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Previous studies have shown that sympathetic nerve stimulation reduces afferent nerve-induced vasodilation by mechanisms unrelated to vasoconstriction in the rat incisor pulp. The present investigation concerned whether similar modulatory mechanisms might also influence neurogenic plasma extravasation in dental pulp. Rat mandibular incisors were electrically stimulated and blood flow reactions in the pulp were recorded by laser Doppler flowmetry. Plasma extravasation in the incisor pulp, gingiva and lip were indirectly assessed by the Evans-blue method. Stimulation of teeth with 50 microA (5 min) did not cause increased dye accumulation in the stimulated pulps whereas stimulation with 100 microA significantly increased the dye content in ipsilateral pulps by 32% as compared to controls; 100 microA stimulation was without effect in unilaterally denervated animals. Tooth stimulation with 50 microA (5 min), in the presence of either the alpha-adrenergic blocker phenoxybenzamine (3 mg/kg), or the alpha 1-adrenergic antagonist prazosin (50 micrograms/kg), as well as in chronically sympathectomized animals, significantly increased the Evans-blue content in the stimulated pulps by 47, 83 and 86%, respectively. Application of short trains of impulses (same number of impulses as for the continuous stimulation but producing minimal vasoconstriction) resulted in some dye accumulation, which was enhanced in the ipsilateral pulps in the presence of prazosin (100 micrograms/kg) or after acute resection of the superior cervical sympathetic ganglion by 70 and 64%, respectively. The Evans-blue content in the lip and gingiva was uninfluenced by the tooth stimulation. The results indicate that activation of sympathetic nerves inhibits the afferent nerve-induced plasma extravasation in rat incisor pulp and this effect is mediated by alpha-adrenoceptors not associated with vasoconstriction.

In 15 subjects, laser-Doppler flowmetry (LDF) was used to investigate whether the nervous control of pulpal blood flow (PBF) is affected by three tests known to excite the sympathetic nervous system. For comparison, skin blood flow was similarly recorded. Dynamic exercise (bicycle ergometer, 5 min, 90–100 W) in eight subjects was accompanied by a rise in PBF. PBF was increased by the cold pressor test (2 min) in eight subjects, while in five the flow decreased or remained unaffected. The isometric hand grip (2 min, 30% MVC) and the subsequent muscle ischaemia (2 min) led to a rise in PBF in two subjects and a fall in four. Following unilateral anaesthesia of the mandibular nerve, PBF in five subjects became unresponsive to dynamic exercise or the cold pressor test, indicating pressure autoregulation. All three tests triggered increases in mean arterial pressure (MAP) and heart rate (HR). Skin blood flow usually increased in response to the tests, but could also decrease, and often changed in a direction opposite to that of PBF. It is concluded that the circulation of blood in the human tooth is affected by evoked changes in autonomic nerve activity, involving activation of both vasodilator and vasoconstrictor nerves to vessels serving the tooth.

This investigation was designed to study the formation of secondary dentin in permanent teeth of young cats after denervation. In eight animals, cervical dentin was exposed bilaterally in the mandibular canines, 7-10 d after unilateral resection of the inferior alveolar nerve. The observation intervals were 30 d, 90 d and 180 d, after which histological examination of dentin was performed. In order to verify the loss and regeneration of pulpal innervation and an intact blood supply, blood flow responses to electrical stimulation of the tooth and to i.v. injections of substance P (SP) were recorded by laser Doppler flowmetry before and at 7-10 d after denervation, at the end of the experiments, and at predetermined intermediate intervals. SP-induced vasodilation was significantly enhanced at 1 wk and 30 d postoperatively and was normalized to control values at 90 and 180 d. Vasodilation in response to electrical tooth stimulation, which was absent after denervation, reappeared after 90 d in two of four cats. There was no irregular dentin formation under the exposed dentin at any time in denervated or control teeth. Formation of regular secondary dentin appeared to be enhanced on the denervated side at 30 d and 90 d postoperatively, whereas at 180 d there was no difference between sides. The results indicate that intradental nerves influence secondary dentin formation in feline permanent teeth.

