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PubMed1987

Arachidonic-acid metabolism in normal and experimentally-inflamed rat dental pulp.

Pulp homogenates were incubated with [14C]-arachidonic acid and the metabolites separated by thin-layer chromatography. The main products of normal pulp were 6-keto-prostaglandin (PG) F1 alpha and 12-hydroxy-eicosatetraenoic acid (12-HETE), further identified by high performance-liquid chromatography. Thromboxane (TX) B2, and PGD2, E2 and F2 alpha were also detected at less than 30 per cent of 6-keto-PGF1 alpha. When the pulp was inflamed by applying bacterial lipopolysaccharide, production of all these metabolites increased; in particular, PGE2 was increased 9.3-fold compared with normal, and 6-keto-PGF1 alpha and HETE 3.8- and 2.0-fold, respectively. An unidentified product, slightly more polar than 12-HETE, was also markedly produced by the inflamed pulp. Thus arachidonic-acid metabolites including lipoxygenase products may be involved in the development of pulpal inflammation.

6-Ketoprostaglandin F1 alpha↗
PubMed1989

Involvement of arachidonic acid metabolites in increases in vascular permeability in experimental dental pulpal inflammation in the rat.

Pulp was experimentally inflamed by applying bacterial lipopolysaccharide (LPS). Changes in arachidonic acid (AA) metabolites were determined by measuring the conversion of exogenously added AA in pulp homogenates. The inflamed pulp produced 12-hydroxy-eicosatetraenoic acid (12-HETE), 6-keto-prostaglandin (PG) F1 alpha greater than PGE2, thromboxane B2 and 11-HETE, which was further identified with high-performance liquid chromatography. The LPS treatment caused a 2.0-fold increase in 12-HETE production at 1 h, a 3.8-fold increase in 6-keto-PGF1 alpha production at 12 h and increases in PGE2 and 11-HETE production of 8.8- and 5.5-fold, respectively, at 24 h. Vascular permeability in the inflamed pulp was measured by quantifying the amount of an extravasated dye; it increased markedly from 6 h and reached a peak at 12 h after the LPS application. When indomethacin (0.3-30 mg/kg, s.c.) was given before LPS, both the production of 6-keto-PGF1 alpha and PGE2 and the increase in vascular permeability were inhibited dose dependently. Exogenously applied PGE2 and PGI2 methyl ester reduced the inhibition of the increase in vascular permeability caused by indomethacin. Thus PGE2 and PGI2 may be involved in increases in vascular permeability in pulpal inflammation.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1990

An immunocytochemical study of the morphological reaction of nerves containing calcitonin gene-related peptide to microabscess formation and healing in rat molars.

Pulpal inflammation was induced by cutting a class V cavity to within 0.1-0.3 mm of the pulp on the mesial aspect of maxillary and mandibular first molars at the cervical line. The exposed dentine was briefly acid-etched and left open to the mouth until the animals were killed. Histological examination of teeth 4 days after injury showed microabscesses, blood vessel dilation and increased numbers of terminal nerve sprouts around the lesion and in radicular pulp and dentine. Specimens at 7, 11, 21 and 35 days after injury showed progressive healing of the lesions with the formation of reparative dentine and a coincident return to a normal patterns of innervation in the remaining pulp. Thus pulpal nerves are not static structures, but rather are capable of rapid change in response to inflammation. The morphological association of CGRP-immunoreactive nerve fibres with the edges of the healing lesions and with zones of reparative dentine suggests a role for these fibres and for the neuropeptide CGRP in the healing response of pulpal tissue.

Abscess↗
PubMed1990

Effects of zinc oxide-eugenol on leucocyte number and lipoxygenase products in artificially inflamed rat dental pulp.

The number of leucocytes and level of endogenous LTC4 in the pulp tissue were measured by a histological method and radioimmunoassay, respectively. When the mandibular incisor pulp was irritated by drilling a hole in the dentine without using any coolant, the number of polymorphonuclear leucocytes and lymphocytes and the concentration of LTC4 increased to 3.2, 1.9 and 1.8 times their respective levels in normal pulp 6 h after the injury. The total leucocyte number in blood collected from these rats was also increased significantly. In contrast, when the cavities cut in dentine were filled with a zinc oxide-eugenol mixture (powder: liquid 100 mg/25 microliters), the increase in the number of cells was significantly curtailed, and the LTC4 level fell to 50% of that in normal pulp within 1 h after the filling. No decrease in the LTC4 level was observed after filling with a zinc oxide-water mixture, but the level decreased in response to an increase in eugenol content in the zinc oxide-eugenol placed in the cavity. Biosynthesis of [14C]-HETE and HPETE from [14C]-arachidonic acid was inhibited by the addition of 10 microM eugenol to the pulp homogenate. Thus eugenol released from zinc oxide-eugenol inhibited the biosynthesis of lipoxygenase products and the early chemotactic accumulation of leucocytes.

