Pulpal diagnosis

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Pulpal diagnosis

  1. 1. Pulpal diagnosis ASGEIR SIGURDSSON Correct pulpal diagnosis is the key to all predictable endodontic treatment. It is paramount that prior to proceeding with a treatment that will affect the contents of the pulp chamber that a clinical diagnosis of the pulp and the periapical tissues is established. This diagnosis should be based on presenting symptoms, history of symptoms, diagnostic tests and clinical findings. If it is not possible to establish the diagnosis or one diagnosis is not dominant within a differential diagnosis, therapy should not be initiated until further evaluation has been performed. In this review, current knowledge on pulpal and periapical status as it pertains to diagnosis will be reviewed. Additionally, most common diagnostic tests will be presented and critically reviewed. In the past, there have been a variety of different pulpal diagnostic terms introduced in the literature (1, 2). Many have been very elaborate and most attempted to describe the histological status of the pulp. However, with the limitations of current technology the attempt to predict the histological status of the pulp is impossible without prior removal of the tissue to be evaluated. In more recent times, the trend has been to move away from these elaborate classifications and use a somewhat modified version of the classification suggested by Morse et al. in 1977 (3). Even though this classification refers to some degree to histological status of the pulp, it directs the clinician to a specific treatment because there is no crossover between classification categories in terms of treatment needs. Healthy pulp According to the classification a healthy pulp is vital, without inflammation. A healthy pulp will be asympto- matic, react to vitality tests such as heat, carbon dioxide (CO2) snow, ice and/or electric pulp tester (EPT). Once the pulp gets ‘older’ it forms increasing amount of secondary dentin in the pulp chamber such that its reaction to thermal test might be diminished, but even in those cases a healthy pulp should predictably react to EPT (4). With the limitations of the diagnostic tests presently available, it would be unrealistic to assume that our diagnosis of a healthy pulp is definitely correct. However, this diagnostic term describes the treatment of a tooth that needs pulp removal because of prosthodontic or restorative needs. Another example would be pulp therapy after a traumatic injury whether it is pulp capping or pulpotomy in an immature tooth or pulpectomy in a mature tooth when it is judged to be the treatment with the best prognosis of preventing apical periodontitis (5). Reversible pulpitis This diagnosis implies that the pulp is vital, but has some local area/s of inflamed tissue that will heal after conservative vital pulp therapy (Fig. 1). Symptoms can be very misleading in this diagnostic category, from none at all to very intense and sharp sensation associated with thermal stimuli. It is well established that there is a poor correlation between clinical symptomalogy and the pulpal histopathological state (1, 2, 6–9). The history of symptoms will most often reveal pain or sensation on stimulation only, such that the tooth will only bother the patient when the tooth is exposed to a stimulus that is hot and/or cold. According to the classification, reversible pulpitis should heal once the irritant is removed or, in case of an exposed dentin surface, the exposed dentin is adequately sealed. The mild trauma with subsequent inflammation can cause small regions of neurogenic inflammation and sufficient mechanical damage to 12 Endodontic Topics 2003, 5, 12–25 Printed in Denmark. All rights reserved Copyright r Blackwell Munksgaard ENDODONTIC TOPICS 2003
  2. 2. stimulate a nerve sprouting reaction (10) and thereby possibly cause exaggerated response to vitality tests, indicating more severe inflammation than actually is present. However, there is a much higher risk of diagnosing a pulp with mild symptoms as being reversible inflamed, when in actuality the pulp is irreversible inflamed (see below). Thus, mistakes in diagnosis of this pulpal category are common and understandable. Therefore, it is essential to recall and test all patients who have had treatment based on this diagnostic category in order to confirm that the progression of pulpal reaction has gone according to expectation, i.e. the pulp has healed. Phone consulta- tion is not enough in these cases, because ‘failure’ of diagnosis and treatment is conceivably pulp necrosis which will in most cases start asymptomatically. The lack of symptoms may be misinterpreted by the patient as resolution of the problem and a successful outcome. Irreversible pulpitis In case of irreversible pulpitis, the pulp is still vital but is severely inflamed so that healing is an unlikely outcome with conservative pulp therapy. Thus, ultimately, pulp necrosis and infection is the predicted outcome if vital pulp therapy is attempted. Apical periodontitis will be the