Whether increased extravasation of plasma protein may occur in the rat incisor pulp as a result of antidromic stimulation of afferent nerves was investigated, and this preinflammatory reaction compared with that in adjacent soft tissues. In anaesthetized rats, the inferior alveolar nerve was exposed and stimulated electrically (10-15 V, 2 ms, 10 Hz for 30 s or 5 min). Blood flow changes in the lower lip and incisor pulp were recorded by laser Doppler flowmetry. Increased vascular permeability in the lip, gingiva and pulp was indirectly determined by means of the Evans blue dye method and spectrophotometric analysis. Stimulation of the inferior alveolar nerve for 30 s, in the presence of the alpha-adrenergic blocker phenoxybenzamine (3 mg/kg), increased blood flow in the lip by 172 +/- 16% and in the pulp by 38 +/- 5% as compared to basal blood flow. Intravenous (i.v.) administration of atropine (1 mg/kg), chlorisondamine (3 mg/kg), timolol (150 micrograms/kg), cimetidine plus mepyramine (3 mg/kg of each), methysergide (1 mg/kg) and diclofenac sodium (3 mg/kg) was without effect on this response. Acute pretreatment with capsaicin (1-3 mg/kg, i.v.), however, abolished the vasodilation in the pulp and reduced that in the lip by 58% (p0.05). In untreated animals, stimulation of the inferior alveolar nerve for 5 min increased the Evans blue content in the ipsilateral lip by 164% (p0.001), gingiva by 55% (p0.01) and pulp by 67% (p0.01). Pretreatment (i.v.) with a combination of cimetidine and mepyramine counteracted the dye extravasation only in the gingiva.(ABSTRACT TRUNCATED AT 250 WORDS)

In order to elucidate a possible influence of the sympathetic nervous system on afferent nerve function, rat mandibular incisors were electrically stimulated and blood flow changes monitored in the incisor pulp of untreated and sympathectomized animals by a laser Doppler flowmeter. Monopolar electrical stimulation of the tooth (200 microA, 5 ms, 40 Hz, 1 s) in normal animals resulted in a transient reduction in pulpal blood flow (PBF) (16% reduction, n = 10) followed by a small but long-lasting increase (11% increase). After administration of phenoxybenzamine or phentolamine (3 mg kg-1, i.v.) the initial dip in PBF was reduced by 59% (P < 0.001) while the subsequent increase was enhanced by 185% (P < 0.001). Similarly, infusion of prazosin (50 micrograms kg-1, i.v.) and idazoxan (0.5 mg kg-1, i.v.) significantly enhanced the increase in PBF by 118 and by 79%, respectively. In chronically sympathectomized animals the increase in PBF was 250% larger than that seen in untreated animals (P < 0.001). This increase in PBF was not further enhanced after alpha-adrenergic blockade. Acute resection of the superior cervical sympathetic ganglion, also resulted in some enhancement (by 56%) of the stimulation-induced increase in PBF (P < 0.01, n = 6). The increase in PBF was unaffected by infusion of timolol (150 micrograms kg-1) and atropine (1 mg kg-1) but was totally abolished by intravenous pre-treatment with capsaicin (1-3 mg kg-1). The present results suggest that activation of sympathetic nerves exerts inhibitory effects on the afferent nerve-induced vasodilation in the rat incisor pulp unrelated to sympathetic vasoconstriction.

