Intradental Nerve Activity Research Articles

Pretty painful: Why does tooth bleaching hurt?

Vital bleaching procedures are a popular means of improving the appearance of discolored teeth. There is a wide array of whitening products for home and dental office use; all involves placing peroxide containing gels or solutions in contact with the teeth. In order to whiten teeth peroxide has to be able to penetrate tooth structure and oxidize colored compounds in the dentin. Unfortunately beauty comes with a price; many patients undergoing peroxide based whitening procedures complain of bleaching sensitivity (BS) arising in the treated teeth. In BS, pain can occur in healthy intact teeth without any provoking stimulus. Currently the mechanism of nociceptors activation in BS is unknown. A more common form of dental pain-dentin sensitivity (DS) occurs when stimuli such as cold or tactile stimulation contact areas of exposed dentin in otherwise healthy teeth. In DS, stimulation of the dentin results in fluid shifts in the dentinal tubules, these fluid shifts activate mechanosensitive nerve endings in the deep dentin and pulp. Since many aspects of BS and DS symptoms differ, it is hypothesized that that the mechanism of pain generation differs for these two conditions. Recently the functional properties of a chemosensitive ion channel-TRPA1 have been described. This channel is activated by a variety of oxidizer compounds including hydrogen peroxide. Pulpal sensory afferents express TRPA1. It is hypothesized that direct activation of intradental nerve activity via TRPA1 is the mechanism of BS pain. If this theory were correct, tooth sensitivity treatments that reduce the excitability of the intradental nerves such as potassium salts, would be the treatment of choice for BS.

Sensory experiences in relation to pulpal nerve activation of human teeth in different age groups

There are no data on the correlation of intradental nerve activity and sensation from intact human teeth. We used microneurography to examine this relation and to determine whether it changes with age. Fifteen informed and healthy male volunteers were divided into three age groups: group A (18.6±1.82 years, mean±standard deviation (S.D.)), group B (38.4±2.70 years) and group C (64.0±4.06 years). Ratings of perceived pain intensity to thermal stimulation were obtained using a visual analogue scale (VAS). In addition, each subject chose one or two words from the short-form McGill Pain Questionnaire to describe perceived pain. A total of 90 single pulpal axons were studied with microneurography at the same time as the sensory experiences were recorded. Mean conduction velocities and variance estimates correlated closely with age. With advancing age, first, the percentage of teeth from which the subjects did not perceive any sensations to thermal stimulation increased, second, units responding to heat stimulus decreased, and third, latencies of sensation induced by thermal stimulation increased. In addition, a burst of afterdischarges following thermal stimulation and neural discharges evoked by thermal stimulation produced no sensation only in some of group B and C units. In contrast, no significant difference was found among three groups in VAS scores and words to describe the perceived pain to thermal stimulation. These results suggest that pulpal afferents were activated by the same mechanism(s); the hydrodynamic mechanism works immediately after thermal stimulation and is possibly followed by direct activation of some nerves, especially slow conducting fibres. In older tooth pulps, the decrease in the number of fast conducting afferents and mineral apposition of dentinal tubules impaired the nerve activation, especially by heat, as per the hydrodynamic mechanism. Spike discharges without sensation in older individuals were suggested to be due to insufficient spatial and temporal summation and may be involved with abnormal uncomfortable sensations.

Effect of HeNe and pulsed Nd:YAG laser irradiation on intradental nerve responses to mechanical stimulation of dentine.

Our study aimed to determine how lasing affected intradental nerve responses to dentine stimulation. Study Design/Materials and Methods Intradental nerve activity was recorded from canine teeth of anaesthetised ferrets. Dentine exposed at the tip of the tooth was stimulated with a glass probe. After determining baseline responses to mechanical stimulation, dentine was lased using a pulsed Nd:YAG laser at 60-150mJ/pulse and 10-30 pulses/sec (total power = 0.3-3.0 W). The HeNe aiming beam alone and Nd:YAG laser at 0.3 W (+ HeNe) had no effect on intradental nerve responses to dentine stimulation. Lasing at 0.6-1. 5 W could either enhance or suppress intradental nerve responses. Lasing at more than or equal to 2.0 W or repeated lasing at lower intensities depressed intradental nerve responses. Lasing often induced intradental nerve firing. HeNe lasing had no effect on intradental nerve excitability. The Nd:YAG laser could depress intradental nerve responses to dentine stimulation.