final outcome. In order to avoid pulp necrosis, the pulp is aseptically removed and the entire space filled with a root canal filling material (Fig. 2). As with reversible pulpitis, symptoms can be very misleading. It has been well documented that in most cases a pulp that is irreversibly inflamed is asymptomatic. It has been reported that dental pulps can progress from vitality to necrosis without pain in 26–60% of all cases (11, 12). According to a recent study, neither gender nor tooth type appears to matter in case of asymptomatic pulpitis; however, the older the patient was (over 53 vs. under 33 years of age) the less likely there was any pain associated with the pulpitis (13). This phenomenon has been in the past termed as ‘painless pulpitis’ (14). Currently, it is not known how asymptomatic pulp death can happen; one suggestion is that at least in some cases, the progression of inflammation to pulp death is so rapid that there is no pain or conversely that the inflammation is so slow that the classical inflam- matory mediators that participate in the pain process never reach a critical level (13). A more likely explanation may be that there is effective modification by local as well as centrally mediated systems. It has been shown that there are several local regulatory factors and systems in the pulp. Several studies have recently indicated that endogenous opioid, adrenergic sympathetic and nitric oxide systems do exist in the pulp (15–17) and there is a good indication for example that somatostatin may inhibit pulpal pain activation under certain conditions (17–19). The effects of the central nervous system (CNS) should not be over- looked either. It is clear that CNS plasticity can both enhance and reduce pulpal pain (20–21); however, the detailed function and ability of the CNS to modulate pain is as of yet poorly understood. If the pulp is symptomatic it is most often very sensitive to thermal changes, and the pain sensation has the tendency to linger as a dull ache after the stimulus has been removed. This fact can be used with caution to predict if the pulp is likely to be irreversibly inflamed or Fig. 1. Moderate carious lesion results in a localized pulpitis. Since nothing in the history points to irreversible pulpitis, it is assumed that after vital pulp therapy this pulp inflammation will heal. Pulpal diagnosis 13
  3. 3. not. It has been established for some time that in a healthy pulp only very intense stimuli will activate the more centrally located C fibers (22, 23). 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 (23). In case of severe inflammation, it is clear that there are several inflammatory mediators that can cause increased sensitivity in the pulpal nociceptors. Initially, these effects will be primarily on the more peripheral A-delta fibers, but when the inflammation reaches deeper structures, the C fibers will be affected. This will cause their firing threshold to be lower and receptive field larger (24). 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 a description of the lingering sensation. The more C-fiber-mediated pain complaint (dull, throb- bing, poorly localized), the more severe the inflamma- tion might be and thus the more likely to be irreversible in nature. It has also been shown that the more severe the pain and the longer it has been symptomatic, the more likely it is irreversibly inflamed (12). Probably though the clearest sign of irreversible inflamed pulp is the history of spontaneous pain, which will ‘hit’ the patient without any thermal stimulation to the teeth, and even wake the patient from sound sleep (6). Necrotic pulp This diagnostic category implies partial (below the cemento-enamel junction) or total pulp space with no vital structures. The distinction between partial and total necrosis can be very important in cases of immature teeth. 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 stump. If the pulp is completely necrotic in a tooth with undeveloped root, it is now possible in some cases to disinfect the canal space and stimulate the root to continue formation (see (25, 26)). In case of a fully formed tooth, root canal therapy is always indicated for both partially and fully necrotic pulp. If the pulpal space is not already infected it will in most cases become so in time if left untreated. Prevention of formation of periapical lesion has been shown to have much more reliable outcome than a treatment on a tooth with a periapical lesion (27–29). The key question is when is a necrotic root canal space infected? It has been shown that all teeth with periapical lesions do have infected pulp space (30). Teeth that do not have periapical lesion may or may not be infected, but because it is well known that there has to be a significant loss of bone structure before it becomes radiographically apparent (31), using lack of radio- graphic signs may be unreliable. Therefore, it is recommended to treat all necrotic teeth as being infected. Disinfection of the canal space will lead to predictable and high success (32). In summary, we do vital pulp therapy in cases when the pulp is healthy or reversibly inflamed but endo- dontic therapy when it is irreversibly inflamed or necrotic. Periapical diagnosis The term apical periodontitis implies that there is inflammation in the periapical tissues. Like pulpal Fig. 2. Irreversible pulpitis due to a carious exposure. The most predictable treatment to prevent apical periodontitis is a puplectomy. Sigurdsson 14