Animals↗
PubMed1991

Regeneration of calcitonin gene-related peptide immunoreactive nerves in replanted rat molars and their supporting tissues.

First maxillary right molars in 66 rats were elevated and replanted and the pulps allowed to regenerate for 1-90 days. The contralateral tooth served as control. Regeneration of nerves in the pulp and periodontium was studied by CGRP-immunohistochemistry and the avidin-biotin-peroxidase method. The pulp and periodontium of the controls were richly supplied with CGRP-labelled nerves. One day after replantation the pulp was completely devoid of CGRP-immunoreactive nerves. After 2 days, axon sprouts were present in the apical, regenerated pulp and in the periodontium. From 3-7 days CGRP-immunoreactive axons were regularly seen to have regenerated in front of the cellular inflammation in the pulp. After 10 days, the pulps were reinnervated up to the horns, although more sparsely than in the controls. From day 20-90 there was a marked divergence in pulpal healing: 17 pulps formed irregular postoperative dentine with a gradual increase in nerve density; 16 pulps remained sparsely innervated and were gradually replaced by bone. Root resorption was most extensive in the teeth with bone replacement of pulp. The soft tissue adjacent to extensive resorbing areas had many more CGRP-labelled axons than in the controls. The reinnervation of the regenerating pulp occurred at the same time as pulpal wound healing, but did not achieve the innervation density of the controls.

Animals↗
PubMed1992

Effect of ageing on responses of nerve fibres to pulpal inflammation in rat molars analysed by quantitative immunocytochemistry.

The response of sensory nerve fibres to inflammation in young adult rat molars has recently been shown to include increases in nerve sprouting and neuropeptide content. The objective was to evaluate neural responses to class V dental preparations in molars of old (1-2 yr) as compared with young adult rats (3-4 months). Tissues were investigated immunocytochemically 4 days post-injury for the sensory neuropeptides calcitonin gene-related peptide (CGRP) and substance P. Quantitative image analysis of the material demonstrated that more immunoreactivity was present for CGRP than for substance P in intact control teeth for each age group. Four days after injury, both immunoreactivities were increased in pulp adjacent to the injury in both young and old teeth. The increase depended on at least three factors: (1) enhanced immunoreactivity of the nerve fibres; (2) increased terminal nerve sprouts near the injury and (3) elevated peptide content of the pulp tissue. Although the incidence of CGRP- and substance P-immunoreactive nerve fibres had decreased in older teeth, the proportional increases in both neuropeptides near the injury were greater in old than in young teeth, owing to a reduction in pulpal volume during ageing. Pulpal tissue was also immunostained for the low-affinity nerve growth factor receptor (p75-NGFR) as an index of pulpal ageing; and an extensive decrease was found in the old adult as compared to young adult rats. These results indicate that old rats maintain the capacity for nerve sprouting despite the decreases in p75-NGFR labelling of pulp cells, pulp volume and nerve fibre numbers that occur as part of dental ageing.

Aging↗
PubMed1993

Role of substance P in neurogenic inflammation in the rat incisor pulp and the lower lip.

Vascular permeability was significantly increased in the incisor pulp and skin of the lower lip in the rat after antidromic electrical stimulation of the inferior alveolar nerve, and this response was significantly inhibited by a substance-P antagonist. The content of substance P in the pulp and lip was also increased after stimulation. The permeability response was reduced by aspirin and bradykinin antagonists (both B1- and B2-receptor types) in the pulp and lip, indicating that prostaglandins and bradykinin may be involved. Mepyramine and methysergide inhibited the vascular response in the lip but not the pulp; the roles of histamine and serotonin differ in the two tissues. Injection of substance P into the incisor pulp and the lip skin caused dye leakage. This response was inhibited by pretreatment with compound 48/80 in the lip but not the pulp. Lip histamine content was decreased significantly after antidromic stimulation of the inferior alveolar nerve and pretreatment with compound 48/80, but was not changed in the pulp. The results suggest that substance P in the lip, after being released from the peripheral sensory-nerve endings, may act on the vascular system via histamine release from mast cells; but in the pulp may cause vascular response directly because of the scarcity of mast cells.

