Inflammatory Response Mechanisms of the Dentine-Pulp Complex and the Periapical Tissues.

The macroscopic and microscopic anatomy of the oral cavity is complex and unique in the human body. Soft-tissue structures are in close interaction with mineralized bone, but also dentine, cementum and enamel of our teeth. These are exposed to intense mechanical and chemical stress as well as to dense microbiologic colonization. Teeth are susceptible to damage, most commonly to caries, where microorganisms from the oral cavity degrade the mineralized tissues of enamel and dentine and invade the soft connective tissue at the core, the dental pulp. However, the pulp is well-equipped to sense and fend off bacteria and their products and mounts various and intricate defense mechanisms. The front rank is formed by a layer of odontoblasts, which line the pulp chamber towards the dentine. These highly specialized cells not only form mineralized tissue but exert important functions as barrier cells. They recognize pathogens early in the process, secrete antibacterial compounds and neutralize bacterial toxins, initiate the immune response and alert other key players of the host defense. As bacteria get closer to the pulp, additional cell types of the pulp, including fibroblasts, stem and immune cells, but also vascular and neuronal networks, contribute with a variety of distinct defense mechanisms, and inflammatory response mechanisms are critical for tissue homeostasis. Still, without therapeutic intervention, a deep carious lesion may lead to tissue necrosis, which allows bacteria to populate the root canal system and invade the periradicular bone via the apical foramen at the root tip. The periodontal tissues and alveolar bone react to the insult with an inflammatory response, most commonly by the formation of an apical granuloma. Healing can occur after pathogen removal, which is achieved by disinfection and obturation of the pulp space by root canal treatment. This review highlights the various mechanisms of pathogen recognition and defense of dental pulp cells and periradicular tissues, explains the different cell types involved in the immune response and discusses the mechanisms of healing and repair, pointing out the close links between inflammation and regeneration as well as between inflammation and potential malignant transformation.

Comprehensive Characterization of 2 Immature Teeth Treated with Regenerative Endodontic Procedures.

INTRODUCTION: Regeneration of the pulp-dentin complex is the penultimate goal of regenerative endodontic procedures (REPs). Histological outcomes have demonstrated reparative tissue formation in human teeth extracted post-REPs. However, lack of accurate characterization has precluded identification of the true nature of tissues formed post-REP. METHODS: Here, we present 2 case reports of tooth #29 and #9 treated with REPs and demonstrate their clinical, radiographic, and histological outcomes. RESULTS: Clinical outcomes revealed healing of apical periodontitis in both teeth and re-establishment of vitality responses in tooth #29. Moreover, radiographic assessments using 2D and 3D-volumetric analyses demonstrate considerable increase in root development for both teeth. Further, histological outcomes evaluated using Hematoxylin and Eosin and immunohistochemical staining demonstrates presence of vascular and lymphatic structures as well as immune cell markers indicative of regeneration of an immunocompetent pulp. Lastly, examination of hard tissue deposition shows dentin-like tissue in parts of tooth #29 demonstrating for the first time, regeneration of a pulp-dentin complex post-REP. CONCLUSIONS: Collectively, this is the first study demonstrating recapitulation of several tissues commonly found as part of a pulp-dentin complex in teeth treated with REPs.

Multiple complex somatosensory systems in mature rat molars defined by immunohistochemistry.

