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K J Heyeraas

Publications and source records attributed to K J Heyeraas.

At least 37 records · Page 2Linked to original sources

Effect of intermittent long-lasting electrical tooth stimulation on pulpal blood flow and immunocompetent cells: a hemodynamic and immunohistochemical study in young rat molars.

Release of sensory neuropeptides after stimulation of afferent nerve fibers has previously been shown to induce vasodilation and increased vascular permeability in the dental pulp, a condition recognized as neurogenic inflammation. In the present study a possible role for the sensory neuropeptides in transendothelial migration of immunocompetent cells was investigated. The dental pulp is an isolated tissue densely innervated with sensory fibers containing neuropeptides, and following electrical stimulation of the crown, the effect on pulpal blood flow and immunocompetent cells can be studied in a noninvasive model. A laser Doppler flowmeter was used to measure relative changes in pulpal blood flow during long-lasting intermittent stimulation of innervated and denervated rat first molars. In the innervated teeth, stimulation promptly increased pulpal blood flow by on average 45% at the start of the experiment, whereas almost no blood flow increase was recorded after 4 to 5 h stimulation. Surgical sectioning of the inferior alveolar nerve abolished blood flow increase upon stimulation. After stimulation, a quantitative analysis of CD43+, CD4+, CD11+, and I-A antigen-expressing cells was performed, and the effect of stimulation on calcitonin gene-related peptide (CGRP)-immunoreactive and substance P (SP)-immunoreactive (IR) nerve fibers was studied. Immunohistochemistry was performed by the avidin-biotin peroxidase method. Stimulation resulted in an almost complete depletion of CGRP- and SP-IR nerve fibers in the first molar pulp, whereas nerve fibers in the gingiva and neighboring teeth were unaffected. A significant increase in the number of CD43+ cells was found in the innervated tooth after stimulation compared to the stimulated denervated (P < 0.01) and unstimulated control (P < 0.05) first molars. For I-A antigen-expressing cells a significant increase (P < 0.05) was found between the innervated stimulated and unstimulated control, but not between the innervated and denervated stimulated first molars. Hence, from the present experiment it is concluded that the pulpal nerves participate in and facilitate transendothelial migration of CD43+ cells during acute neurogenic inflammation.

Afferent Pathways↗

Pulp interstitial fluid pressure and blood flow after denervation and electrical tooth stimulation in the ferret.

The effects of sensory and sympathetic denervation on simultaneously measured interstitial fluid pressure and blood flow in the canine pulp before, during and after electrical tooth stimulation were investigated in 25 ferrets. The micropuncture technique was used to measure interstitial fluid pressure and laser-Doppler flowmetry was used to record pulpal blood flow. Animals with an intact innervation (group 1) served as controls. Sensory denervation was by axotomy of the left inferior alveolar nerve 10 days before the experiment (group 2) and sympathectomy by removal of the left cervical ganglion 5 days before the experiments (group 3). The study was designed to verify whether denervation affected basal pulp blood flow and interstitial fluid pressures during control conditions and/or after tooth stimulation. During control conditions the interstitial fluid pressure averaged 1.32 +/- 0.07 kPa in group 1, whereas the mean was only 0.51 +/- 0.13 kPa in the axotomized animals (group 2). The difference was highly significant, indicating decreased blood or interstitial fluid volume in the pulp after inferior alveolar nerve axotomy. In the sympathectomized group neither the interstitial fluid pressure nor the pulp blood flow was significantly different from those of group 1. Electrical tooth stimulation caused an almost simultaneous increase in interstitial fluid pressure and pulp blood flow in groups 1 and 3, whereas stimulation did not significantly change either variable in the axotomized animals (group 2). It is concluded that a resting nervous vasodilator tone of sensory origin exists in the ferret dental pulp, and that the sensory nerves are responsible for the increased interstitial fluid pressure and pulp blood flow during tooth stimulation.

Animals↗

Neuropeptide Y expression in the trigeminal ganglion and mandibular division of the trigeminal nerve after inferior alveolar nerve axotomy in young rats.