  4. 4. inflammation, the periapical inflammation can be symptom free and then may only be diagnosed on a periapical radiograph; however, it is very important to appreciate that a periapical lesion is most likely caused by an infection in the root canal system, irrespective of the patient having history or being symptomatic (30). As always, if the patient is symptomatic then it is very important to be able to diagnose the source, prior to any treatment. Treatment of such is always to remove the irritant that causes the symptoms or lesion. This could be accomplished by simple occlusal adjustment in case of occlusal trauma, but more likely the cause is bacteria in the root canal system and the only predictable treatment is to effectively disinfect the canal space followed by filling of the canal and coronal cavity. Antibiotics cannot penetrate into a root canal space with necrotic tissue since the blood supply that would transport the antibiotic is not viable. Therefore, antibiotics will not accomplish disinfection and any relief in symptoms will be temporary (33). Acute apical periodontitis This diagnostic category suggests that there is an acute inflammation in the periodontal ligament space that causes the involved tooth to be tender to touch/ percussion and/or palpation. By definition, there are minimal or no radiographic changes associated with this diagnostic term. 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, but in case of bacteria the pulp is either obviously irreversibly inflamed or more likely already necrotic. In case of occlusal trauma, evaluation of the dentition will point to a new filling in the opposite arch or in the tooth involved or the patient will reveal that he/she was chewing and happen to accidentally bite into something unexpectedly hard. If the trauma is recent then there will be no signs on a radiograph, but if the traumatic occlusion has been there for a long time, the periodontal ligament space could be slightly widened all around the tooth. When the acute apical periodontitis (Fig. 3) is caused by a severely inflamed or necrotic pulp the signs of pain to chewing, percussion (both in a vertical and a lateral direction) and periapical palpation will precede radio- graphic signs of apical periodontitis. Vitality tests should confirm the diagnosis of a severely inflamed or (more likely) a necrotic pulp. Chronic apical periodontitis This diagnostic category implies that the patient is asymptomatic with the only sign a periapical lesion radiographically (Fig. 4). Frequently, the patient will deny any previous history of pain in the tooth. Vitality test and test cavity preparation will confirm a necrotic pulp. Occasionally, an acute flare up occurs in a chronic lesion that will cause swelling and/or pain in the area. This is commonly termed Phoenix abscess or acute exacerbation of a chronic apical periodontitis (Fig. 5). Apical periodontitis with abscess When the pulp space infection and the periapical inflammation cause purulent breakdown there is a possibility of accumulation of pus in the periodontium or subperiosteal. This, as with the Phoenix abscess, commonly occurs in an area of chronic apical periodontitis (Fig. 5). As stated before, treatment should be primarily aimed at eliminating the source of the abscess, the pulpal space, and antibiotics only used as supplemental treatment if the patient is showing systemic effects of the infection. Fig. 3. Acute apical periodontitis: May result from traumatic occlusion, AP with acute pulpitis or an acute exacerbation of CAP. Pulpal diagnosis 15
  5. 5. Apical periodontitis with sinus tract Similar to the apical periodontitis with abscess, the infection in the pulpal space and subsequent reaction in periapical area is causing purulent breakdown but in this case rather then collect subperiosteally and thereby cause pain and swelling, the exudate has found its way to a surface, most commonly on the gingiva or mucosa, but sometimes on to the surface of the skin. Because of the lack of pressure buildup there is usually very minimal pain associated with this diagnostic category and after the tract has found its way to the surface swelling will not occur. Once the source of the infection has been eliminated, by disinfection the pulpal space of the involved tooth, the sinus tract should heal within a few days without any specific need for treatment (Fig. 6). Diagnostic procedures It has been stated by Dr Okeson (34) that dentists are disadvantaged by their dental training because it focuses primarily on diagnosing a problem by visual means. However, when diagnosing the origins of pain, most of the diagnosis should be done by what we