OBJECTIVE: Intradental sensory receptors trigger painful sensations and unperceived mechanosensitivity, but the receptor bases for those functions are only partly defined. We present new evidence here concerning complex endings of myelinated axons in rat molars. DESIGN: We sectioned mature rat jaws in sagittal and transverse planes to analyze neural immunoreactivity (IR) for parvalbumin, peripherin, neurofilament protein, neurotrophin receptors, synaptophysin, calcitonin gene-related peptide (CGRP), or mas-related g-protein-receptor-d (Mrgprd). RESULTS: We found two complex sensory systems in mature rat molar dentin that labeled with neurofilament protein-IR, plus either parvalbumin-IR or peripherin-IR. The parvalbumin-IR system made extensively branched, beaded endings focused into dentin throughout each pulp horn. The peripherin-IR system primarily made unbeaded, fork-shaped dentinal endings scattered throughout crown including cervical regions. Both of these systems differed from neuropeptide CGRP-IR. In molar pulp we found peripherin- and parvalbumin-IR layered endings, either near special horizontal plexus arrays or in small coiled endings near tangled plexus, each with specific foci for specific pulp horns. Parvalbumin-IR nerve fibers had Aß axons (5-7µm diameter), while peripherin-IR axons were thinner Aδ size (2-5µm). Mechano-nociceptive Mrgprd-IR was only found in peripherin-IR axons. CONCLUSIONS: Complex somatosensory receptors in rat molars include two types of dentinal endings that both differ from CGRP-IR endings, and at least two newly defined types of pulpal endings. The PV-IR neurons with their widely branched, synaptophysin-rich, intradentinal beaded endings are good candidates for endodontic non-nociceptive, low threshold, unperceived mechanoreceptors. The complex molar dentinal and pulpal sensory systems were not found in rat incisors.

Influência do tratamento do substrato com plasma não térmico na resistência de união em cimentação adesiva / Influence of the substrate treatment with non-thermal plasma on bond strength of adhesive cementation

Objetivo: avaliar a influência do tratamento de superfície com plasma não térmico de argônio (PLA) na resistência de união de cimentos resinosos ao esmalte, à dentina e à cerâmica de dissilicato de lítio. Observar, no esmalte e na dentina, através de espectroscopia de infravermelho por transformada de Fourier (FTIR) os compostos inorgânicos e da cromatografia gasosa a alteração dos compostos orgânicos voláteis nas condições experimentais propostas. Material e Método: Foram avaliados 3 cimentos resinosos: Variolink Esthetic LC e N (Ivoclar Vivadent), e Panavia V5 (Kuraray). Foram utilizados 240 dentes bovinos, dos quais 150 tiveram a superfície do esmalte exposta e 90 a de dentina. Foram obtidas 150 lâminas de cerâmica de dissilicato de lítio (12 x 14 x 0,5 mm). Os grupos foram divididos de acordo com o tratamento de superfície e o substrato. Os tratamentos para as superfícies de esmalte e dentina foram: EA (esmalte/ácido fosfórico); DA (dentina/ácido fosfórico); EPS (esmalte/PLA 30 s); EPM (esmalte/PLA 1 min); DPS (dentina/PLA 30 s); EAPS (esmalte/ácido fosfórico/PLA 30 s) e EAPM (esmalte/ácido fosfórico/PLA 1 min); e, DAPS (dentina/ácido fosfórico/PLA 30 s). Os tratamentos para as superfícies da cerâmica foram: CA (cerâmica/ácido fluorídrico), CPS (cerâmica/PLA 30 s); CPM (cerâmica/PLA 1 min); CAPS (cerâmica/ácido fluorídrico/PLA 30 s) e CAPM (cerâmica/ácido fluorídrico/PLA 1 min). Posterior aos tratamentos, cilindros dos cimentos resinosos (0,8 mm/1,5 mm) foram confeccionados sobre as superfícies dos substratos. Após 48 h, os espécimes foram submetidos ao ensaio mecânico de microcisalhamento (10 Kgf/1 mm/min) até a fratura. A área fraturada foi analisada em estereomicroscópio. As superfícies tratadas e a interface adesiva foram analisadas por Microscopia Eletrônica de Varredura (MEV). Através do FTIR foram observados os espectros de amostras tratadas de esmalte e dentina. Os dados da resistência de união foram submetidos à análise estatística ANOVA e teste de Tukey (5%). Resultados: Para o esmalte os tratamentos de superfície não apresentaram diferença estatisticamente significante entre si; para a dentina o grupo DPS apresentou os maiores valores de resistência de união; e, para a cerâmica o tratamento CA apresentou os maiores valores de resistência de união. Para esmalte e dentina, o FTIR, mostrou alterações do conteúdo da água, carbonato e fosfato e a cromatografia gasosa das substâncias orgânicas voláteis. Conclusão: O tratamento de superfície com PLA não influencia a resistência de união de cimentos resinosos ao esmalte, aumenta à dentina e diminui ao dissilicato de lítio. As análises observacionais no FTIR sugerem que o plasma não altera compostos do esmalte e da dentina(AU)