Neuropeptide Y (NPY) is a 36-amino-acid peptide residing in sympathetic nerve terminals, originating from the superior cervical ganglion in oral tissues. NPY exerts vasoconstrictor action together with noradrenalin and has been found to inhibit the release of neurotransmitters from primary afferent fibers. During regeneration of the axotomized inferior alveolar nerve (IAN), NPY-immunoreactive (IR) nerve fibers have been shown in the odontoblast layer and dentin, an area normally innervated by afferent nerve fibers. The dynamic shift in neuropeptide expression in the trigeminal ganglion and in the dental pulp was studied by immunohistochemistry 1, 2, 3, and 8 weeks after IAN axotomy. In the ipsilateral first mandibular molar a temporal loss of pulpal sensory nerves lasting for approximately 1 week was found after axotomy. An upregulation of NPY was shown in neurons located in the mandibular area of the trigeminal ganglion, concomitant to a reduction in number of neurons expressing substance P (SP). To study an alternate and possible trigeminal origin of some of the peripheral nerve fibers IR to NPY in the dental pulp, double immunofluorescence labeling was performed for NPY and calcitonin gene-related peptide (CGRP). Coexistence of NPY and CGRP was shown in neurons located in the trigeminal ganglion and in nerve fibers in the tooth pulp during IAN regeneration. Furthermore, retrograde tracing with Fluorogold revealed NPY-IR neurons projecting to the first molar pulp 3 weeks after axotomy. Hence, we conclude that after IAN axotomy NPY is produced in trigeminal ganglion neurons and transported in afferent regenerating fibers to the dental pulp. These results add further evidence for a plasticity in peptide transcription in sensory neurons after nerve injury and indicate a trigeminal origin of at least some of the pulpal NPY-IR fibers during nerve regeneration.

Age Factors↗

Effect of capsaicin treatment or inferior alveolar nerve resection on dentine formation and calcitonin gene-related peptide- and substance P-immunoreactive nerve fibres in rat molar pulp.

The aim of this study was to investigate whether decreased sensory innervation induced by capsaicin treatment or axotomy of the inferior alveolar nerve has an effect upon dentine formation in the rat first molar. Dentine formation was visualized by intravital injection of Procion brilliant Red H8BS and denervation was verified immunohistochemically for the neuropeptides calcitonin gene-related peptide (CGRP) and substance P. The observation times were 6 weeks for the capsaicin-treated group and 11 days for the axotomized group. Capsaicin injections caused a consistent reduction in numbers of CGRP- and substance P-immunoreactive fibres in the pulps and a somewhat smaller reduction in the periodontal tissues. Unilateral axotomy of the inferior alveolar nerve induced an almost complete loss of immunoreactive fibres in the pulp and in the mesial gingiva of the first molar. Dentine formation at the mesial pulp horn and at the central pulp floor was significantly reduced in both groups compared to controls. The results suggest that sensory neuropeptides such as CGRP and substance P may play a part in dentine formation.

Animals↗

Effect of inferior alveolar nerve axotomy on immune cells and nerve fibres in young rat molars.

Denervation has been a useful approach to the investigation of interactions between nerve fibres and the pulp-dentine complex. Information on the immunological implications of axotomy is still lacking. The effect of axotomy on CD43+, CD4+, CD11b+ and I-A antigen-expressing cells in both the distal segment of the cut inferior alveolar nerve and in the first molar pulp of young rats was evaluated. Nerve fibres immunoreactive to protein gene product (PGP) 9.5, the neuropeptides substance P and calcitonin gene-related peptide (CGRP), and neuropeptide Y were visualized also by use of the avidin-biotin peroxidase complex method. Recruitment of macrophages was found in the distal segment of the sectioned inferior alveolar nerve 2 days after axotomy, with a further increase in number during the 6-day observation period. However, in the dental pulp, the number of CD43+, CD4+, CD11b+ and I-A antigen-expressing cells was almost unaffected. An almost complete sensory denervation of the first mandibular molar pulp was obtained 2 days after axotomy. After 6 days, the mesial part of the coronal pulp still remained denervated, while regenerated nerve fibres had reached both the root pulp and the distal part of the coronal pulp. Nerve fibres immunoreactive to neuropeptide Y were slightly reduced in density 2 days after axotomy, and after 6 days the localization of neuropeptide Y-immunoreactive fibres was changed compared to the control, with fibres also distributed in the odontoblast layer close to dentine. Hence, following axotomy in young rats, an almost complete sensory denervation is achieved in the first molar, whereas nerve fibres immunoreactive to neuropeptide Y change their distribution pattern, with fibres located close to the dentine after 6 days. Due to the almost unchanged number and distribution of immunocompetent cells in the pulp after axotomy, the young rat molar pulp may represent a suitable and useful experimental model to study neuro-immune interactions.