hear and not what we see. In fact, visual clues might throw us off track resulting in incorrect diagnosis. Therefore, it is essential to carefully listen to the patient and system- atically review his/her present symptoms as well as the pain history prior to coming to any conclusions about the cause. It is often stated that once a comprehensive history has been taken the practitioner should in most cases know the diagnosis of the problem. The clinical examination and diagnostic tests should then be done to ascertain which tooth fits this diagnostic category. Pain complaint As stated previously, pulpitis is as a rule painless (4, 8, 11–13); therefore, lack of pain is not a good indicator of severity of pulpal/periapical inflammation. However pain, when present, is obviously an indicator of disease. If the pain is short and directly associated with a stimulus, it is likely to be mediated by the A-delta Fig. 5. Apical periodontitis with abscess. Fig. 4. Chronic apical periodontitis. Sigurdsson 16
  6. 6. neurofibers (only) that are normally active throughout the dentin–pulp complex. Thus, complaints of sharp provoked pain indicate mild and reversible inflamma- tion and that vital pulp therapy would be sufficient to reverse the pulpal inflammation. Examples would be the removal of a shallow carious lesion, replacing a leaky restoration or covering exposed root surfaces. There is building evidence that the classical inflam- matory mediators, capable of causing pain, are released in the pulp in direct proportion to the insult. Serotonin (5-TH) is for example able to sensitize intra-dental A- fibers resulting in increased responsiveness (35) and bradykinin have shown to be in significant higher concentration in irreversibly inflamed human pulps (36). In addition, recently in a ferret model where lipopolysaccharide (LPS) was used to induce inflam- matory changes in deep class V preparations in canine teeth, there was strong correlation between change in the animal’s behavior and C-fos expression in the area of subnucleous caudalis and interpolaris. The findings were consistent with mild-to-moderate pain felt by the animals for some time after the exposure to the LSP (37). 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 found in significantly higher concentrations in symptomatic pulp compared with healthy pulps (38–40). The history of the pain has been found to be as important as the presenting symptoms. As stated before there is a difference between the pain sensations conveyed by the two main pain fibers in the pulp. The rapid pain sensation associated with the A-delta fibers is part of the normal function of the pulp, the deeper seated slower and unmyelinated C-fiber are for most part unresponsive to all but very intense stimulus in normal, uninflamed pulp (16, 40). When asking about the history of the pain it can be very revealing to note that the pain initially started as primarily temperature sensitivity, with sharp defined pain episodes, but then changed to more dull throbbing ache that has become more severe in nature. This is important for many reasons, first it indicates a shift to pain consistent with activation of the C-fibers indicating increased inflam- mation and second it has been shown that self-reports of intensity and quality of dental pain is a valid predictor of whether or not the pulpal inflammation is reversible or not (41, 42). It is extremely important to remember that the primary source of the pain does not have to be in the location of chief complaint of the patient. Therefore, all possible sources need to be investigated and ruled out because in order for a treatment to be effective it must be directed towards the source of the pain and not the site of the pain. Dr Glick (43) in 1962 investigated the referral pattern from teeth with toothache. He noticed certain trends that still for most part hold true. He concluded that toothache never crossed the midline, the pain was frequently referred from one tooth to another and the referred pain was not only felt in the deep but also to the superficial or cutaneous tissues. There were also certain patterns observed, the upper teeth tended to refer the pain up to the upper face and temporalis Fig. 6. Histological, clinical and radiographic appearance of a apical periodontitis with sinus tract. Pulpal diagnosis 17