Increased blood flow and nerve firing in the cat canine tooth in response to stimulation of the second premolar pulp

Mustard oil or mechanical stimulation was applied to maxillary second premolar tooth pulps and pulpal blood flow and/or intradental nerve activity in the ipsilateral canine tooth were recorded in the cat. Mustard oil application to the second premolar pulp significantly increased blood flow in the canine tooth pulp to 162.0±65.8% ( n=16) of the prestimulation flow compared to control data obtained with application of mineral oil (107.0±5.1%, n=6) (Mann–Whitney U-test, p=0.0009). Sectioning of the infraorbital nerve and its branches on the experimental side ( n=4) did not affect this increase in pulpal blood flow. The paraperiosteal injection of 2% lidocaine (1.0 ml) without vasoconstrictor significantly inhibited the increase in canine pulpal blood flow induced by mustard oil application to the second premolar pulp (109.8±6.8% of the prestimulation level, n=7) (Mann–Whitney U-test, p=0.0013). Sporadic firing or sometimes bursts of action potentials in the canine pulp nerves were recorded during and/or after the mustard oil application to the second premolar pulp in three of 16 cases. Four single pulp nerve units firing in synchrony with the mechanical stimulation of the second premolar pulp were recorded in two of eight canines, which substantiated the existence of branched afferents innervating both teeth. These findings suggest that stimulation of the second premolar pulp may induce axon reflex-related vasodilation and intradental nerve firing in the canine pulp via branched afferent fibres innervating both the second premolar and canine teeth.

Pathophysiology of TMD and other related disorders

The tooth pulp has many attractive features for the study of peripheral pain mechanisms because of its rich innervation, its unique distribution of nerve fibers and its general disposition to give rise to pain upon stimulation. An experimental model has been developed for simultaneous recordings of intradental multi-unit A-delta nerve activity and the subjective intensity and quality of pain evoked by tooth pulp stimulation in conscious, alert humans. The only teeth to be considered for this kind of investigations are those having such a periodontal condition that they have to be extracted. The nerve activity was recorded from two electrodes placed in the dentin on the labial tooth surface, one at the level of the most incisal part of the pulp, and the other as far apically as possible. Brief cold stimulation was produced by using evaporating ethyl chloride administered between the recording electrodes. The magnitude of perceived pain was estimated by means of an intermodal matching technique (finger span) in combination with verbal descriptors. Of three response criteria selected — average response amplitude, peak amplitude and area under the response curve (integral)—for describing the relationship between intradental nerve activity and sharp, shooting pain, the integral yielded the highest mean correlation coefficient.

Effect of interstimulus interval on perceived sensation and intradental nerve activity during thermal tooth stimulation in man

The effect of interstimulus interval on nerve responses and subjective sensory ratings evoked by thermal stimulation of the teeth were studied in man. A total of 30 unitary discharges during heat stimulation of the lower incisor teeth were recorded from the inferior alveolar nerves using microneurographic technique. Fifteen of them had threshold sensory ratings above 3 (pain related-units) and 15 had ratings of less than 2 (non-pain-related units). Repetitive heat stimulation was applied to the teeth with interstimulus intervals of 180 s (ISI 180) and 30 s (ISI 30). Repetitive (ISI 180 and ISI 30) non-painful heat stimulation of the teeth did not alter either the intensity ratings or unitary discharge activities of non-pain-related units (P > 0.05). Repetitive painful heat stimulation of the teeth with ISI 180 did not alter the intensity ratings of pain-related units (P > 0.05), whereas that with ISI 30 significantly reduced the intensity ratings of pain-related units during a second session of heat trials (P > 0.05). On the other hand, repetitive heat stimulation of the teeth with ISI 180 caused a slight reduction in the firing frequency of pain-related units (P > 0.05). Repetitive painful heat stimulation with ISI 30 significantly reduced the firing frequency of pain-related units (P < 0.05).