Animals↗

Effect of venous stasis and hypoproteinemia in gingival fluid formation in rats.

Experiments were performed to provide information on the mechanisms of the formation of gingival fluid in rats and on the determinants of its flow and composition. For this purpose we studied the effect of increasing net capillary filtration by venous stasis induced by multiple ligations of the jugular vein or by hypoproteinemia induced through puromycine nephrosis. A 1 microliter glass capillary was placed in the sulcus of the first maxillary molar for collection of gingival fluid (GF). Colloid osmotic pressure (COP) was determined in GF, in wick fluid from attached gingiva and buccal mucosa, and in plasma. Interstitial fluid hydrostatic pressure (Pi) was measured by micropuncture technique and the fractional removal rate of radio-labelled human serum albumin (kAlb) was recorded in attached gingiva and buccal mucosa. During venous stasis the gingival fluid flow increased from 1.7 microliters/h to 3.8 microliters/h, whereas COPGF fell from 14.1 mmHg to 8.8 mmHg. COP in wick fluid from gingiva was reduced from 10.3 to 4.3 mmHg. Pi increased from 6.8 to 13.1 mmHg, and kAlb in sham-operated controls increased from 0.068 to 0.189 h-1. In buccal mucosa COPi was significantly decreased to 7.1 mmHg in rats with venous stasis, whereas Pi and kAlb remained unchanged compared to the sham-operated controls. In hypoproteinemic rats COPGF was 5.0 mmHg and COPp was reduced from 18.9 to 8.0 mmHg. COPi declined from 8.9 mmHg to 2.4 mmHg in gingiva and from 8.1 mmHg to 2.7 mmHg in buccal mucosa.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Recruitment of immunocompetent cells after dentinal injuries in innervated and denervated young rat molars: an immunohistochemical study.

The dental pulp represents a peripheral end-organ deprived of a collateral nerve supply. After inferior alveolar nerve (IAN) axotomy, rat molar pulp is denervated over a period of at least 6 days. Therefore, rat molar pulp was used as an experimental model to study the effect of sensory nerve fibers on influx of immunocompetent cells after dentinal injury. In the present study we performed a quantitative analysis of CD43+, CD4+, CD11b+, and I-A antigen-expressing cells subjacent to dentinal cavities in denervated and innervated first mandibular molars. For visualization of nerve fibers, antibodies to protein gene product (PGP) 9.5, the sensory neuropeptides substance P (SP) and calcitonin gene-related peptide (CGRP), and the sympathetic neuropeptide Y (NPY) were used. Immunohistochemistry was performed by the avidin-biotin-peroxidase method. In the innervated teeth, a correlation between increased sensory nerve density and influx of immunocompetent cells was found. Compared to the contralateral innervated molars, a significant reduction in recruitment of immunocompetent cells was found in the denervated pulp tissue subjacent to the dentinal cavities. The rat molar represents a unique model to illustrate the influence of sensory nerves and neuropeptides on inflammation and recruitment of immunocompetent cells.

Animals↗

Effect of electrical tooth stimulation on blood flow, interstitial fluid pressure and substance P and CGRP-immunoreactive nerve fibers in the low compliant cat dental pulp.

The effect of vasodilation on simultaneously measured interstitial fluid pressure (IFP, micropuncture) and blood flow (laser-Doppler) in the low compliant pulpal connective tissue was investigated in 10 cats. Vasodilation was induced by electrical stimulation of the tooth after pretreatment with the sympathetic blocker guanethidine. Visualization of the sensory neuropeptides calcitonin gene-related peptide (CGRP) and substance P (SP) was performed using immunocytochemistry. The study was designed to answer the following questions. (1) Does vasodilation promptly increase IFP in low compliant tissues? (2) Does an increase in IFP counteract the blood flow increase? (3) Does repeated electrical stimulation cause reduced staining of CGRP- and SP-immunoreactive nerve fibers in the dental pulp? Electrical stimulation resulted consistently in a nearly synchronous increase in both blood flow and IFP. IFP was nearly doubled, from 6.3 +/- 0.18 mm Hg in control to 11.7 +/- 0.44 mm Hg, whereas blood flow increased by 28%. However, despite continued vasodilation the IFP fell to control level, or even lower, within 1-5 min. The results indicate that the increased IFP will promote fluid absorption into the blood, counteracting a further IFP increase in low compliant tissues during vasodilation. Accordingly, transmural pressure is only transitorily reduced and compression of vessels does not take place. There was considerably less CGRP- and SP-immunoreactive fibers in the stimulated teeth than in the contralateral controls, suggesting that the vasodilation was caused by liberation of these sensory neuropeptides.