  7. 7. muscle area, where the lower teeth tended to be referred to the body of the mandible and back to the ear. However, not only the pulp can refer pain to a remote area. It has been shown that certain muscle groups can refer pain from myalgia to the dentition (44) confusing the patient into thinking that he/she is suffering from toothache when they actually are suffering from myofacial pain (muscle ache). Therefore, clearly it is very important to palpate facial structures where pain is felt by the patient. If pain is felt in a tooth that is made worse by palpation of the temporalis muscle it is much more likely that the patient is suffering from myalgia than toothache (see Table 1). Diagnostic tests Unfortunately, many clinicians rely solely on diagnostic tests to make a definitive diagnosis. It is very important to remember that most commonly used test systems do not actually assess the vitality (blood circulation) of the pulp and most do not give much if any indication about presence or severity of inflammation in the pulp. So why are these tests used? The main reasons for doing pulpal test are to reproduce the symptoms, to localize the symptoms and to access the severity of the symptoms. With every test it has to be remembered that the responses are going to be subjective and some patients will have the tendency to exaggerate while others will understate the pain felt (45, 46). Electric pulp tester (EPT) The EPT uses electric current to stimulate the sensory nerves of the dental pulp (47–49), specifically, the fast- conducting myelinated fibers (A-Delta) at the pulp dentin junction. The unmyelinated (C) fibers of the pulp may (50) or may not respond (51). Measurement of electric voltage in teeth may be inconsistent due to thickness of enamel and dentin, dryness and electrical resistance of enamel (52), infractions, restorations, pits, fissures and caries. In addition, the movement of the electric current to the pulp may be impossible if the tooth is covered with a crown or large restoration. Bipolar and monopolar are the two stimulating modes available. The bipolar mode is presumably more accurate because the current is confined the coronal pulp (53, 54). However, most EPTs are still monopolar (51). A positive response to the electric pulp test is an indication of vital pulp tissue in the coronal aspect of the root canal space. However, it is not an indication of the reversibility of the inflammation within the pulp. No correlation has been found between the pain thresholds and the condition of the pulp (6, 55, 56). A negative response was found by Seltzer et al. (6) to indicate a total necrosis in 72% of cases and localized necrosis in 25.7 % of cases. Thus, if it is accepted that even localized necrosis is an indication for the need of pulpectomy in a mature tooth, in 97.7% of cases a negative response to the electric pulp test would indicate that clinically a pulpectomy or debridement of a necrotic pulp should be performed. The response of the young pulps (teeth with open apices) to the EPT is unreliable (4, 57) since the complete development of the plexus of Raschkow does not occur until the final stages of root development (58). Thus, pulpal nerves do not end amongst the odontoblasts, predentin or dentin, as in fully developed teeth in occlusion (59). In young teeth, sensitivity testing with cold is a more effective method (57). Where the electric pulp tested is placed on the tooth crown is critical. It has been shown that the incisal edge on anterior teeth and the mesio-buccal incisal edge on lower teeth is the optimal placement site for the EPT to determine the lowest response threshold (60). This is true of the cold tests as well (Fig. 7). Thermal tests These tests are thought to work by hydrodynamic forces in the dentin-initiating generator potentials in the nerve endings by displacing surface membranes. By this theory, fluid movement in the tubules (due to the thermal stimulation) is responsible for activation of sensory receptor units in the pulp (61). Cold test The most effective cold tests are those with frozen sticks of carbon dioxide ( À 781C; CO2 snow) or a cotton pellet sprayed with difluordichlormethane (DDM) ( À 501C) (57). Older techniques of using refrigerator ice or ethyl chloride ( À 41C) are less reliable (57) and should be replaced by the newer techniques. A major advantage of these newer thermal tests may be their ability to effectively move cold Sigurdsson 18
  8. 8. through crowns and large restorations. Concern about the potential for extreme cold to cause cracks in the dentin or irreversibly damage the pulp have been shown to be unfounded (62, 63). Abnormal but positive responses are equally distrib- uted among the pulps of teeth in all diagnostic categories (6, 8). Therefore, a positive response is an indication that the pulp is vital but does not indicate if inflammation is reversible. The same authors showed that a negative response is highly indicative of necrosis and this test result can be used to predict the need for root canal therapy. The advantages of frozen CO2 over other sensitivity tests is that it can be used with metallic restorations, orthodontic bands, metallic splints, temporary and permanent crowns, and is also the most effective vitality test for immature teeth (4, 57, 64). Heat test The heat test is a difficult test to perform since too much heat can in itself cause irreversible harm to the pulp. The reaction to heat has been described as biphasic. Initially, there is a sharp localized pain reaction due to stimulation of A-delta fibers (65), and with continued stimulation, a dull radiating pain follows (66) due to activation of the C fibers (22, 40). No correlation has been found between an abnormal Table 1. Formulation of a pulpal diagnosis Vital pulp Symptom, test, supporting information Necrotic pulp Irreversible inflammation Reversible inflammation 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 Deep throbbing lingering pain Present Absent Pain to hot relieved by cold Present Absent Factors related to treatment plan Age, periodontal disease, previous pulpal insults Questionable Questionable Fig. 7. Correct placement of pulp-testing devices. Left: CO2 ice stick placed on the incisal edge. Right: the electric pulp tester placed on the mesio-buccal cusp of the lower molar. Pulpal diagnosis 19