Effects of capsaicin on KCl-induced blood flow and sensory nerve activity changes in the tooth pulp

Potassium ion-containing solutions have been shown to initially excite then depress intradental nerve activity (INA) when applied into deep dentinal cavities. The INA reflects activity originating in intradental A fibers. Application of KCl to deep dentinal cavities also induces an increase in pulpal blood flow (PBF). Capsaicin is known to exert a highly selective desensitizing effect on polymodal C-fiber nerve endings. These C fibers are generally believed to release vasoactive substances in response to stimulation. In order to determine if KCl exerts its vascular effect via activation of capsaicin-sensitive nerve fibers, we examined blood flow and sensory nerve responses to KCl obtained before and after capsaicin desensitization. The A-fiber nerve activity was determined by using INA recording technique. Blood flow was measured simultaneously from the same tooth using laser Doppler flowmetry. Local application of 0.25 M KCl to a deep dentinal cavity induced a brief spike burst and an increase in PBF of 76.0 ± 14.6% ( n = 8). Repeated applications of 0.25 M KCl caused a consistent increase in the peak PBF amplitude ( n = 8). Local application of 100 μM capsaicin to a deep dentinal cavity caused an increase in PBF of 116.8 ± 26.3% ( n = 8) lasting 12–18 min, but capsaicin application did not appear to evoke any INA response. The amplitude of PBF in response to capsaicin application declined during repeated applications. Following repeated applications of capsaicin the PBF response to KCl was significantly reduced (9.9 ± 4.3%, n = 8). Capsaicin treatment, however, had no effect on the vasodilatory response to papaverine, a known smooth-muscle relaxant, which was used as a control. The brief excitation of KCl on the INA after repeated applications of capsaicin did not seem to be affected by comparing the oscillographic spike activity. These results suggest that the inhibition of KCl-induced vasodilation by capsaicin may be caused by desensitization of capsaicin-sensitive nerve fibers and that local application of KCl into a deep dentinal cavity can stimulate both A fibers and capsaicin-sensitive nerve fibers.

Sensitizing effects of leukotriene B 4 on intradental primary afferents

Previous studies have established that leukotriene B 4 (LTB 4) sensitizes cutaneous nociceptors. In this study the effects of LTB 4 on spontaneous and stimulus-evoked nerve activity from primary afferents innervating the dentin of canines in adult cats were examined. LTB 4 treatment (25 μg/ml) significantly enhanced stimulusevoked intradental nerve activity (INA) for at least 20 min after the removal of the compound from the recording preparation. Teeth treated with LTB 4 demonstrated enhanced spontaneous nerve activity following the removal of hypertonic saline used to evoked INA. These findings provide additional evidence that LTB 4 is able to sensitize nociceptors and may be a long-lasting hyperalgesic factor which may contribute to pain of pulpal origin.

Comparisons of the sensation perceived and intradental nerve activity following temperature changes in human teeth

The relationship between the intradental nerve responses and subjective sensory ratings evoked by thermal stimulation of the teeth was studied in man. Recordings were taken from a total of 12 thermally sensitive units from the inferior dental nerve following thermal tooth stimulation, of which seven responded to both heating and cooling, two were exclusively cold-sensitive and three exclusively heat-sensitive. The early and late sensory responses following both cold and heat stimulation of the tooth were observed. The late sensory responses were more unstable than the early sensory responses. The mean threshold of the early sensory responses to tooth cooling was 13.6 +/- 1.9 degrees C (n = 9) and that to heat stimulation was 48.4 +/- 4.8 degrees C (n = 10). The firing frequency of the heat-sensitive, but not the cold-sensitive, units increased linearly in proportion to the increase in magnitude of the early sensory ratings.

Decreasing intradental nerve activity in the cat with potassium and divalent cations