Objective: to evaluate the influence of surface treatment with non - thermal argon plasma (PLA) on bond strength of resin cements to enamel, dentin and lithium disilicate glass ceramic; and, to observe, through Fourier Transform Modified Infrared Spectroscopy (FTIR), the inorganic compounds and through gas chromatography, the alteration of the volatile organic compounds, on the enamel and dentin, under the experimental conditions. Material and Method: Three resin cements: Variolink Esthetic LC and N (Ivoclar Vivadent) and Panavia V5 (Kuraray) were evaluated. Twenty hundred and forty bovine teeth were used, among which 150 specimens with enamel surface exposure and 90 with dentine exposure. One hundred and fifty lithium disilicate glass ceramic slices (12 x 14 x 0.5 mm) were obtained. The groups were divided according to the substrate and surface treatment. The treatments for enamel and dentin surfaces were: EA (enamel / phosphoric acid); DA (dentin / phosphoric acid); EPS (enamel / PLA 30 s); EPM (enamel / PLA 1 min); DPS (dentin / PLA 30 s); EAPS (enamel / phosphoric acid / PLA 30 s) and EAPM (enamel / phosphoric acid / PLA 1 min); and, DAPS (dentin / phosphoric acid / PLA 30 s). The treatments for the ceramic surfaces were: CA (ceramic / hydrofluoric acid), CPS (ceramic / PLA 30 s); CPM (ceramic / PLA 1 min); CAPS (ceramic / hydrofluoric acid / PLA 30s) and CAPM (ceramic / hydrofluoric acid / PLA 1 min). After the treatments, resin cement cylinders (0.8 mm / 1.5 mm) were built on the substrate's surfaces. After 48 h storage bond strength tests (µSBS) were performed in a universal testing machine (10 Kgf / 1 mm / min) until failure to fracture, and failure mode was analyzed under a stereomicroscope. The treated surfaces and the adhesive interface were analyzed by Scanning Electron Microscopy (SEM). The FTIR was used to observe the spectra of enamel and dentin treated samples. Bond strength data were submitted to ANOVA and Tukey test (5%). Results: for the enamel there was not a statistically significant difference among surface treatments; for the dentin, the DPS group presented the highest bond strength; and for the ceramic the AC treatment presented the highest values of bond strength. For the enamel and the dentin samples, the FTIR observations showed changes in water, carbonate and phosphate contents and the gas chromatography in the volatile organic substances. Conclusion: Surface treatment with PLA does not influence the bond strength of resin cements to the enamel, increases the bonding to dentin and decreases to the lithium disilicate. Observational analysis on FTIR suggest that non-thermal plasma does not alter enamel and dentin compounds(AU)

Immunohistochemical localization of SNARE core proteins in intrapulpal and intradentinal nerve fibers of rat molar teeth.

OBJECTIVE: The present study was designed to elucidate whether three soluble N-ethylmaleimide-sensitive fusion protein attachment protein receptor (SNARE) core proteins, syntaxin-1, synaptosomal-associated protein of 25kDa (SNAP-25), and vesicle-associated membrane protein-2 (VAMP-2), are present in the dental pulp of the rat molar at both the light and electron microscopic levels. DESIGN: Immunohistochemistry for protein gene product 9.5 (PGP 9.5), a pan-neuronal marker, syntaxin-1, SNAP-25, and VAMP-2 was performed on decalcified rat molars for light and electron microscopic analyses. Double-immunolabeling of PGP 9.5 and the SNARE core proteins, as well as combinations of the SNARE core proteins, was also carried out. RESULTS: PGP 9.5-immunoreactive nerve fibers ran toward the coronal region, ramified at the subodontoblast layer, and formed the subodontoblastic nerve plexus. Most nerve fibers penetrated the predentin and dentin along the dentinal tubules. Most, if not all, nerve fibers displayed immunoreactivity for syntaxin-1, SNAP-25, and VAMP-2. Immunoelectron microscopic analyses confirmed the presence of immunoreactivity for the SNARE core proteins within the intradental axonal elements. CONCLUSIONS: The present findings suggest that, since SNARE core proteins participate in the docking and exocytosis of synaptic vesicles in the central nervous system, they may contribute to vesicle exocytosis from the dental nerve fibers even though there are no apparent synapses.