  9. 9. response to heat and a histologic diagnosis including liquefaction necrosis. A negative response is indicative of necrosis in the pulp (6, 8). Thus, as with the other sensitivity tests, this test only differentiates a vital from a non-vital pulp. Degrees of inflammation or the reversibility of an inflamed pulp cannot be ascertained from this test. Mechanical tests Percussion and palpation These are not true vitality tests but rather are indicative of periodontal ligament inflammation (67). Pain is elicited on percussion more frequently in all pulp conditions where partial or total necrosis is present (49) and as such is an indirect method of assessing the status of the pulp. Also, the presence of percussion and/or palpation sensitivity in conjunction with a vital pulp is indicative of a pulp that is severely and thus (probably) irreversibly inflamed. Percussion (Fig. 8). This test is performed with digital pressure or more commonly with the handle of a mouth mirror. The aim of this test is to determine the presence/absence of inflammation in the apical period- ontium. A positive percussion test indicates inflamma- tion of the periradicular tissues. However, a negative percussion test does not rule out the presence of such inflammation (6). As already mentioned, a positive response to percussion in a tooth which tests vital to sensitivity testing is an indication of severe and probably an irreversible inflammation in that pulp (49). Care must be taken, when interpreting the results of the percussion tests, to rule out a positive response due to marginal periodontitis, i.e. due to periodontal disease. This is particularly difficult in those cases where the pulp vitality tests indicate a vital pulp. The results of other diagnostic tests are used to differentiate period- ontitis of periodontal or endodontic origin. Palpation (Fig. 9). This test is used to detect inflammation in the mucoperiosteum around the root of the tooth. It may be possible to detect tenderness, fluctuation, hardness or crepitus before extensive swelling is present. Diagnostic information As has been discussed for 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 (6). Radiographic examination The radiographic examination is one of many tests and the findings should always be evaluated together with those of the other tests and the clinical examination. Initial sensitivity tests can suggest which type of radio- graph will be most advantageous. If a vital tooth is evaluated, a bitewing radiograph would be advantageous to detect caries or other causes of pulpal inflammation. If periapical disease is suspected by the previous tests, a periapical radiograph is indicated. 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 biteblock so that the angulation of follow-up radio- graphs will be as similar as possible (Fig. 10). The radiograph cannot detect pulpal inflammation directly. However, caries or defective restorations seen on the radiograph will suggest pulp inflammation (68). Condensing apical periodontitis is a near-pathFig. 8. Percussion test. Fig. 9. Palpation test. Sigurdsson 20
  10. 10. gnomonic sign of pulpitis. 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. Additional tests Test drilling This test has been used when full coverage restorations are present making other forms of testing impossible. The use of CO2 frozen sticks has diminished the need for test drilling. Some practitioners use the test drill method as the ‘final diagnosis’ of pulp necrosis. As with the other sensitivity tests, a positive response to this test indicates a vital pulp but gives no information about the pathologic involvement of the pulp. Experimental testing methods Attempts have been made to demonstrate pulpal circulation rather than the neural integrity of the pulp. Tests include: Ultrasonic pulse echo Barber et al. (69) used an ultrasonic pulse echo instrument to detect the dentino–enamel and denti- no–pulpal interfaces using transmission and reflection of sound from the dental hard tissues. Crown surface temperature Fanibunda (70–72) has performed extensive research in the field of crown surface temperature. This pulp vitality technique is based on the hypothesis that vital teeth are warmer and will rewarm quicker after cooling than non-vital teeth. Fanibunda’s experiments con- cluded that time–temperature curves comparing the warming of vital vs. non-vital teeth were diagnostically informative. Additionally, it has been attempted to use color change of cholisteric liquid crystals as a diagnostic tool to measure crown temperature change (73) with some success. And a more recent study using an infrared thermographic camera showed crown temperature patterns of non-vital teeth to be slower to re-warm than those of vital teeth (74). 