Nerve activity was recorded from deep dentinal cavities in the canine teeth to assess the possible influence of potassium and divalent cations in decreasing this activity in hypersensitive teeth. The decreased activity after the topical application of 0.756 mol/l KCl to the cavity was primarily due to the cation. KCl elicited a biphasic response from intradental nerves, an initial transient excitatory response followed by a prolonged inhibitory period. During the inhibitory period 3mol/l NaCl, an effective excitatory stimulus, failed to evoke intradental nerve activity. However, with time the response to 3 mol/l NaCl eventually recovered to its previous control level. Close, intra-arterial injection of KCl showed the same biphasic response and time-course of intradental nerve activity as with topical application. Therefore, whether KCl was applied topically or injected its effectiveness in altering the nerve activity was similar. Pretreatment of the dentinal cavity with CaCl 2, MgCl 2 or SrCl 2 greatly reduced the response of intradental nerves to KCl. Therefore these divalent cations seem to have a depressant action on pulpal nerve fibres. The mechanism of action of KCl seems to be an alteration of K + concentration immediately surrounding the intradental nerves which presumably depolarizes the nerve fibre membrane and elicits an initial firing of action potentials. Because of the persisting high levels of extracellular potassium a sustained depolarized state occurs that results in an inactivation of the action potential. Divalent cations appear to depress the excitability of the nerve cell membrane without altering membrane potential. Such ionic agents could be used in conjunction with KCl as a possible treatment for hypersensitive teeth.

The intensive aspect of information processing in the intradental A-delta system in man—a psychophysiological analysis of sharp dental pain

The tooth pulp has many attractive features for the study of peripheral pain mechanisms because of its rich innervation, its unique distribution of nerve fibers and its general disposition to give rise to pain upon stimulation. An experimental model has been developed for simultaneous recordings of intradental multi-unit A-delta nerve activity and the subjective intensity and quality of pain evoked by tooth pulp stimulation in conscious, alert humans. The only teeth to be considered for this kind of investigations are those having such a periodontal condition that they have to be extracted. The nerve activity was recorded from two electrodes placed in the dentin on the labial tooth surface, one at the level of the most incisal part of the pulp, and the other as far apically as possible. Brief cold stimulation was produced by using evaporating ethyl chloride administered between the recording electrodes. The magnitude of perceived pain was estimated by means of an intermodal matching technique (finger span) in combination with verbal descriptors. Of three response criteria selected--average response amplitude, peak amplitude and area under the response curve (integral)--for describing the relationship between intradental nerve activity and sharp, shooting pain, the integral yielded the highest mean correlation coefficient.

Intradental nerve activity and jaw-opening reflex in response to mechanical deformation of cat teeth.

Mechanical stress was applied to canine teeth in anaesthetized cats to excite intradental A-fibres and to produce digastric muscle EMG responses. Activity in the intradental sensory units was recorded by two electrodes, one inserted in a dentinal cavity, the other in contact with the gingival sulcus. A pneumatically driven piston was used to cause a mechanical stress (10-150 N) on the stabilized tooth crown for 30 s, with instantaneous onset and release. Application of a load of 30 N produced a momentary burst of impulses in 2 of 12 teeth; 8 out of 10 teeth responded when 150 N was used. Digastric EMG responses were obtained at and above 60 N. Removal of the coronal pulp or cooling of the tooth crown with ethyl chloride abolished this reflex, whereas percussion of the tooth still produced a digastric response. Our results suggest that load-induced deformation of teeth activates intradental sensory mechanisms and a reflex withdrawal reaction unrelated to periodontal stimulation.

Effects of ionic and non-ionic solutions on intradental nerve activity in the cat

Intradental nerve activity (INA) was recorded from cat canine teeth to determine whether solutions altering intradental nerve sensitivity were strongly correlated to the osmotic concentration of the solution or via a more direct action on intradental nerve excitability. The effects of various ionic and non-ionic solutions were tested in both deep and shallow dentinal cavities. With saline in the deep dentinal cavity a very low firing rate or resting nerve spike (action potentials) activity was recorded. When 3 M NaCl was placed in the same or similar cavity a high discharge rate of nerve spike activity was obtained. This 3 M NaCl elicited activity was utilized to determine the inhibitory or excitatory effects of various test agents on the intradental nerves. The following agents: MgCl 2, MgSO 4, and CaCl 2 were inhibitory to the INA response elicited by 3 M NaCl. Non-ionic solutions of urea or sucrose failed to evoke INA and they were also minimally effective in altering 3 M NaCl elicited activity. Shallow cavities were utilized to maintain the tubular structure of dentin relatively intact. In the shallow cavity preparations hypertonic sucrose or urea failed to evoke INA, even when dentin was etched with 50% citric acid for 2 min. The results suggest that the osmolarity of these solutions is a poor indicator of the INA.