Animals↗

Nerve fibres and cells immunoreactive to neurochemical markers in developing rat molars and supporting tissues.

The distribution of nerve fibres immunoreactive to calcitonin gene-related peptide (CGRP), substance P (SP) and neuropeptide Y (NPY) was compared to the general neurochemical markers for nerves and neuroendocrine cells protein gene product 9.5 (PGP 9.5) and neurone-specific enolase (NSE), by use of the avidin-biotin peroxidase complex method in developing dental structures in rats aged 13 to 27 days. A substantially greater part of the nerve fibres was immunoreactive to CGRP and SP than to NPY. In the bell stage, nerve fibres immunoreactive to PGP 9.5, CGRP and SP were found in the dental follicle but not in the dental papilla and stellate reticulum. In the advanced bell stage, after initiation of dentine and enamel formation, PGP 9.5, CGRP- and SP-immunoreactive fibres were found in the dental papilla, while the first NPY-immunoreactive fibres were observed in the papilla when root formation started. Concomitant with the beginning of root development, a subodontoblastic nerve plexus was gradually formed and PGP 9.5-, CGRP- and SP-immunoreactive fibres were found within the dentinal tubules. From the start of root formation, CGRP-, SP- and NPY-immunoreactive nerves were shown in the developing periodontal ligament, although a mature distribution pattern was not observed until root formation was nearly completed. Ameloblasts, odontoblasts and cell-like structures in the outer enamel epithelium and within the dental lamina were PGP 9.5-immunoreactive at the bell stage. As the tooth matured, the immunolabelling gradually decreased, but was still present in some odontoblasts after tooth eruption. NSE-immunoreactive, cell-like structures were found in the periphery of the dental follicle, and persisted close to alveolar bone in the periodontal ligament when the tooth reached occlusion. Hence, it may be concluded that sensory nerves containing SP and CGRP are present in the pulp in advance of sympathetic nerves immunoreactive to NPY.

Alveolar Process↗

Changes in blood circulation in teeth and supporting tissues incident to experimental tooth movement.

Fluorescent microspheres (FM) were used to semi-quantify the effect of orthodontic forces on blood flow in oral tissues in young rats. Forty-five animals had an orthodontic appliance inserted on the first maxillary molar on one side exerting a mesial force of approximately 50 g. Ten animals served as unoperated controls. On days 1, 3, 7, 14, and 21 after the start of the experiment, FM were injected into the left ventricle through an abdominal approach in the experimental and control animals. FM were counted in serial sections from the jaws in the periodontal ligament, pulp, and alveolar bone in a fluorescent microscope. The number of FM per tissue volume and/or tissue weight was taken as a measure of blood flow. The experimental side had significantly lower numbers of FM/mm3 in the periodontal ligament of the first and the second molar on the first day, compared with the contralateral side. However, a steady, significant increase in the number of FM/mm3 in the periodontal and pulpal tissues, and FM/mg in the alveolar bone could be observed on the third and seventh days on the experimental side of the first, second, and third molars compared with the contralateral side, while in the later stages the values of the two sides approached each other. The results of this study indicate that a localized experimental tooth movement initiates a more generalized blood flow response in the periodontal ligament, dental pulp and alveolar bone.

Alveolar Process↗

Increased pressure in venous sinusoids during decongestion of rat nasal mucosa induced by adrenergic agonists.

The haemodynamic effects of sympathetic agonists causing decongestion of the nasal mucosa have been investigated in rats. Access to mucosa was obtained from the dorsal side through a small cavity drilled in the nasal bone. The pressures in the venous sinusoids and in the interstitial fluid of nasal mucosa were recorded by micropuncture technique. The local red cell flux (LDF) was monitored by laser Doppler flowmetry, and the blood volume in the mucosa was measured by radio-labelled erythrocytes and albumin. In control rats the tissue blood volume was 0.25 +/- 0.03 g (g wet wt)-1. The interstitial fluid pressure (IFP) was 2.4 +/- 0.6 mmHg and the average blood pressure in venous sinusoids (Ps) was 12.8 +/- 2.7 mmHg. After topical application of noradrenaline (NA) the local blood volume was reduced to 0.12 +/- 0.03 g g-1. Ps was increased to 18.0 +/- 4.0 mmHg, whereas IFP was maintained and LDF was reduced to 40.4% of control, indicating a greater rise in post than in presinusoid vascular resistance. Blocking of both alpha 1 and alpha 2-receptors by phentolamine caused a rise in mucosa blood volume and in LDF by 16 and 20% of control, respectively. Ps increased significantly to 15.2 +/- 3.3 mmHg. Specific stimulation or blocking of alpha 1-receptors by phenylephrine or prazosin induced similar or slightly smaller vascular responses than NA or phentolamine. The effects of the specific alpha 2-agonist (clonidine) or antagonist (yohimbine) on rat mucosa were small, indicating a domination of the alpha 1-receptors. Thus, application of NA caused a rise in blood pressure in the venous sinusoids of nasal mucosa. As LDF fell simultaneously, the reduced blood volume must be due to an increased tone in the muscular wall of venous sinusoids.