133Xenon radioisotope Radioactive materials for measurement of pulpal blood circulation were previously used in the radiolabelled microsphere injection method (75, 76). A method utilizing a radiation probe with 133 xenon radioisotope to differentiate between vital and pulpless teeth on the basis of blood supply has been found effective (77). However, the use of radioactive materials is expensive, restricted on humans, and requires special licencing requirements. To this point the most promising of these experimental methods are those using the measurement of light passing through or deflected from the blood in the pulp. Laser Doppler flowmetry This technique was developed to assess blood flow in microvasculature systems, e.g. retina, mesentery, renal cortex and skin (78) (Fig. 11). It has recently been used in intact teeth in animals (79, 80) and in man (79, 81). It utilizes a light beam (Helium Neon 632.8 nm), which is scattered by moving red blood cells (82). Newer machines have varied the wavelength between 600 and 700 nm depending on the light absorption properties of tissue which is tested. This light beam undergoes a frequency shift, according to the principle of Doppler. The back-scattered light is picked up by photodetectors, and produces a signal which is proportional to the red cell flux (number of cells  average velocity). This can be used as a measure of pulpal blood flow, expressed as a percentage of full- scale deflection at a given gain. The technique appears objective, non-invasive and accurate. A growing number of reports indicate that it is a method which can easily be adapted to the testing of Fig. 10. Bite stent used for every radiography to ensure that positioning is consistent. Pulpal diagnosis 21
  11. 11. a tooth and which is promising as a pulp vitality tester. It is especially effective in young traumatized teeth with large pulps that do not respond well to other forms of sensitivity testing (79, 81, 83). Pulse oximetry This technique has been used to detect vascular integrity in the tooth (84). A modified probe was used and two wavelengths used to provide a ratio of the absorption of wavelengths for oxygenated and deox- ygenated blood. This gives the percentage of oxygena- tion of blood (84). This method has the potential of not only assessing the presence of a vital pulp but also of assessing pathological processes (84). Dual wavelength spectrophotometry Oximetry by spectrophotometry uses a dual wave- length light source (760 and 850 nm) to determine the oxygen saturation level of the pulpal blood supply (85– 87). Preliminary tests on teeth were promising since the blood oxygenation and volume could be detected (88) (Fig. 12). Thus, the instrument might be useful not only in determining pulp necrosis, but also the inflammatory status of the pulp. The instrument shows promise as a pulp tester as it is non-invasive, objective, small and portable. Clinical findings The findings of the clinical examination in addition to an extensive knowledge of the pulpal reaction to external irritants is important for arriving at a correct diagnosis. A thorough clinical examination is critical since pulpitis is usually painless and also because of the lack of correlation between symptomatology and diagnostic tests and the histopathologic state of the pulp. Clinical findings of significance Carious pulpal exposure Scientific evidence indicates that when the pulp is exposed to caries, bacteria have penetrated the pulp directly with abscess formation (68). Long-term vital treatment of a cariously exposed pulp has reported success rate from just over 20% to below 50% (89, 90) so that the pulp should be considered irreversibly inflamed. Only in cases where root development is incomplete should an attempt be made to estimate the level at which the pulp is uninflamed and apexogenesis attempted. Age Through the years, the pulpal space will be reduced and thereby the pulp tissue becomes less. At the same time, the cellular components decrease with increased thick- ness of the collagen fibers and number of nerves and blood vessels are lost (6, 91). It is not clear how much effect all these changes do have on the defense capability of the pulp. It could be speculated that the pulp has less ability to reverse an inflammatory response to an insult; however, there is neither any research that has confirmed that nor is there any indication that older patients are more likely to need root canal therapy. Therefore, increased age on its own does not seem to be very much of clinical significance in the decision of need for endodontic care, only it needs to be remembered Fig. 11. Laser Doppler flowmeter. Left set up and computer read out of pulp status. Right, probe showing the small dimensions suitable for accurate placement on the tooth. Fig. 12. Dual wavelength spectrophotometer. Machine attached to recorder (left) and light source and detector (right). Sigurdsson 22