Experimental procedure to test the efficacy of chemical agents in altering intradental nerve activity

The present report is a detailed description of an animal model that can be used to evaluate the efficacy of chemical agents in altering intradental nerve activity. Intradental nerve activity was recorded in cat canine teeth using a bipolar electrode recording arrangement. An incisal cavity provided an avenue for the administration of test agents and also for the site of the active electrode, while a gingival cavity accommodated the indifferent electrode. Both electrodes were fixed to the tooth surface with dental acrylic cement. For the incisal cavity, a wall of Plastibase provided for the containment of fluids. The active electrode tip was suspended in this solution to eliminate all hard tissue contact with the electrode. The cavity depth can be deep (25 to 50 μm above the pulp) to achieve direct contact between the test agent and the extracellular fluids bathing the pulpal tissue, or a shallow cavity can be used to evaluate the osmotic effects of such agents. The results indicate that this model can effectively evaluate the effects of various ionic and nonionic agents on intradental nerves.

Chronically sensitized C nociceptors in skin. Patient with hyperalgesia and ongoing pain: [formula omitted], J. Ochoa and E. Torebjörk (Departments of Neurology, Good Samaritan Hospital and Medical Center, Portland, OR, U.S.A., Neurophysiology, University of Wisconsin, Madison, WI, U.S.A., Clinical Neurophysiology, Uppsala, Sweden)

Potassium ion-containing solutions have been shown to initially excite then depress intradental nerve activity (INA) when applied into deep dentinal cavities. The INA reflects activity originating in intradental A fibers. Application of KCl to deep dentinal cavities also induces an increase in pulpal blood flow (PBF). Capsaicin is known to exert a highly selective desensitizing effect on polymodal C-fiber nerve endings. These C fibers are generally believed to release vasoactive substances in response to stimulation. In order to determine if KCl exerts its vascular effect via activation of capsaicin-sensitive nerve fibers, we examined blood flow and sensory nerve responses to KCl obtained before and after capsaicin desensitization. The A-fiber nerve activity was determined by using INA recording technique. Blood flow was measured simultaneously from the same tooth using laser Doppler flowmetry. Local application of 0.25 M KCl to a deep dentinal cavity induced a brief spike burst and an increase in PBF of 76.0 ± 14.6% (n = 8). Repeated applications of 0.25 M KCl caused a consistent increase in the peak PBF amplitude (n = 8). Local application of 100 μM capsaicin to a deep dentinal cavity caused an increase in PBF of 116.8 ± 26.3% (n = 8) lasting 12–18 min, but capsaicin application did not appear to evoke any INA response. The amplitude of PBF in response to capsaicin application declined during repeated applications. Following repeated applications of capsaicin the PBF response to KCl was significantly reduced (9.9 ± 4.3%, n = 8). Capsaicin treatment, however, had no effect on the vasodilatory response to papaverine, a known smooth-muscle relaxant, which was used as a control. The brief excitation of KCl on the INA after repeated applications of capsaicin did not seem to be affected by comparing the oscillographic spike activity. These results suggest that the inhibition of KCl-induced vasodilation by capsaicin may be caused by desensitization of capsaicin-sensitive nerve fibers and that local application of KCl into a deep dentinal cavity can stimulate both A fibers and capsaicin-sensitive nerve fibers.

The relation between intradental nerve activity and pulpal pain after heat stimulation

The effects of tooth surface stimulation on intradental nerve activity (INA) and subsequent pain perception were studied in human lower incisors later to be extracted for periodontal reasons. The INA elicited by hot gutta-percha briefly applied to the tooth surface was monitored by means of labial electrodes deeply implanted in the dentin and perceived pain was continuously rated using a finger-span technique. After each stimulation the subject was also requested to select a sensory descriptor that was appropriate to describe the maximal pain intensity. The very first application of heat induced a typical pattern of nerve activity consisting of three phases. An initial burst of 3-5 s duration, phase I, was followed by a depression relative to the baseline lasting for 20-30 s, phase II, that gradually turned into phase III constituting a slowly increasing firing rate. The spontaneously emerging activity (phase III) in the absence of a physical stimulus passed unnoticed by all the subjects despite an average increase in firing rate of 67% relative to the prestimulus noise level. Repeated heat applications at short intervals led to a decrease and finally to abolishment of the whole nerve response. The lack of pain during phase III may be explained in two ways: the rate of increase in firing frequency may be too slow to trigger those perceptual pathways involved in processing of pain; the slow development of the increased sensory nerve activity may lead to central habituation.(ABSTRACT TRUNCATED AT 250 WORDS)

