulp [84, 108]. If a tooth that has large restoration or crown there is increased risk that the odontoblastic layer has been damaged if care was not taken to cool the bur and preparation done without adequate moisture [52].
7.5 Diagnostic Testing
Unfortunately, many clinicians solely rely on diagnostic tests for their diagnosis. It is important to remember that most commonly used test systems do not actually assess the vitality (blood circulation) of the pulp and they do not give much if any indication about presence or severity of inflammation in the pulp. The main reasons for doing a pulp test are to reproduce and, primarily, to localize the symptoms and to assess the severity of the symptoms. With every test it has to be remembered that the responses are subjective and some patients will have the tendency to exaggerate while others understate the pain felt [32, 64].
7.5.1 Sensibility Tests
Sensibility tests include the electric pulp test (EPT) and thermal tests. The primary function of these tests it to differentiate a vital from a non-vital pulp [56, 116]. By the use of these tests the nerve fibers in the pulp are activated, eliciting a reaction from the patient. The patient response is subjective, so that care must be taken to differentiate a “fearful” positive response from a true one [32, 64]. This is usually accomplished by comparing the patient's response with that of a contralat- eral or neighboring tooth and revisiting the tested teeth to ensure consistency. Care must also be taken to clean and dry the teeth so that conduction of the stimulus to the periodontal ligament or to adjacent teeth is minimized.
It is important to ask the patients prior to applying these sensibility test about recent intake of pain medications. This is because it has been shown that taking 800 mg of ibuprofen one hour before doing cold, percussion, palpation, and bite force tests significantly affected the diagnostic testing results in patients that had been diagnosed with endodontic pain [99].
As stated above, the main disadvantage of these tests, apart from their subjectivity, is the fact that an assumption has to be made that the presence of nerve fibers in the pulp correlates to a vital blood supply. While this assumption is mostly valid, in a number of cases the blood supply in the pulp will be lost before the degeneration of nerves in the pulp, resulting in an incorrect diagnosis of pulpal vitality [97]. Conversely it is known that, especially after luxation injury, vital pulps sometimes do not respond to sensitivity tests shortly after the trauma, but at a fol- low-up appointment a few weeks to few months later, normal responses are observed [78, 111].
7.5.1.1 Electric Pulp Test
The electric pulp testers activate the nerve bundle in the pulp, probably mainly the A- delta fibers. The unmyelinated C fibers of the pulp may [83] or may not respond [87]. The main problem with this type of test is the many variables that needs to be taken into account, some of which cannot be controlled. Key issues are location of the probe on the tooth (as far as possible from the gingival); conductivity between the instrument and the tooth; rate of stimulus intensity increase; isolation of the tooth tested from adjacent teeth and prevention of shunting to the gingiva by drying the crown. It is not possible to control for the thickness and electric resistance of the enamel and dentin, the presence of restorations and caries, and the functionality of the nerve complex in the pulp.
Procedure
The tooth and surrounding teeth are dried. The pulp test probe is placed on the incisal edge or cusp tip corresponding to the pulp horn of the tooth [8, 39] (Figure 7.1). Contact between the probe and tooth is facilitated by the use of conducting medium such as tooth- paste or fluoride gel. The circuit must be completed with a lip contact or the patient holding the handle of the electric pulp tester. The amount of current is increased slowly with the patient instructed to indicate (e.g. by raising the hand) if a tingling or other sensation is felt.
Diagnostic Information
A response, within reasonable intensity, to a stimulus is an indication of a vital pulp tissue. The response level however does not indicate the health of the pulp or reversibility of inflammation that might be present in the pulp, because no correlation has been shown between the electric pain threshold in a pulp and histological condition [69, 83]. No response is, however, a strong indicator of a necrotic pulp in most teeth [97, 108]. Seltzer et al. found complete necrosis in 72% and localized necrosis of the pulp in 25.7% of those teeth that did not respond to EPT. Thus, if it is accepted that even localized necrosis is an indication for the need of pulpectomy in a mature tooth, 97.7% of cases with no response to EPT will require a pulpectomy or the debridement of a necrotic pulp. And a more recent study confirmed these findings from 1963 as it showed that EPT results had overall accuracy of 75%. However, the negative predictive value was 90%, indicating that if there is no response and there is a good contact with the tooth, the likelihood of the pulp being necrotic is high. The reverse was not true, because positive predictive value was only 58% [56].
Figure 7.1 The electric pulp tester (EPT) probe is placed on the incisal edge of a maxillary anterior tooth. Theo tooth is thoroughly dried and contact between the probe and surface of the crown is facilitated by conduction medium like toothpaste or fluoride gel.