Glial network responses to polymicrobial invasion of dentin.

This study investigated the distribution patterns of glial networks disclosed by reactivity for glial fibrillary acidic protein (GFAP) and S100B in healthy and carious human teeth. The objective was to determine the assembly and collapse of glial networks in response to encroaching infection. 15 healthy and 37 carious posterior teeth from adults were studied. Immediately after extraction, teeth were cleaned and vertically split and the half with pulp fixed and prepared for resin or frozen sections. Sections were stained with toluidine blue and for immunofluorescence, with observation by confocal laser microscopy and analysis by ImageJ software. Carious teeth were subdivided into three groups according to degree of carious involvement: microbial penetration through enamel (stage A), extension into dentin (stage B) and advanced penetration into dentin but without invasion of underlying pulp tissue (stage C). In stage A lesions there was marked increase in glial networks in dental pulp tissue that extended beyond the zone of microbial invasion. This response was maintained in stage B lesions. In advanced stage C lesions these networks were degraded in the zone of invasion in association with failure to contain infection. Cells expressing the glial markers GFAP and S100B showed a response to initial microbial invasion of dentin by increase in number and altered anatomical arrangement. The late stage of dentinal caries was marked by collapse of these networks in the region adjacent to advancing bacteria. This behaviour is important for understanding and explaining the defensive response of the neurosensory peripheral dental pulp apparatus to infection.

Cellular and molecular mechanisms of dental nociception.

Due, in part, to the unique structure of the tooth, dental pain is initiated via distinct mechanisms. Here we review recent advances in our understanding of inflammatory tooth pain and discuss 3 hypotheses proposed to explain dentinal hypersensitivity: The first hypothesis, supported by functional expression of temperature-sensitive transient receptor potential channels, emphasizes the direct transduction of noxious temperatures by dental primary afferent neurons. The second hypothesis, known as hydrodynamic theory, attributes dental pain to fluid movement within dentinal tubules, and we discuss several candidate cellular mechanical transducers for the detection of fluid movement. The third hypothesis focuses on the potential sensory function of odontoblasts in the detection of thermal or mechanical stimuli, and we discuss the accumulating evidence that supports their excitability. We also briefly update on a novel strategy for local nociceptive anesthesia via nociceptive transducer molecules in dental primary afferents with the potential to specifically silence pain fibers during dental treatment. Further understanding of the molecular mechanisms of dental pain would greatly enhance the development of therapeutics that target dental pain.

How can sensitive dentine become hypersensitive and can it be reversed?

This paper reviews a number of studies in oral biology and endodontics that deal with the reactivity of the pulpo-dentine complex in response to mechanical and immunological stimuli. It can be hypothesized that these reactions could also apply to changes in dentine sensitivity following periodontal procedures. Some of these changes involve neurogenic inflammation of the pulp under exposed open tubules; this increases the rate of outward fluid flow through the tubules, making the overlying exposed dentine more sensitive. Other changes may be due to inflammation-related nerve sprouting of pulpal nerves, which can lead to innervation of more tubules than normal. Changes may also involve upregulation of new, more sensitive ion channels in the membranes of these nerves. The goal of the paper is to increase awareness of the complex issues involved in dentine sensitivity, so that future investigators may develop agents or techniques to stimulate mechanisms that mitigate dentine sensitivity, or to block mechanisms that aggravate the condition, for therapeutic effect.

Nerve-targeted desensitizing toothpastes occlude dentin tubules and induce mineral precipitation.