Perception of pulpal pain as a function of intradental nerve activity

The purpose of the present investigation was to find neurophysiological correlates of pain perception. The magnitude and time course of perceived pain was successfully related to the neural discharge evoked by rapid cooling of the tooth surface in 6 dental patients whose lower incisors were to be extracted for prosthodontic reasons. Two cavities were prepared on the facial surface of human lower incisors. The cavities were deepened using hand driven instruments until the pulp was visible through a thin layer of dentin. A metal tube was placed in contact with amalgam on each cavity bottom and fixed in place by composite filling material. The tubes were connected to standard equipment for electrophysiological recordings by a flexible circuit. The magnitude of perceived pain was assessed by a cross-modality matching to finger span in combination with sensory verbal pain descriptors and magnitude estimation. The striking agreement between the integrated nerve activity, probably of the Aδ type and pain perception, is of great importance from the methodological point of view since it strongly argues in favor of the appropriateness of the techniques applied here to elucidate the neural substrate of some types of nociception and also to evaluate various means of relieving such pain.

Relation between intradental nerve activity and estimated pain in man —a mathematical model

Intradental nerve activity (INA) induced by cold stimulation of human teeth is regularly accompanied by pain perception. In this study a mathematical model was developed in order to quantify the relationship between INA and pain. In 5 patients (45 experiments) INA was recorded using electrodes implanted in lower incisor teeth. Brief cold stimulations induced bursts of INA. The intensity of the resulting pain was simultaneously evaluated by means of an intermodal matching technique, finger span. The relationship between perceived pain and the integrated INA was analyzed using various mathematical operations (inter alia Fourier analysis) by means of a computer. A transfer function which describes the pain response following INA was found. This preliminary mathematical model, which is characterized by 5 parameters, consists of 2 parts, one which responds to fast changes in the afferent nerve signal, and another which reacts with a delay. The validity of the model has been tested, and it was found that the model consists of an adequate number of parameters and their cross-interaction is low. The analysis indicates that the parameters which determine the pain response following INA can be quantified and that they might be used as a measure of the efficacy of various pain relieving procedures.

The effect of some metal ions on the intradental sensory nerves of the cat.

Intradental nerve activity from canine teeth of anesthetized cats was recorded during the application of different metal ion solutions in a dentinal cavity. The application of Ag2+, Ca2+, Cd2+, Cr3+, Hg2+, Mg2+, Mn2+, Ni2+, Pb2+, Sn2+, and Zn2+ reduced the nerve activity induced by NaCl 0.76 M and compound 48/80. The application of Cu2+ and Co2+ excited the intradental sensory nerves.

Intradental nerve activity induced by reduced pressure applied to exposed dentine in the cat.

In order to study the excitation of intradental nerves by fluid flow in dentinal tubules the following experiments were performed. The fluid flow was caused by reduced hydrostatic pressure applied to the exposed dentine surface of the canine teeth in the anesthetized cat. In one series of 7 cats the intradental nerve activity was recorded by means of electrodes inserted in dentinal cavities. Provided that the pressure was sufficiently reduced and applied to acid-etched dentine in preparations of sufficient depth, intradental nerve activity of different impulse amplitudes was recorded. The responding pressure sensitive units were found to be sensitized by a brief local application of veratrine and desensitized by potassium chloride. In the second series 26 single functional pulp nerve fibre units were dissected from the inferior alveolar nerve in 7 cats. Nerve impulses were recorded by means of platinum-iridium wire electrodes. The conduction velocities of the 9 fibres responding to reduced pressure varied from 8.3 to 43.0 m/s. Five of these fibres also responded to elevated pressure. None of the 9 fibres conducting impulses with a velocity below 2 m/s responded to a reduction in pressure. thus, the present data strongly suggest that intradental nerve endings with myelinated axons are activated by fluid flow in dentinal tubules. Our results support the hydrodynamic mechanism of dentine sensitivity.