It is also important to remember that responses to EPT are unreliable shortly after dental trauma [111] as well as in teeth with incomplete root formation [39, 40]. This is likely due to the fact that the nerve plexus of Raschkow does not fully develop until very late stages of root formation. Thus the pulpal nerves do not reach the odontoblasts, pre- dentin, or dentin, as in fully developed teeth that have reached normal occlusion. In young teeth the cold test, especially with CO2 ice, is more reliable than EPT [39].
7.5.1.2 Cold Test
Probably the most commonly used test in dental offices is some form of a cold test [98]. It is important to realize that this testing method also, like the EPT and heat, only gives indication of functional nerve fibers, rather than information about the vitality status (blood flow) of the pulp.
The initial response to any cold stimulus is generated by cold-sensitive A-delta fibers [59] activated by the hydrodynamic forces. The temperature change causes a rapid movement of fluids in the dental tubules, a movement which then activates the intratu- bular nerves [17, 18]. Moreover, in animal models, the cold-sensitive A-delta fibers respond uniformly to rapid lowering of the tooth temperature [59], while the initial high-frequency discharge rate falls off as the rate of temperature change decreases and stops completely when the temperature reaches a steady level. This is a good indication that the sharp initial sensation when a cold stimulus is applied to the tooth is caused by the A delta fibers and subsides when those fibers stop firing once the movement of the intratubular fluid stops. The C fibers also show a quite uniform but very different reaction. The C fibers start to discharge after a short latency and then the discharge rate is low [59]. In an experimental study in human [77], the subjects reported sensations that could be interpreted as being comparable to these phasic type of activation of the A and C fibers in the animal study. There was a distinct, sharp, and short- latency (1.6 sec) pain felt when the tooth was rapidly cooled. The latter pain was described as dull, burning pain, which was difficult to localize. These findings support the assumption that the response behavior of the human pulp nerves are comparable to those of the animal model: the first sharp pain is evoked by intradental A delta fibers and then later, once the interdental temperature is raised sufficiently, the C fibers are activated and are responsible for the dull, throbbing, and aching sensation. Subsequently other research groups have come to similar or same con- clusions, though with somewhat different research approaches. It is important to note, however, that the studies providing the data for these mechanisms were done on relatively normal, healthy pulps [2].
Very few studies have been done to investigate pain sensation in inflamed human pulps. There appears to be only a poor correlation between estimates of pain magnitude and the total A delta nerve activity in patients that were clinically diagnosed with pulpitis [3]. However, abnormal but positive responses are equally distributed among the pulps of teeth with varying degree of inflammation. Therefore a positive cold test response only indicates vitality but not if the pulp is revers- ible or irreversible inflamed; however, no response is very indicative of a necrotic pulp.
Historically, ice and ethyl chloride spray have been used for cold testing but both of those have several problems that have led to new approaches. Both are not very cold; ethyl chloride is only about -4° C and ice is at or just above 0° C. An additional problem with water is that once it melts very cold water can drip on adjacent teeth and thereby give false positive responses. Carbon dioxide (CO2) ice pencils have now been available for over twenty years. They are safe to use on vital pulps and will not cause damage to enamel or pulpal tissue in vivo. [54, 95, 96]. The CO2 ice may also be more dependable than ethyl chloride and water ice in producing a positive response, and in young patients with incomplete root formation CO2 ice seems to be more reliable than EPT [40]. Additionally the CO2 ice appears more reliable than EPT in patients undergoing orthodontic movement of teeth [24].
More recently refrigerant spray, 1,1,1,2 tetrafluoroethane, has been introduced. It has the advantage that it is supplied in spray cans; it can be stored at chairside; and it has less start-up cost compared to the CO2 ice. It is, however, not as cold as CO2 ice (-26.2° C, -15.4°F). It appears that there is no difference between tetrafluoroethane and CO2 ice in producing a pulp response regardless of tooth type or presence of restoration [57].
If several vitality tests are planned on a patient, it seems that the sequence and interval between electric pulp testing and cold vitality testing with refrigerant spray does not affect the reliability of pulpal diagnostic testing [93].
Procedure
As with the EPT, care needs to be taken to dry the tooth and surrounding teeth. The cold object should be placed on the incisal edge or close to a pulp horn for optimum results. The cold test should be administered gently, as a placement of the very cold ice or object could cause rapid and severe pain, especially in the anterior teeth (Figure 7.2).
Diagnostic Information
Abnormal but positive responses are equally distributed among the pulps of teeth in all diagnostic categories [31, 108]. Therefore a positive response is an indication that the pulp is at least partially vital, but it does not indicate if inflammation is reversible if present. Despite the lack of an apparent clear correlation between cold response and histological appearance of the pulp, clinical expe- rience indicates that an exaggerated response, which quickly turns into a dull aching pain, coupled with other signs, like history of pain and spontaneous pain strongly indicates a pulpal inflammation that is most likely irreversible.