Adrenergic alpha-Agonists↗

Neurogenic inflammation in rat trachea is accompanied by increased negativity of interstitial fluid pressure.

The present experiments were performed to investigate whether neurogenic inflammation in rat trachea (with edema formation and protein extravasation when the circulation is intact) induced by electrical field stimulation of neuropeptide-containing C fibers in the vagal nerve is accompanied by increased negativity of interstitial fluid pressure (P(if)). Increased negativity of P(if) in the trachea occurs in dextran anaphylaxis and mast cell degranulation and facilitates edema formation under these circumstances. Experiments were performed after circulatory arrest had been induced in pentobarbital anesthesia to prevent edema formation, which will raise P(if) and potentially cause underestimation of an increased negativity of P(if). After induction of circulatory arrest, the vagal nerve was isolated and placed in a stimulating electrode. The trachea was then exposed and covered with mineral oil, and measurement of P(if) was started as soon as possible thereafter. P(if) was measured with sharpened glass capillaries (tip diameter, 3 to 7 microns) connected to a servocontrolled counterpressure system. P(if) in the control group (n = 12) did not change throughout the observation period. Electrical stimulation of the left vagal nerve caused P(if) to fall in all experiments, from -1.1 +/- 1.1 mm Hg in the control condition to an average of -10.6 +/- 3.4 mm Hg (n = 9, P < .01). In some experiments, a continuous recording of P(if) was obtained, showing that the reduction of P(if) started within 30 seconds after onset of stimulation to reach and later remain at a stable level within a few minutes. The experimental protocol was repeated after the C fibers had been nearly depleted of neuropeptides with capsaicin.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Nerve fibers immunoreactive to protein gene product 9.5, calcitonin gene-related peptide, substance P, and neuropeptide Y in the dental pulp, periodontal ligament, and gingiva in cats.

The distribution patterns of nerve fibers immunoreactive (IR) to calcitonin gene-related peptide (CGRP), substance P (SP), and neuropeptide Y (NPY) in the dental pulp, periodontal ligament (PDL), and gingiva were studied and compared with the complete innervation visualized by antibody to protein gene product (PGP) 9.5 in adult cats. The pulp showed considerably denser nerve supply for PGP 9.5, CGRP, and SP than the periodontal tissues. Most of the pulpal fibers were CGRP-IR, and approximately three to four times more IR fibers were labeled with CGRP than SP. Most fibers in the odontoblast area penetrating into the dentin tubules were CGRP-IR. NPY-IR nerves were mainly observed in connection with the larger blood vessels in pulp and PDL. In the PDL most nerves were localized in the apical third in connection with blood vessels, but CGRP-IR fibers extending close to root cementum were often observed. Immunoreactivity to PGP 9.5 and CGRP was frequently found in cell-like structures in connection with Malassez epithelium in the PDL and in some round epithelial-like cells located in the base of gingival rete pegs.

Animals↗

Effect of traumatic occlusion on CGRP and SP immunoreactive nerve fibre morphology in rat molar pulp and periodontium.