  12. 12. that responses to tests might be greatly diminished with increased age. Periodontal disease Severe periodontal disease can prematurely age the pulp (6, 60, 92). However, again the ‘aging’ of the pulp will not necessary cause the pulp to be less able to defend it self and it has been demonstrated that there is no difference in the pulp status of teeth with or without periodontal disease (93). Previous pulpal insults It is clear that any pulpal insult will affect the pulp in someway and the more severe it was, the more reaction will be seen (6). If a tooth has history of deep restorations, possible incomplete caries removal or carious pulp capping the more likely is that the pulp has been damaged beyond repair and therefore a root canal therapy would be needed. Again if tests are inconclusive especially when there is no reaction to thermal tests but some reaction to EPT then a ‘test cavity preparation’ is advisable. Then the access is cut into the tooth without anesthesia. It is important to explain to the patient that there is a good likelihood that the pulp is necrotic and therefore no pain is expected, but he/she is instructed to give a signal if and when any sensation is felt. If the patient feels sensation as soon as the dentin is exposed, then it is likely that the periodontitis is of different origin that needs then to be further investigated. References 1. Baume LJ. Diagnosis of diseases of the pulp. Oral Surg Oral Med Oral Pathol 1970: 29: 102–116. 2. Seltzer S. Classification of pulpal pathosis. Oral Surg Oral Med Oral Pathol 1972: 34: 269–280. 3. Morse DR, Seltzer S, Sinai I, Biron G. Endodontic classification. J Am Dent Assoc 1977: 94: 685–689. 4. Fulling HJ, Andreasen JO. Influence of maturation status and tooth type of permanent teeth upon electrometric and thermal pulp testing procedures. Scand J Dent Res 1976: 84: 291–296. 5. Heide S, Mjo¨r IA. Pulp reaction to experimental exposures in young permanent monkey teeth. Int Endod J 1983: 16: 11–19. 6. Seltzer S, Bender IB, Zionitz M. The dynamics of pulp inflammation: correlation between diagnostic data and actual histologic finding in the pulp. Oral Surg Oral Med Oral Pathol 1963: 16: 846–871. 7. Lundy T, Stanley HR. Correlation of pulpal histopathol- ogy and clinical symptoms in human teeth subjected to experimental irritation. Oral Surg Oral Med Oral Pathol 1969: 27: 187–201. 8. Dummer PMH, Hicks R, Huws D. Clinical signs and symptoms in pulp disease. Int Endod J 1980: 13: 27–35. 9. Garfunkel A, Sela J, Almansky M. Dental pulp pathosis: Clinicopathologic correlation based on 109 cases. Oral Surg Oral Med Oral Pathol 1987: 35: 110–117. 10. Byers MR, Narhi MV, Mecifi KB. Acute and chronic reactions of dental sensory nerve fibers to hydrodynamic stimulation or injury. Anat Rec 1988: 221: 872–883. 11. Barbakow F, Cleaton-Jones P, Friedman D. Endodontic treatment of teeth with periapical radiolucent areas in a general practice. Oral Surg Oral Med Oral Pathol 1981: 51: 552–559. 12. Bender IB. Reversible and irreversible painful pulpitides: diagnosis and treatment. Aust Endod J 2000: 26: 10–14. 13. Michaelson PL, Holland GR. Is pulpitis painful? Int Endod J 2002: 35: 829–832. 14. Hasler JE, Mitchell DF. Painless pulpitis. J Am Dent Assoc 1970: 81: 671–677. 15. Olgart LM. Neural control of pulpal blood flow. Crit Rev Oral Biol Med 1996: 7: 159–171. 16. Byers MR, Narhi MVO. Dental injury models: Experi- mental tools for understanding neuroinflammatory interactions and polymodal nocicpetor functions. Crit Rev Oral Biol Med 1999: 10: 4–39. 17. Hirvonen T, Hippi P, Narhi M. The effect of an opioid antagonist and a somatostatin antagonist on the nerve function in normal and inflamed pulp. J Dent Res 1998: 77(abstract): 1329. 18. Taddese A, Nah S-Y, McClesky EW. Selective opioid inhibition of small nociceptive neurons. Science 1995: 270: 1366–1369. 19. Casasco A et al. Peptidergic nerves in human dental pulp: an immunocytochemical study. Histochemistry 1990: 95: 115–121. 20. Dubner R, Ruda MA. Activity-dependent neuronal plasticity following tissue injury and inflammation. Trends Neurosci 1992: 15: 96–103. 21. Sigurdsson A, Maixner W. Effects of experimental and clinical noxious counter irritants on pain perception. Pain 1994: 57: 265–275. 22. Narhi MVO, Hirvonen T, Hakumaki MOK. Activa- tion of intradental nerves in the dog to some stimuli applied to the dentin. Arch Oral Biol 1982: 27: 1053– 1058. 23. Jyvasjarvi E, Kniffki DK. Cold stimulation of teeth: a comparison between the responses of cat intradental A – and C – fibers and human sensations. J Physiol 1987: 391: 193–207. 24. Narhi MVO, Yamamoto H, Ngassapa D, Hirvonen T. Function of interadental nociceptors in normal an inflamed teeth. In: Shjimono M, Maeda T, Suda H, Takahashi K, eds. Dentin/pulp Complex. Tokyo: Quin- tessence Publ., 1996, 136–140. 25. Hoshino et al. In-vitro antibacterial susceptibility of bacteria taken from infected root dentine to a mixture of Pulpal diagnosis 23
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