Figure 7.2 Thermal sensitivity test with (a) CO2 frozen stick (-70°C), (b) cotton pellet sprayed with 1,1,1,2 tetrafluoroethane, (-26°C), (c) prophy rubber cup without any lubrication used to heat the tooth surface, (d) single-tooth rubber dam isolation and irrigation with hot water. Courtesy of Dr. Sigurdsson.
7.5.1.3 Heat Test
A less common, but probably a more clinically informative, temperature test is some form of heat test. The main problem with this approach is that many commonly used tests can cause excessive heat that may dam- age the pulp or adjacent tissue, and others are cumbersome to apply. Therefore, the clinical use of heat tests is somewhat limited.
The normal pulp reaction and sensation to heat is similar to cold. It is in most cases biphasic where initially the A delta fibers are activated and then later, if the stimulus is maintained, a dull, radiating pain follows [18, 86]. It has been shown in vivo human studies that hot gutta-percha induced a more complex neural response pattern than ethyl chlo- ride. The hot gutta-percha evoked a response in three phases, where the third phase was a slow spontaneous emerging activity in the absence of physical stimulus, and this activity was not felt by the test subjects, indicating more C-fiber activity [3].
Procedure
Several heat tests have been advocated. One is to heat gutta-percha over flame and then place it on a lubricated surface of the crown towards the incisal edge [83]. The problem with this approach is that there is little control over the heat and the gutta-percha tends to stick on the tooth and thereby cause con- tinued heating of the tooth after the bulk materials is removed. Using a prophy cup or a rubber wheel without lubrication has also been advocated, but again there is no control over the heat generated. A better, but cumbersome, approach is to put the patient in supine position, isolate a single tooth with rubber dam and then bathe the exposed tooth in hot water. Once a response has been noted, the rubber dam is moved mesially by one tooth and the procedure repeated. One starts distal to the suspected tooth so that if there is a leakage thorough the dam, the hot water will not drip on the suspected tooth and thereby give a false positive response.
Diagnostic Information
No correlation has been found between an abnormal response to heat and histologic diagnosis [31, 108]. It is, however, generally accepted that when there is severe inflammation in the pulp there seems to be a tendency for heat sensitivity. Studies on this are scarce but clinical experience indicates that when a patient complains about severe heat sensitiv- ity, the pulp is usually irreversibly inflamed. This is confirmed to some degree in animal studies, where it has been shown that the nerves stimulated by heat are located in similar areas as markers for pain responses in symptomatic pulpitis. [26, 27].
7.5.2 Mechanical Tests
Percussion and palpation test are not technically vitality tests but rather give indication about periodontal and/or periapical inflammation. It has been stated that pain is more likely to be elicited on percussion when there is a partial or total necrosis present in the pulp [106] and as such an indirect assessment of the status of the pulp. Other causes for percussion sensitivity, like recent traumatic occlusion, high filling etc, obviously need to be ruled out. The same seems to be the case when the periapical area is sensitive to palpation but the pulp is still vital. Presence of percussion and/or palpation sensitivity in conjunction with a vital pulp with hypersen- sitivity to thermal stimulation is indicative of a pulp that is severely and thus most likely irreversibly inflamed [106]. However, if the tooth is not sensitive to percussion and/or palpation, inflammation is not necessarily absent [10].
Percussion
This test is properly performed with the han- dle of a mouth mirror. The aim is to deter- mine the presence/absence of inflammation in the apical periodontium.
Procedure
The mouth mirror handle is used to percuss not only the occlusal, but also facial and lingual surfaces of the teeth. The teeth should be percussed in a random order so that the patient does not respond to “anticipates” rather than real pain.
Diagnostic Information
As stated before, a positive percussion test indicates inflammation of the periradicular tissues. Care must be taken, when interpreting the results of the percussion tests, to rule out a positive response due to periodontal diseases or cuspal fracture. This is particularly difficult in cases where the pulp vitality tests indicate a vital pulp. The results of other diagnostic tests and presenting symptoms need to be used to differentiate periodontitis of marginal or endodontic origin.
Palpation
This test is used to detect inflammation in the mucoperiosteum around the root of the tooth. It may be possible to detect tender- ness, fluctuation, hardness, or crepitus before extensive swelling is present.
Procedure
The index finger is pressed against the bone through the mucosa. When pressure is felt, the finger is rolled causing sensitivity if inflammation is present. As with percussion, the test should be performed in a random fashion and the results obtained should be compared to a contralateral tooth or neigh- boring teeth.