Traumatic occlusion provides a trauma that affects the whole tooth and its supporting tissues. To study the effect of this trauma on CGRP and SP immunoreactive nerve morphology in pulp and periodontium, traumatic occlusion was induced in 2-months-old rats. The occlusal surface of the first maxillary molar in 30 rats were unilaterally raised 1 mm with a composite material. At different observation periods up to 30 days, the rats were transcardiacally perfused, the jaws demineralized, sectioned and processed for immunohistochemistry with the avidin-biotin-peroxidase method. Changes in nerve morphology, distribution and density in first and second molars and their supporting tissues were analyzed and compared in experimental (n = 30) and control rats (n = 14). Already after 5 days with traumatic occlusion, 22% of the experimental teeth had increased density of CGRP and SP immunoreactive nerves locally in gingiva, the periodontal ligament and the pulp, while in 15%, axonal proliferation and changed nerve morphology were found in the whole pulp (severe reaction). During a 20-day period, the pulpal nerve reactions progressed and included the whole pulp in 46% of the experimental teeth. The periodontal nerve responses were still localized only to the cervical and apical regions, and they remained local in these areas throughout the experimental periods. After 20 days the number of teeth with severe nerve changes seemed to decrease. The study shows that an unilateral change in occlusion of the first molar initiate nerve responses in the total molar dentition. In this experimental model the pulpal axons containing CGRP and SP reacted more serious to occlusal trauma than the nerves in the periodontium. The results indicate that the nerve changes in some cases might be transient.

Animals↗

Micropuncture measurements of interstitial fluid pressure in normal and inflamed gingiva in rats.

Interstitial fluid pressure (IFP) in normal and inflamed gingiva of rats was measured by sharpened glass capillaries (diameter 2-4 microns) connected to a servocontrolled counterpressure system ad modum Wiederhielm. Gingival inflammation was induced by a steel ligature placed unilaterally around the first maxillary molar. After 8 weeks, the ligature was removed and measurements of IFP in normal and experimentally inflamed gingiva were made by puncture through the intact oral epithelium. Average IFP on the control side was 3.5 mm Hg in free, and 7.4 mm Hg in attached gingiva. Compared to the control side, IFP on the experimental inflamed side was elevated significantly (p less than 0.05) both in free and attached gingiva. In the ligated inflamed side IFP in free gingiva averaged 6.7 mm Hg, whereas in attached gingiva it showed a mean value of 10.4 mm Hg. Histological examinations showed a dense infiltrate of inflammatory cells in the connective tissue, while the contralateral control side showed normal features of epithelial and connective tissue. The present finding of increased IFP in the inflamed gingiva may in theory contribute to augmented crevicular fluid flow during inflammation.

Animals↗

Effect of experimental traumatic occlusion on periodontal and pulpal blood flow.

Fluorescent microspheres (FM) were used to visualize and semi-quantify flood flow in the periodontal ligament (PDL) and dental pulp during experimental traumatic occlusion of the maxillary and mandibular molar teeth in young rats. At different observation points FM were injected systemically, and the number of FM was counted in serial sections from the jaws in the PDL and pulp of the molar teeth in a fluorescent microscope. Blood flow was related to the number of FM in the tissues and in a reference blood sample. In the early stages an increase in blood flow in the PDL and dental pulp was found on the experimental side compared with the contralateral side. Furthermore, there was an increase in blood flow on both sides of the jaws compared with an unoperated control material. The study thus indicates that a local unilateral occlusal trauma initiates blood flow responses in the total molar dentition in rats.

Animals↗

Effects of dental trauma on pulpal and periodontal nerve morphology.

Regeneration and morphological changes in sensory peptidergic nerves in pulp and periodontium were studied after general dental trauma by means of immunohistochemistry. In control teeth also the total nerve supply was demonstrated by using antibody to the general neuronal marker, protein gene product (PGP)9.5. Two experimental rat models were used, i.e. tooth replantation and induced traumatic occlusion. Results from these studies are reviewed here. In the controls, the PGP9.5-immunoreactive(IR) nerve supply in pulp and periodontium was generally denser compared to CGRP-IR and SP-IR nerves. In the replanted teeth, regeneration of CGRP-IR nerves closely followed the pulp cell renewal. Density and distribution of the regenerated nerves showed two different patterns which seemed to depend on the capacity of the renewed pulp to form postoperative dentine. The nerve density never reached the same level as the controls. In teeth not able to form irregular dentine, the pulp was sparsely innervated and the pulp cavity was filled with innervated bone. Nerve responses in CGRP-IR and SP-IR nerves after unilateral induced traumatic occlusion in the first maxillary molar were studied at different observation periods up to 30 days. After 5 days, localized morphological nerve changes were found both in the pulp and periodontium within the total rat molar dentition. With increasing observation periods, the pulpal neural changes progressed and were extended to all pulpal areas compared to the periodontium, where the nerve responses remained localized to cervical and apical tissues throughout the experiment.

Animals↗