Animals↗
PubMed1994

Dynamic plasticity of dental sensory nerve structure and cytochemistry.

Hypersensitive dentine responds to normal changes in touch or temperature with abnormal pain sensations. This paper reviews studies that have shown dynamic changes in sensory nerve structure, cytochemistry and location after tooth injury, suggesting that those changes contribute to dentine hypersensitivity. Nerve fibres containing calcitonin gene-related peptide (CGRP) are the main type of sensory fibre to innervate dentine. Evidence that many of those dentinal nerve endings originate from small myelinated fibres is presented here. The location of CGRP nerve terminals correlates with the pulpal gradients of nerve growth factor that have been demonstrated in normal teeth by in situ hybridization histochemistry. When shallow cavities are drilled into the outer dentine of rat molars a five-to-eight-fold increase in pulpal nerve growth factor precedes the extensive structural changes in the sensory nerve reactions eventually subside if healing occurs, but both continue if inflammation continues. Evidence correlating pulpal inflammation with long-term changes in central trigeminal pain pathways is reviewed. There can be extensive neuroplasticity after tooth injury, both within dental pain fibres and in central pain pathways. The timing of those alterations of nerve structure, location, and cytochemistry is consistent with their involvement in mechanisms of dentine hypersensitivity.

Animals↗
PubMed1994

Endogenous vasoactive substances and oxygen-derived free radicals in pulpal haemodynamics.

An adequate blood supply to the dental pulp is essential to the health of the tooth. A recent concept is that repeated stimulation of sensitive teeth may induce pulpal changes; this could occur through induction of neurogenic inflammation and alteration of pulpal blood flow. One possibility is that production of oxygen-derived free radicals at sites of inflammation contributes to alterations in local blood flow. The first target of free radicals, generated in several pathological processes, is the vascular system (essentially the endothelium). Although the exact mechanism by which free radicals induce changes in vascular conductance is still uncertain, they may act directly on vascular smooth muscle or modify vascular tone by interacting with the production and/or biological activity of endogenous vasoactive mediators. Recent data indicate that the oxygen-derived, free radical-generating system can decrease pulpal blood flow in the dog via endothelial dysfunction when applied locally in deep dentinal cavities. In addition to the part played by oxygen-derived free radicals, the measurement of pulpal blood flow and the effects of endogenous vasoactive substances on flow are discussed.

Animals↗
PubMed1994

Nerve-pulp interactions.

Pulpal haemodynamics are naturally intermeshed with inflammatory responses. Cellular and humoral factors may be the vehicles that aid in physiological regulation, but when these systems are overly activated, they may lead to pathological changes. Sensory nerves may initiate inflammatory reactions when activated, and interestingly, recent findings show that vasoconstrictor nerves in the pulp can inhibit the release of neurally stored vasoactive and inflammatory mediators. Thus, there are options for endogenous control of inflammation. Perhaps a variation in the effectiveness of such control can explain why symptoms of hypersensitivity and pain are so unpredictable and individual. What naturally occurring agents are involved in early tissue changes and how do they act? Some agents exert their effects both on vessels and nerves. Thus, there is an intriguing mutual interplay between nerves and tissue reactions. A prolonged, painful stimulation may generate increased blood flow and inflammation, and vice versa, inflammation may lead to pain. This complexity of mechanisms generates many questions that need answers.

Animals↗
PubMed1995

Immunohistochemical study on the immunocompetent cells of the pulp in human non-carious and carious teeth.

The condition of the pulp tissue was classified into seven groups according to the depth of carious lesions from stage (S) 0 (non-carious teeth) to S6 (exposed pulp). A substantial change in the infiltration of immunocompetent cells occurred between S3 and S4; all types were markedly increased in S4 as compared to S3, with a remarkable increase in the number of helper T lymphocytes, B-lineage cells, neutrophils and macrophages. Therefore, the pulpal immune reaction to carious stimuli could be classified into early (S1-S3) and advanced phases (S4-S6). In the early phase a cellular immunoresponse would be induced by T-lineage cells, and in the advanced phase the humoral immunoresponse is furthered by B-lineage cells concomitant with the destruction of pulp tissue by proteolytic enzymes released from infiltrating neutrophils and macrophages. Human dental pulp is thus equipped with a functional immune response that is sufficient as a biodefensive mechanism. Dental caries should be treated before S4.

Adult↗