Diagnostic Information
Similar to the percussion test, a positive response when palpating over the root tip is a reliable indicator of periapical inflammation. However, if a positive response is not elicited, inflammation is not necessarily absent [10].
7.5.3 Radiographic Examination
The radiographic examination is one of many tests, and the findings should always be evaluated together with those of presenting symptoms, clinical examination as well as with those of the other tests. All radiographs should be taken using holders which allow parallelism and standardization. If comparative radiographs will be required on follow up, it is useful to fabricate a rubber bite-block so that the angulation of the follow-up radiographs will be as similar as possible (Figure 7.3).
Diagnostic Information
The radiograph cannot detect pulpal inflammation directly. However, caries or defective
restorations seen on the radiograph will indicated pulp inflammation [73]. Condensing apical periodontitis is a near pathognomonic sign of pulpitis (Figure 7.4). Signs of obliteration and calcification (diffuse or as pulp stones) may be considered but are not directly correlated with inflammatory reactions in the pulp. Also, the presence of an apical radiolucency of endodontic origin may be a good indication that necrosis or a necrotic zone is present in the pulp space.
7.5.4 Experimental Testing Methods
Sensitivity test of pulp vitality require functional nerves to respond to a stimulus. Pulp with effective circulation and vital cells, but with severed or compromised nerves, may be misdiagnosed as being necrotic or non-vital by these tests. Therefore, attempts have been made to demonstrate pulpal vitality based on blood circulation. Several experimental methods have been proposed, like crown surface temperature measurements [36, 37], Xenon-133 radioisotope injection [61], pulse oximetry [104], dual wavelength spectropho- tometry [90], and laser Doppler flowmetry [43]. Of those alternative methods the laser Doppler flowmetry and pulse oximetry seems to be most likely to be accurate in determining the vitality of the pulp [71]. However, and very unfortunately, they have a limited ability to assess the level of inflammation that might be present in the pulp, and most of these approaches, despite experimental demonstration of very accurate and reliable findings, have never been made available commercially for pulp vitality assessment.
Figure 7.3 (a) All radiographs should be taken using holders which allow parallelism and standardization. (b) If comparative radiographs will be required on follow up, it is useful to fabricate a customized rubber bite-block using putty impression material. (c) The bite registration is then stored along with the film holder. Courtesy of Dr. Sigurdsson.
Figure 7.4 A radiograph showing condensing apical periodontitis associated with the mesial root of a lower molar. The tooth had been restored some years earlier, with what appears to be direct pulp capping. The patient reported hypersensitivity to cold for some weeks prior to seeking help.
7.6 Formulation of a Pulpal Diagnosis
The diagnosis is made using the information obtained above (see Table 7.1).
Table 7.1 The formulation of a pulpal diagnosis.
|
Symptom, test, supporting information |
Necrotic pulp |
Vital pulp |
|
|
Irreversibly inflamed |
Reversibly inflamed |
||
|
Pulp test |
Negative |
Positive |
Positive |
|
Key factors |
|||
|
Pulpal exposure |
Present |
Absent |
|
|
Pain to percussion |
Present |
Absent |
|
|
Related factors |
|||
|
Severe pain |
Present |
Absent |
|
|
Spontaneous pain |
Present |
Absent |
|
|
Past history of pain |
Present |
Absent |
|
|
Pain that lingers |
Present |
Absent |
|
|
Pain to hot, relieved by cold |
Present |
Absent |
|
|
Factors related to treatment plan |
|||
|
Age, periodontal disease, |
Questionable (complex |
Questionable (simple |
|
|
previous pulpal insults |
treatment plan) |
treatment plan) |
|
7.6.1 Key Factors
Necrotic Versus Vital
Using the patient's presenting symptomatology and the results of as many diagnostic tests as possible, it should be possible to accurately determine if the pulp is necrotic or vital. If the pulp is necrotic, the choice of treatment is root canal therapy if the tooth is to be maintained for an extended period.
It is a much greater challenge to differentiate a reversible from an irreversible pulpitis. For this determination, the presenting symptomatology and its history (subjective) and clinical findings are used.
Pulp Exposure
As already discussed, if on excavation the pulp is found to be exposed to bacteria, an irreversible pulpitis can confidently be diagnosed. Treatment is then extirpation of the whole pulp and root canal filling as a preventive measure. An exception would be a case of a very young tooth with incomplete root formation. In those cases, a temporary (few months to a year) partial pulpotomy would be indicated in an attempt to allow the apex to fully form prior to initiation of complete root canal therapy.
7.6.2 Related Factors
A history of severe pain, spontaneous pain, a past history of pain in the same tooth, or referred pain, are all indications of an irreversible pulpitis.
All other related factors, such as age, periodontal status, and previous pulpal and treatment history, must be considered but are less suggestive.