PURPOSE: To examine the laboratory dentin tubules occlusion and mineral precipitation capability of two potassium salts-containing desensitizing toothpastes. METHODS: 40 dentin disks were obtained and divided into four groups, including artificial saliva (AS), distilled water (DW), Sensodyne Freshmint (SF) and Colgate Sensitive (CS). Dentin permeability measurement was performed after EDTA etching, initial brush, 3-day brush, 7-day brush and citric acid challenge, respectively. Attenuated total reflection Fourier transform infrared spectroscopy (ATR-FTIR) was used to monitor the variation of mineral content before and after treatments. The ultra-morphology of dentin surface was examined using scanning electron microscopy (SEM) to evaluate tubule occlusion. RESULTS: The two potassium salts-containing desensitizing toothpastes significantly reduced dentin permeability to less than 40% after 7-day treatment (P<0.05). The ATR-FTIR analysis showed increase of the intensity of the phosphate peak after a 7-day brushing period using both of the tested toothpastes. However, the dentin permeability significantly increased and the intensity of phosphate peak decreased after acid etching for all groups. The SEM examination revealed partially occluded dentin tubules after toothpaste treatments, but after the acid challenge the tubules were opened again.

Effect of nitrous oxide on the efficacy of the inferior alveolar nerve block in patients with symptomatic irreversible pulpitis.

INTRODUCTION: The inferior alveolar nerve (IAN) block does not always result in successful pulpal anesthesia. Anesthetic success rates might be affected by increased anxiety. Nitrous oxide has been shown to have both anxiolytic and analgesic properties. Therefore, the purpose of this prospective, randomized, double-blind, placebo-controlled study was to determine the effect of nitrous oxide on the anesthetic success of the IAN block in patients experiencing symptomatic irreversible pulpitis. METHODS: One hundred emergency patients diagnosed with symptomatic irreversible pulpitis of a mandibular posterior tooth were enrolled in this study. Each patient was randomly assigned to receive an inhalation regimen of nitrous oxide/oxygen mix or room air/oxygen mix (placebo) 5 minutes before the administration of the IAN block. Endodontic access was begun 15 minutes after completion of the IAN block, and all patients had profound lip numbness. Success was defined as no or mild pain (visual analog scale recordings) on access or instrumentation. RESULTS: The success rate for the IAN block was 50% for the nitrous oxide group and 28% for the placebo group. There was a statistically significant difference between the 2 groups (P = .024). CONCLUSIONS: For mandibular teeth diagnosed with symptomatic irreversible pulpitis, administration of 30%-50% nitrous oxide resulted in a statistically significant increase in the success of the IAN block compared with room air/oxygen.

Dentin hypersensitivity and its management.

Dentin hypersensitivity is a common patient complaint that is more prevalent than the profession realizes. It is important for dentists to diagnose dentin hypersensitivity by exclusion and provide appropriate treatment recommendations for patients. Various treatment methods have been proposed but no universally accepted desensitizing agent or treatment has been identified. When a patient has symptoms that can be attributed to dentin hypersensitivity, a thorough clinical examination should be carried out to rule out other likely causes prior to diagnosis and treatment. Depending on the identified cause, a combination of individualized instructions on proper oral health behaviors, use of at-home products, and professional treatment may be required to manage the problem.

Management of dentinal hypersensitivity: a review.

Dentinal hypersensitivity is a very common clinical finding that can cause considerable concern for the patient. Clinicians must understand the various etiological factors, their complexities, and numerous treatment options available. This article reviews the etiology, management, and prevention of dentinal hypersensitivity.

Electrophysiological observations on the effects of potassium ions on the response of intradental nerves to dentinal tubular flow in the cat.