A unilateral resection of the mandibular nerve ( n = 20) was made 10–14 days before investigation of the contribution of afferent nerves in vasodilator reactions in the dental pulp. Lower canine teeth were subjected to various stimuli and pulp blood-flow responses monitored by laser Doppler flowmetry. An absence of response to bipolar electrical (5 impulses, 50 μA, 5 ms, 2 Hz) stimulation on the tooth surface was used to demonstrate a successful chronic nerve lesion. Local application of capsaicin (10 −4 M) in a deep dentinal cavity induced a long-lasting increase in pulpal blood flow in control teeth only. Bradykinin (10 −3 M) induced significantly larger responses in control than in denervated teeth (58.3 ± 9.8% and 24.5 ± 4.9%, respectively, p n = 8); in addition, the onset was slower and the duration of the response significantly (60%) shorter than in control teeth. Intermittent grinding of surface dentine instantly increased flow in control teeth by 53.0 ± 12.5% ( n = 12) whereas in denervated teeth the response was delayed and significantly (70%) smaller. Deeper preparation produced responses of similar magnitude in control and denervated teeth (69 and 50%, respectively) but the onset was delayed in denervated teeth. Low-intensity ultrasonic stimulation caused vasodilation in intact teeth (38% increase) but had no effect in denervated teeth. This effect was abolished after local anaesthetic (mepivacaine) injection. Sympathectomy ( n = 3) did not influence stimulation-induced blood-flow responses in the dental pulp. The results show that afferent nerves make an important contribution to haemodynamic reactions in the pulp in response to experimental and clinical procedures directed at the tooth.

It can be concluded that the sympathetic vasoconstrictor regulation is dominant among the remote control mechanisms of pulpal blood flow. The local systems, neurogenic and humoral, probably act by modulating t h e sympathetic vasoconstrictor tone. The basal vascular tone, of fundamental importance in other vascular beds, has not been analyzed in the dental pulp.

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)

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.

In order to investigate the origin of intradentinal nerve-like structures, unilateral transection of the sensory (inferior alveolar nerve) and/or the autonomic (cranial cervical sympathetic ganglion) supply was performed in 6 cats. After 2—4 weeks, when degenerative change was expected in the cut nerves, electrophysiological recordings from the dentin showed total absence of impulse activity in teeth subjected to sensory denervation regardless of whether or not the autonomic innervation was intact. Control teeth, on the other hand, responded to different local pain stimuli. Electron microscopic study of predentin and inner dentin in control teeth showed intratubular nerve-like structures similar to «associate cells» earlier described in human teeth. In teeth subjected to sensory nerve resection, however, the intradentinal «associate cells» showed advanced degenerative change or were absent. Resection of the sympathetic nerve supply did not influence the appearance of these intratubular structures.The pres...

The rate of disappearance of radioactive iodide from a deep dentinal cavity has been used as a means to measure the influence of various cavity washing agents on pulpal microcirculation. Hydrogen peroxide in concentrations of 2–4% exerted a pronounced influence when it was allowed to act in deep dentinal cavities where the red colour of the pulp was barely visible through the dentin. Repetitive treatments of 3 % hydrogen peroxide of 40 sec duration caused a potentiated depression of the microcirculation. This was true when the dentinal wall between the cavity and the pulp was intact. In cases of pulp exposure the influence seemed to be much less. All other agents tested failed to influence the pulpal microcirculation as reflected by the present method.

Because of discrepancies between results from animal and human experiments on nervous activity of teeth, experiments were done on human teeth to find clinical relevance. When a dentist manipulates a tooth with a probe, an air blast, or a bur, the patient suffers from hydrodynamic excitation of the A-delta nerves. Dull pain is more likely to be the result of C-fiber stimulation and is associated with tissue damage and inflammation of the pulp.