7.6.3 Treatment Planning
It has been continually stressed that with methods of diagnosis available today, the diagnosis of an irreversible pulpitis is at best an “educated guess” and mistakes are inevitable. Because of this fact, the overall treatment plan for the patient should play a role in the choice of pulpectomy or conservative therapy.
For example, if a tooth is the only tooth in the arch needing treatment and the longterm restoration is to be a simple amalgam or resin (Figure 7.5), a conservative approach can be attempted without pulpec- tomy, even though some of the related factors suggest a moderate inflammation is present. With the same presenting signs and symptoms, a tooth planned as an abutment for a bridge which would be difficult to treat endodontically subsequent to possible failure of conservative treatment, might preferentially be subjected to immediate pulpectomy without an attempt at conservative treatment.
Figure 7.5 Radiograph (a) showing two lower molars both with extensive and deep carious lesions. Patient complained about sever pain of few days duration but was unable to determine which tooth was causing the pain. Pulpal test were inconclusive on which tooth had more severe pulpal inflammation. After caries excavation a caries perforation was found in the second molar but not the first. The second molar was treated with root canal therapy. The first with vital pulp therapy and restoration. (b) At one year re-evaluation the first molar responded normally to pulpal tests and both teeth were normal to percussion and palpation.
7.7 Periapical Diagnosis
The term “apical periodontitis” implies that there is an inflammation in the periodontal ligament caused by infection of the pulp or of the necrotic pulp space. The noxious material and bacterial byproducts have passed to the periodontium through the apical foramina. If communication between the pulp space and surrounding periodontium is present through furcation or accessory canals, periodontal inflammation can result in these locations as well. Histologically the lesion is predominated by chronic inflammatory cells with the overall appearance of a granuloma or cyst [15].
Like pulpal inflammation, the periapical inflammation can be symptom-free and then only diagnosed in a chronic phase on a periapical radiograph. However, if there is a periapical lesion detectable on a radiograph it is almost certainly caused by an infection in the root canal system, irrespective of the tooth's history or the occurrence of symptoms [11]. As always, if the patient is symptomatic it is important to be able to diagnose the source prior to treatment. Treatment is always to remove the irritant that causes the symptoms or lesion. This could be accomplished by simple occlusal adjustment in cases of occlusal trauma, but as the cause is usually bacteria in the root canal system, the only predictable treatment is to completely disinfect the canal space followed by obturation and a good coronal seal. Antibiotic therapy alone is not effective [38].
7.7.1 Normal Apical Tissues
7.7.1.1 Symptomatic Apical Periodontitis (SAP)
This term usually implies that the apical inflammation started in the acute phase causing clinical symptoms like biting and percussion sensitivity and/or palpation sensitivity. Often there are minimal or no radiographic changes associated with SAP. However, this diagnostic term might be associated with an apical radiolucent area. There can be several causes for this inflammation. Most benign would be occlusal trauma. If that is the case, the pulp should be vital and unaffected. However, in case of bacterial infection, the pulp is either severely or irreversibly inflamed and usually partly or totally necrotic. An acute apical periodontitis can also be superimposed on a previously chronic lesion (see 7.7.1.3).
7.7.1.2 Asymptomatic Apical Periodontitis (AAP)
This term implies that the apical periodontitis is of some duration without symptoms. The condition may be suspected when the pulp is necrotic with radiographic signs of apical periodontitis (radiolucency or rarely a radiopacity).
7.7.1.3 Acute Apical Abscess (AAA, Phoenix Abscess)
Here the periapical inflammation has caused a purulent breakdown of periapical tissues with accumulation of pus in the periodontium, subperiosteally, submucosally, and/or subcutaneously, often characterized by rapid onset of pain, and tenderness to pressure and swelling. Commonly, this acute inflammation is superimposed on a previous chronic apical periodontitis and has been termed a Phoenix abscess.
7.7.1.4 Chronic Apical Abscess
This term is used when there is a slow and gradual inflammatory reaction due to pulpal necrosis and ensuing infection. Most often there is little or no discomfort and there is a traceable sinus tract associated, where the periapical exudate discharges onto a body surface (intraor extra-orally), establishing a traceable sinus tract with periapical drainage (Figures 7.6 and 7.7).
Figure 7.6 A radiograph of a sinus tract that has been traced with size 40 gutta-percha. Note that the exit of the tract was distal to the left central incisor but traced to the right central incisor.
7.7.1.5 Condensing Osteitis
These are usually asymptomatic findings that are associated with a diffuse radiopaque area usually close the apex ofthe tooth (Figure 7.4). It is thought that this is associated with a low-grade inflammatory stimulus on the pulp and from evaluating human cadavers exhibited areas of inflammation or no inflammation, occupied by connective tissue bordered with a rim of varying widths of dense lamellar-type bone replacing the cancellous bone and marrow [45].