OBJECTIVE: To determine the effects of K(+) on the sensitivity of sensory receptors in teeth to fluid flow through dentine. METHODS: Evoked discharges were recorded from intradental nerves in anaesthetised cats during the application of 5s hydrostatic pressure stimuli to exposed dentine through either normal Ringer's or Ringer's containing up to 255 mmol/lK(+). The stimuli ranged between -500 and +500 mm Hg. RESULTS: The number of impulses evoked by a positive pressure stimulus increased, and the latency of the response decreased, as either the pressure or the K(+) concentration of the Ringer's was increased. The response to a negative pressure stimulus applied 2s after a positive pressure pulse of equal but opposite amplitude decreased as either the intensity of the stimulus or the K(+) concentration of the Ringer's was increased. CONCLUSIONS: Potassium ions that were transported into the dentine and pulp by bulk flow during the application of positive pressure stimuli increased the sensitivity of the receptors to inward tubular flow but decreased their sensitivity to outward flow.

Teaching dental pain with and without underlying oral physiology: learning implications.

This study investigated whether teaching undergraduate dental students the diagnosis and management of acute dental pain alongside the underpinning oral physiology helped them to understand the topic better than teaching them acute dental pain as a separate entity. Each of three clinical years of dental students at the same dental school was taught in two groups. Each group was taught the signs/symptoms of five acute dental pain conditions by the same member of the staff. However, the teaching for one group of students in each year reminded the students about the physiology that underpinned the clinical symptoms. One week later, the students completed an open-ended questionnaire that required them to list signs/symptoms of the five dental pain conditions. For each year of dental students that was examined, the mean student marks were significantly higher (p<0.05) for those who were taught dental pain and the underlying physiology compared with students who were only taught dental pain as a stand-alone subject. This suggests that integrating biomedical science and clinical teaching is beneficial.

Management of dentinal hypersensitivity.

Dentinal hypersensitivity is a complex condition that can cause considerable concern in the dental office. Despite the large number of available treatment modalities, no current desensitizing agent is considered ideal for managing this uncomfortable condition. Selecting the right therapy requires a complete understanding of how applying a stimulus to the exposed dentin surface can influence the nerve fibers and produce hyperesthesia. This article reviews the etiology and critically analyzes management of dentinal hypersensitivity by reviewing laboratory and clinical investigations.

In-office treatment of dentinal hypersensitivity.

Dentinal hypersensitivity is a common dental complaint, especially in periodontal patients. It is believed to be mediated by a hydrodynamic mechanism in which various stimuli result in increased fluid flow in dentinal tubules, thereby generating action potentials in associated nerve fibers. Although it is often perceived as mild discomfort by the patient, it can be severe. A variety of interventions has been used, although few have been subjected to rigorous study. This article surveys those in-office treatments that are available, and suggests directions for research so that clinicians may treat patients based on best evidence. Until such evidence is available, it seems prudent to employ therapies that are least likely to cause harm and are reversible.

Pulpal status of human primary teeth with physiological root resorption.

OBJECTIVE: The overall aim of this study was to determine whether any changes occur in the pulpal structure of human primary teeth in association with physiological root resorption. METHODS: The experimental material comprised 64 sound primary molars, obtained from children requiring routine dental extractions under general anaesthesia. Pulp sections were processed for indirect immunofluorescence using combinations of: (i) protein gene product 9.5 (a general neuronal marker); (ii) leucocyte common antigen CD45 (a general immune cell marker); and (iii) Ulex europaeus I lectin (a marker of vascular endothelium). Image analysis was then used to determine the percentage area of staining for each label within both the pulp horn and mid-coronal region. Following measurement of the greatest degree of root resorption in each sample, teeth were subdivided into three groups: those with physiological resorption involving less than one-third, one-third to two-thirds, and more than two-thirds of their root length. RESULTS: Wide variation was evident between different tooth samples with some resorbed teeth showing marked changes in pulpal histology. Decreased innervation density, increased immune cell accumulation, and increased vascularity were evident in some teeth with advanced root resorption. Analysis of pooled data, however, did not reveal any significant differences in mean percentage area of staining for any of these variables according to the three root resorption subgroups (P > 0.05, analysis of variance on transformed data). CONCLUSIONS: This investigation has revealed some changes in pulpal status of human primary teeth with physiological root resorption. These were not, however, as profound as one may have anticipated. It is therefore speculated that teeth could retain the potential for sensation, healing, and repair until advanced stages of root resorption.