The present investigation was undertaken to ascertain whether local insults can affect the sympathetic vasoconstrictor regulation of pulpal blood flow. The rate of disapperance (k-value) of iodide from dentinal cavities was measured in anaesthetized cats. Changes in k-value reflected changes in blood flow. It has previously been shown that stimulation of sympathetic vasoconstrictor nerve fibres generally causes a clearcut decrease in the k-value. Deep cavity preparation was found to inhibit the vasoconstrictor response in a few cases in experiments on mature cats. Heating or cooling the tooth during cavity preparation induced a more frequent inhibition, which proved to be reversible within a few hours. Compound 48/80 applied locally to the cavity was also found to induce inhibition of the vasoconstrictor effect, but in this case no sign of reversibility was observed. Chronic insults were produced by exposing the cavity to oral microorganisms during 1-4 weeks before the experimental procedure. In this case, the sympathetic vasoconstrictor response was not inhibited. A histological study was performed to examine the pulp tissue after cavity preparation and the application of insults. It was found that cavity preparation and acute insults caused little or no disturbance, while chronic insults resulted in severe damage to the pulpal tissue.

The ability of a mathematical model to evaluate the effects of two different pain modulating procedures (partial nerve block and vibration) on acute experimental pulpal pain was studied. The results were also compared with placebo procedures and it was shown that the model could accurately quantify the parameters that determine the pain response following cold-induced intradental nerve impulse activity (INA). The most effective pain relieving method was found to be partial nerve block which induced significant parameter alterations reflecting decreased pain sensation and increased reaction time. Thus, it was shown that the present mathematical model is a useful tool enabling detailed analysis of differences in pain relieving procedures on human pulpal pain mediated by nerves of the A type.

Laser Doppler flowmetry was applied to human teeth to study whether blood How in the pulp can be recorded. In sensitive, intact incisors the level of the output signal Ironi the flowmeter was clearly distinguishable from that obtained in adjacent nonsensitive or pulpeetomized teeth. Heart beat synchronous oscillations, which were present in the recording signal from normal teeth, were absent in nonvital teeth. Local injection of lidocaine (20 mg/ml) with adrenaline (12.5 μg/ml) caused a pronounced and long-lasting reduction of the flowmetric values in healthy teeth. The oscillations were also reduced in amplitude. Repeated recordings showed good reproducibility. Thus, changes in blood (low may be assessed in a tooth by tin's non-invasive method. The instrument is a promising tool in the clinical evaluation of pulp vitality following traumatic injuries.

Changes in intra-alveolar tooth position and local 125I clearance from the periodontal ligament (PDL) were monitored simultaneously in cats. Axial tooth movements, reflecting periodontal ligament volume changes, were measured with an ultrasonic transit time technique. Local blood flow changes in the PDL were studied indirectly by measuring the local clearance of 125I-. Stimulation of the cervical sympathetic trunk caused an intrusive movement of the tooth with a concomitant reduction of the 125I- clearance. Infusion of noradrenaline induced a similar response. Stimulation of the inferior alveolar nerve during systemic treatment with phentolamine caused an extrusive movement of the tooth with a concomitant increase in the clearance of the tracer from the PDL. Intra-arterial infusion of the vasodilator substance P mimicked that response. Fixation of the tooth to the jaw bone, thus preventing an intrusive movement, did not change the reductions in clearance seen on sympathetic stimulation, indicating that this blood flow reduction was not dependent on tooth movement. A qualitative relation between PDL blood flow (as measured by local 125I clearance) and PDL volume (as measured by tooth position) is shown. The two variables measured are suggested to reflect two aspects of blood flow in the PDL.

Publisher Summary This chapter discusses the existence of nervous control of blood circulation in the dental pulp and the periodontal tissues. The influence of sympathetic nerve activation on the blood circulation in the dental pulp and the periodontal tissues has been estimated by measuring the change of rate of disappearance or clearance of diffusible tracers from local depots. The chapter presents an experiment in which to study the effect of the sympathetic vasomotor control in the different tissues, the appropriate sympathetic nerves to the jaws of the dog and cat were stimulated and the rate of disappearance of tracer from depots in the pulp, gingival, and periodontal membrane was measured. Such stimulation elicited reduction in tracer disappearance in all the tissues studied, which was related to the frequency of stimulation. The chapter discusses that the activation of the sympathetic nerves to the oral tissues results in a pronounced reduction of blood flow in the pulp and the periodontal tissues.