7.8 Symptomatology of Periapical Disease
The same diagnostic steps should take place for the diagnosis of periodontal pathosis as described above for the pulp. The patient's presenting symptoms are carefully evaluated, diagnostic tests are performed, clinical findings recorded, and the information is compiled to make the tentative diagnosis (see Table 7.2).
Figure 7.7 (a) The patient with that has epilepsy (grand mal) had been treated by multiple physicians for a "chin cyst') which led to the scar tissue on the chin as well as a localized paresthesia. Eventually she was seen by an endodontist that traced the sinus tract with gutta-percha point. (b) The point traced to lower left central incisor. The pulp did not respond to sensibly tests and there was a periapical lesion evident on the radiograph. After first appointment where the canal was debrided and Ca(OH)2 the sinus tract closed and was still closed at two-year re-evaluation. (Courtesy of Dr Buttke.)
Table 7.2 Differential diagnosis of an endodontic sinus tract versus a periodontal pocket.
|
Test applied |
Periodontal pocket |
Endodontic sinus tract |
|
Vitality testing |
Within normal limits |
No response |
|
Perio probing |
Wide pockets |
Narrow tract |
|
Clinical status of the tooth |
Minimal caries/restorations |
Evidence of caries/restorations |
|
General periodontal condition |
Poor |
Within normal limits |
|
Dark field spirochete count |
>30% |
<10% |
7.8.1 Symptomatic Apical Periodontitis (SAP)
Traumatic Occlusion
Presenting symptoms: Patients complain of pain on biting, eating or “when the teeth come into contact"
History: Commonly the patient has recently had a dental procedure performed which has resulted in a restoration where the occlusion is not balanced, leaving high contact.
Clinicalfindings: There is often evidence of a new restoration(s) in the area.
Diagnostic tests: Response to thermal and electrical sensitivity testing are normal. Pain is elicited to percussion, and on rare occasions to palpation as well. Radiographic findings are usually non-specific.
Treatment: The occlusion should be adjusted so that premature contacts are removed, including all interference in acentric contacts. The patient should return for a follow-up visit to ensure that the acute apical inflammation has subsided and the pulp has remained vital.
Symptomatic Apical Periodontitis with Acute Pulpitis
This condition has already been discussed in pulpal diagnosis. Acute apical periodontitis in conjunction with an acute pulpitis indicates an irreversible pulpitis.
Treatment: Pulpectomy/endodontic ther- apy (see Chapter 10). A permanent restoration should be placed as soon as possible after obturation to prevent coronal leakage with subsequent chronic apical periodontitis [70].
Acute Exacerbation of Asymptomatic Apical Periodontitis
Presenting symptoms: Patient complains of pain on biting, eating, or “when the teeth come in to contact" There may also be epi- sodes of spontaneous and intense pain, as well as swelling and malaise.
History: The history in these cases is varied. In some cases, the patient reports episodes of previous pain or there is a recent restoration placed in the tooth. In other cases, the patient may tell a previous history of pulpal pain which later subsided. Sometimes root canal therapy has previously been performed on the tooth.
Clinicalfindings: These are consistent with a tooth with a necrotic pulp or a previous root filling. Examples would be a deep carious lesion, a previous pulp capping, a large restoration, or full-coverage crown.
Diagnostic tests: There is no response to thermal and electrical sensitivity tests. There will be pain to percussion and/or palpation. An apical radiolucency is present on radiographic examination, indicating the presence of chronic apical periodontitis in addition to the acute exacerbation.
Treatment: The treatment involves complete root canal instrumentation and disinfection with antibacterial irrigation and intracanal medication of the root canal system [22] (see Chapter 10). Since abscess formation has not yet occurred, drainage is not possible. For the same reason antibiotic therapy is not required. Pain medication is prescribed as needed. Re-evaluation should be after 1-4 weeks for confirmation that the apical inflammation has subsided, after which the canal is obturated. A permanent restoration is placed as soon as possible for prevention of coronal leakage.
7.8.2 Asymptomatic Apical Periodontitis
Presenting symptoms: By definition the patient is asymptomatic or at least reports very minimal discomfort associated with the tooth. The condition may be diagnosed on a routine recall radiograph, or a restoration may have been required on a tooth which when tested for vitality shows no response.
History and clinical findings: These are as in acute exacerbation of AAP, and pain may have been completely absent.
Diagnostic tests: There is no response to thermal and EPT tests. Percussion and/or palpation tests are usually negative, although slight sensitivity may be present.