Time-dependent activation of ERK1/2 in nerve terminals of the dentin-pulp complex following bradykinin treatment.

The extracellular signal-regulated kinases 1 and 2 (ERK1/2) have been implicated in the inflammation-dependent sensitization of nociceptors, and the inflammatory mediator bradykinin (BK) led to a reduced threshold in the nociceptor terminals, activating intracellular signaling by phosphorylating receptors and ion channels. The effects of BK on the non-transcriptional modulation of the ERK1/2 in the peripheral nociceptor terminals, including in nerve endings of the dentin-pulp complex, are unknown. The time-dependent effects of BK (10(-7) M) on the ERK1/2 phosphorylation in nerve terminals of the dentin-pulp complex were investigated by quantitative and double immunolabeling with organ bath experiments. In nerve terminals, total and p-ERK1/2 were detected. In comparison with the controls, the numbers of p-ERK1/2-positive nerve endings increased after 1 and 3 min and decreased after 10 min of BK treatment. Analysis of the data indicates that BK induces phosphorylation-mediated local activation of ERK1/2 in nerve terminals modulating nociception in the dentin-pulp complex.

Sympathetic nerve fibers sprout into rat odontoblast layer, but not into dentinal tubules, in response to cavity preparation.

This study was designed to determine if sympathetic nerve fibers exist in dentinal tubules in rat normal dental pulp, and if they sprout into the dentinal tubules in response to artificial cavity preparation in dentin. Sympathetic nerve fibers in rat molar dental pulp were labeled using an anterograde axonal transport technique involving injection of wheat germ agglutinin-horseradish peroxidase (WGA-HRP) into the superior cervical ganglion (SCG). They were then observed using light and electron microscopes. In normal dental pulp (control), scattered WGA-HRP reaction products were observed in unmyelinated nerve endings in the odontoblast layer and subodontoblastic region. In injured pulp 3 weeks after cavity preparation, reaction products were about 1.8-times more plentiful in the above areas (versus control pulp). However, no labeled nerve fibers were observed in the dentinal tubules in either control or injured dental pulp. These results indicate that although sympathetic nerve fibers do indeed sprout in rat dental pulp in response to cavity preparation, they do not penetrate into the dentinal tubules in which postganglionic nerve endings derived from the SCG were not originally present.

The relationship between the discharge of intradental nerves and the rate of fluid flow through dentine in the cat.

OBJECTIVE: To investigate further the relationship between dentinal tubular flow and the discharge evoked in intradental nerves. DESIGN: In anaesthetised cats, recordings were made of fluid flow through dentine during the application of hydrostatic pressure stimuli of 5 s duration in the range +500 to -500 mm Hg to exposed dentine and of the nerve impulses evoked by these stimuli. Single unit recordings were obtained from filaments dissected from the inferior alveolar nerve and multi-unit recordings, from the exposed dentine. RESULTS: Of 20 single units tested, 10 (conduction velocities: 2.4-36.2 m s(-1)) responded to negative pressures and four of these, also to positive pressures. None responded to only positive pressures. The pressure thresholds of the units (single and multi-unit preparations) ranged from -100 to -500 and +100 to +500. In terms of flow (measured 1 s after the start of a stimulus) the thresholds ranged from 0.4 to 2.2 nl s(-1) mm(-2) exposed dentine with outward flow, and 0.4-2.1 nl s(-1) mm(-2) with inward flow. The outward flow per tubule at the threshold of the most sensitive units was estimated to be 21 fl s(-1) and the corresponding mean velocity of the contents of the dentinal tubules at their pulpal ends, 27 microm s(-1). Although the thresholds to outward and inward flow were similar, with outward flow the mean discharge rate increased with stimulus intensity; whereas with inward flow few impulses were evoked and the number was little affected by the stimulus intensity. CONCLUSION: The transduction mechanism that generates impulses in hydrodynamic intradental afferents is much more responsive to outward than inward flow through the dentinal tubules, although the thresholds in both directions are similar.