Radiographic findings: Since these cases are largely asymptomatic, the diagnosis of chronic apical periodontitis is made primarily on radiographic evidence of the presence of radiolucency (or rarely on opacity) (see Chapter 6) (Figure 7.8). It is possible for an apical periodontitis to go undetected radiographically [9, 10]), so that pulp necrosis and infection is evident only after initiation of endodontic therapy. A revised diagnosis of probable AAP should then be made and the tooth treated accordingly (Chapter 11).
Treatment: Effective disinfection of the root canal system will result in reversal of the chronic apical periodontitis.
7.8.3 Acute Periodontitis with Abscess
During acute phases of apical periodontitis (primary acute or an exacerbation of chronic lesion), the infection may develop to produce an accumulation of pus and formation of an abscess. From this point, the inflammation may become chronic, but in some cases continues with formation of a clinical abscess. There is an increase in tissue pressure, bone resorption is initiated by inflammatory mediators, and the pus escapes first through the bone and under- neath the periosteum and then, if the periosteum is penetrated, into the tissue spaces.
Figure 7.8 13-year-old patient asymptomatic apart from noticing some firm enlargement facial to his lower anterior teeth. Radiographic evaluation revealed large periapical radiolucency with the roots of the central incisors pushed distally (a). The right central incisor did not respond to cold, but the left one did. Diagnosis of necrotic pulp with chronic apical periodontitis (CAP) was made. Six weeks after placing calcium hydroxide in the root canal system there was significant improvement of the periapical lesion (b). After three months of calcium hydroxide treatment there was almost complete resolution of the lesion (c).
The exact location of the accumulation of fluids is dependent on the anatomical location of the root apex relative to the facial muscles [81]. Most commonly the drainage is buccal into the oral vestibule. A rare complication is spread from maxillary and mandibular third molars via the pterygoid plexus, causing a cavernous sinus thrombophlebitis and impairment of cerebral vascular drainage [50] (Figure 7.9). In the mandibular teeth the most serious spread would be from the premolar or molar teeth lingually under the mylohyoid muscle and into the retropharyn- geal space. Ludwig's angina is a bilateral ret- ropharyngeal spread which may become serious through a blockage of the airway [112]. In most cases the pus will break through the intraoral mucosa to a surface. Occasionally the abscess will drain extraorally on or under the chin or below the mandible.
Presenting symptoms: Symptoms will vary according to the stage of progression of the inflammatory process. Initially, the symptoms may be minor with pain on biting, eating or occlusal contact. As pus builds under the periosteum, the pain increases in intensity and can in time be excruciating. When the periosteum is penetrated by the pus, diffuse swelling may develop (Figure 7.9). The penetration of the periosteum by the pus is usually accompanied by a release of pressure and a considerable reduction in the pain.
Figure 7.9 Severe swelling due to an abscessed maxillary first premolar tooth. Pus has broken through the periosteum and caused severe and very serious swelling around the orbit.
History and clinical findings: These are the same as in SAP.
Diagnostic tests: There is no response to thermal or electrical sensitivity tests. Pain on percussion and/or palpation is elicited which can sometimes be severe, depending on the stage of the process.
Radiographic findings: The stage of devel- opment of the abscess determines the radiographic picture. At the early state of abscess formation radiographic signs of inflammation may be minimal if any. As the abscess spreads and more bone is destroyed, the radiographic signs of apical periodontitis will be more obvious. In the case of an acute exacerbation of a chronic lesion, the signs of apical periodontitis are present throughout.
Treatment: Treatment principles are the same as for all teeth with apical periodontitis, i.e. the disinfection of the root canal (see Chapter 9). Additionally, in the case of an acute abscess, concerns of spread of the infection in the tissue spaces (cellulitis) and pain control must be addressed in the treatment protocol. Emergency treatment is primarily aimed at eliminating the source of the abscess, the infection of the pulpal space, and antibiotics are only used as supplemental treatment if the patient is showing systemic effects of the infection. In severe cases when a spread is suspected in to the retropharyn- geal space or orbit an emergnecy consultation with oral surgeon or emergency room is recommended.
7.8.4 Chronic Apical Abscess
This occurs when the apical inflammatory exudate drains to a body surface, intraor extra-orally. The formation of a sinus tract may be the mechanism with which the body controls the infection, or it may indicate a specific infection of some - as yet unknown - bacterial combination. It may develop as a result of an abscess as described above or be without preceding symptoms, and the diagnosis may be made without the patient even being aware of its existence. When long-standing, the tract can become completely epithelialized [6]. With adequate disinfection of the root canal and resolution of the periapical inflammation, the epithelium, if present, will in most cases disintegrate. Commonly, the sinus tract will drain on the mucosa adjacent to the offending tooth. However, the opening may be at some distance from the involved tooth (Figure 7.6), drain through the periodontal ligament mimicking a periodontal pocket or even extraorally, where it might be misdiagnosed (Figure 7.7). For these reasons, it is important to perform a thorough diagnostic examination and not rely on the presence and location of the sinus tract opening.
Presenting symptoms: Generally, when a sinus tract is present in conjunction with the apical periodontitis, pain is absent or very mild and swelling is minimal. This is due to the lack of pressure build-up under the peri- osteum or adjacent tissues.
History and clinical findings: A history consistent with that described for AAP or SAP
Diagnostic tests: The pulp is nonresponsive to thermal or EPT tests. There is no or only light pain to percussion and/or palpation.
Radiographic findings: Radiographic evidence of chronic apical periodontitis is usually present, but the location of the sinus tract on the mucosa does not always correspond to the offending tooth. Therefore, it is important to trace the sinus tract with an opaque object, for instance a size 35 or 40 gutta-percha cone, to determine the origin of the tract. Care must be taken to not force the cone and thereby create a false tract, which could lead to an incorrect diagnosis.
Treatment: Disinfection of the root canal system should result in reversal of the chronic apical periodontitis and the sinus tract will disappear within days to few weeks. In rare cases the sinus tract will not heal because the infection is primarily located extraradicular and antibiotic therapy and/or surgical treatment my become necessary.
7.8.5 Condensing Osteitis
As stated before, this is a diffuse radiopaque area usually close to the apical area of a tooth [118].
Presenting symptoms: Generally, this is an asymptomatic identity and the pulp is viatl in most cases. However, it can be hypersensitive to sensibility tests.
History and clinical findings: It has been theorized that there is a long standing chronic irritation to the pulp, like deep and/ or leaky fillings that causes a low-grade inflammation in it, along with the periapical bony changes where there is replacement of marrow spaces and cancellous bone by dense, compact bone along with areas of fibrosis replacing fatty marrow [45].
Diagnostic tests: The pulp is usually responsive to thermal or EPT tests. There is no pain to percussion and/or palpation.
Radiographic findings: Diffuse radiopaque areas that are concentrically arranged around a root apex that may or may not have a radio- lucent inflammatory lesion that does not alter the PDL space [35].
Treatment: No treatment is recommended, except ruling out source of the irritation to the pulp by evaluating the restoration(s) in the tooth.
7.9 Formulation of a Periapical Diagnosis
The diagnosis is only possible to make after obtaining all the information listed above, see summary in Table 7.3.
7.9.1 Key Factors
Periapical diseases associated with the root canal system are nearly always caused by bacteria and/or bacterial by-products. Therefore, elimination of those should ensure resolution of the disease and healing.
Table 7.3 The formulation of periapical diagnosis.
|
Presenting symptoms |
||||
|
Pain |
Swelling |
Radiographic signs |
Other findings |
|
|
Acute apical periodontitis |
Yes |
No |
Normal PDL |
|
|
Chronic apical periodontitis |
No |
No |
Periapical radiolucency |
|
|
Apical periodontitis with abscess |
Yes/No |
Yes |
Initially normal PDL Late stage some widening |
|
|
Apical periodontitis with sinus tract |
No |
No |
Usually periapical radiolucency |
Draining sinus tract |
7.9.2 Related Factors
Diagnosis of periodontal versus endodontic causes for periapical diseases is crucial for correct and proper treatment of the disease (see Table 7.2).
7.10 Future ofPulpal and Periapical Diagnosis
Recently it has been suggested that various biomarkers, like for example matrix metalloproteinase, could be a useful tool to assess the level of pulpal inflammation [119]. This is because it has been shown, that at least in general, irreversible pulpitis is associated with different expression of various biomarkers compared to healthy pulps and many of those could be even collected non-invasively from crevial fluid or from dentinal/interdentin fluids collected prior to accessing the pulp in case of caries or other restorative procedures [100]. The interplay of these biomarkers could not only be used to assess the level of pulpal inflammation but also have the potential to provide enough information to differentiate between periapical cysts from granuloma [28, 33, 94, 100]. However, we are not quite there yet, because according to a recent systematic review on biological markers for pulpal inflammation the authors concluded that the main current challenges in the clinical application of biomarkers lie in the identification of biomarkers or biomarker subsets that reliably correlate with pulpal inflammation, the improvement of sample collection, and the interference of the biomarkers with inflammation of other than pulpal origin [100].
Determining the endodontic diagnosis prior to any invasive endodontic, or even any dental, procedure is paramount. It is clear that it takes clinical skills, good understanding of clinical signs and symptoms, as well as recognition of the limitations of commonly used sensitivity tests to make a clinical diagnosis - an acquired skill that does take some time to develop and always is at risk of subjectivity or bias.
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