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Eight ingredients of composite materials were evaluated individually for pulp irritation. None caused significant inflammation as evidenced by its average response. No abscess formations or lesions predominating in leukocytes occurred.
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ATP-degrading enzyme activities in pulps of healthy and carious human teeth were quantitatively analyzed using the bioluminescence method. The patterns of both Ca2+- and MG2+-activated ATP hydrolysis resembled each other. Increased enzyme activities were observed during injured states.
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The findings from the recent literature on pulpal cell responses to the application of calcium hydroxide to exposed pulps are described. The effect of calcium hydroxide on healthy and inflamed pulp is discussed. The effect of incorporation of calcium hydroxide in various pulp-capping agents is presented. The initial effect of calcium hydroxide applied to exposed pulp is the development of a superficial three-layer necrosis. The beneficial effect of calcium hydroxide is regarded as the result of the chemical injury caused by the hydroxyl ions, limited by a zone of firm necrosis against the vital tissue, and the toleration of calcium ions by the tissue. The firm necrosis causes slight irritation and stimulates the pulp to defense and repair. The observed sequence of tissue reactions is that which is expected when connective tissue is wounded. It starts with vascular and inflammatory cell migration and proliferation, to control and elimination of the irritating agent. This is followed by the repair process, including migration and proliferation of mesenchymal and endothelial pulp cells and formation of collagen. When the pulp is protected from irritation, odontoblasts differentiate, and the tissue formed assumes the appearance of dentin, i.e., the function of the pulp is normalized. The mineralization of the collagen starts with dystrophic calcification of both the zone of firm necrosis and the degenerated cells in the adjacent tissue, leading to deposition of mineral in the newly-formed collagen. The presence of calcium ions stimulates precipitation of calcium carbonate in the wound area and thereby contributes to the initiation of mineralization.(ABSTRACT TRUNCATED AT 250 WORDS)
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Lipopolysaccharides (LPS) from Bacteroides oralis and Veillonella parvula and cell wall material from Lactobacillus casei were studied for their capacity to induce leukocyte migration in the dental pulp and in an implanted wound chamber. Three adult monkeys were challenged using lyophilized material sealed into buccal Class V cavities prepared in dentin. Pulp tissue responses were observed histologically eight and 72 hours after initiation of the experiment. Subjacent to cut dentinal tubules, bacterial materials induced polymorphonuclear leukocyte (PMN's) infiltration in the pulp tissue of the majority of test teeth examined. Responses were similar for the three bacterial test materials at both time periods. Topical applications of bovine serum albumin (BSA), used as a control, induced significantly less accumulation of PMN's. Assessments of induced exudate volumes and leukocyte densities in chambers implanted in rats showed comparable rankings with pulpal experiment between test (i.e., bacterial) and control (BSA) materials. Analysis of the data indicates that high-molecular-weight complexes of bacterial cell walls may adversely affect pulpal tissue across freshly exposed dentin.
The most common method of evaluating pulp tissue reactions to injury is by a qualitative assessment of pulp tissue alterations. This evaluation method is subjective and difficult to quantify; stereological methods are more suitable, for they can quantify important tissue components, and so more objectively describe pulp tissues. This study compares a morphometric and a descriptive method of classification for pulp tissue analysis by using 15 teeth with inflamed pulp tissue, and 12 teeth experimentally pulp-capped with calcium hydroxide. Morphometric analysis allowed for volumes of remaining dentin, pulp tissue, inflamed pulp tissue, and reparative dentin to be calculated. In addition, volume densities of polymorphonuclear and mononuclear leukocytes, odontoblasts, fibroblasts, erythrocytes, vessels, and residual tissue were calculated for comparison among different experimental teeth. The morphometric method provided a quantitative description of tissue reactions. The descriptive method of classification was adequate when inflamed tissue subjacent to the cavity was evaluated, but was less precise than the morphometric method in describing reactions deeper in the tissue. The descriptive method could delineate the amounts and types of inflammatory cells only in non-quantified terms, while the morphometric method could quantify and locate them. It also yielded a quantified evaluation of the healing sequence of experimentally pulp-capped teeth. In conclusion, a morphometric method can yield more quantitative data on pulp tissue reactions than can a descriptive method of classification.
The occurrence and distribution of the regulatory peptide endothelin in normal and inflamed human dental pulp was studied by immunocytochemistry. Endothelial cells in both normal and inflamed pulp displayed endothelin-like immunoreactivity. Neither pulp cells nor dental nerves were immunoreactive. No significant change in the distribution of endothelin immunoreactivity could be detected in the samples of inflamed pulp tissue, the immunoreactive material being detectable only within the endothelium. However, the intensity of the immunostaining was less intense in the samples of inflamed pulp. It is reasonable to presume that endothelin, produced and released locally by endothelial cells, may participate via a paracrine mechanism in the regulation of blood pressure and flow in normal and pathological human dental tissues.
Components of primary (azurophilic) granules of polymorphonuclear leukocytes (PMNs) have been implicated as important mediators in pulpal inflammation. This anatomical study used ultracryoimmunocytochemical techniques and characterized and contrasted the subcellular distributions of human PMN elastase (PMN-E), PMN cathepsin-G (PMN-CG), and alpha-2 macroglobulin (alpha-2M) in healthy and inflamed dental pulps. Inflamed pulpal tissue sections revealed an intense distribution of PMN-E in the extracellular domain throughout the collagen matrix. PMN-E was also localized in the perinuclear cytoplasm of PMNs and distributed in a random fashion. PMN-CG was localized intensely in the intracellular granules of PMNs and observed moderately within the extracellular matrix. Healthy pulpal tissues exposed to PMN-E and PMN-CG antibodies revealed no evidence of PMN infiltration and no specific labeling. alpha-2M, a natural serum inhibitor of PMN-E and PMN-CG, was distributed in an intense fashion within the intravascular compartments of both inflamed and healthy pulpal samples. Immunogold-labeling for alpha-2M was observed in moderate amounts within the extravascular domain of inflamed pulpal samples but only in mild amounts within the same area of healthy tissues. These results suggest that PMN-E and PMN-CG are released to the extracellular matrix of irreversibly inflamed teeth, enabling them to facilitate pulpal connective tissue destruction. Conversely, moderate extravascular labeling for alpha-2M within inflamed samples suggests a physiological attempt at inhibiting the pulpal connective tissue destruction mediated by human PMN-E and PMN-CG.
In previous work, the diffusion of monomers from composite and bonding resins through dentin was demonstrated in vitro. The monomers triethylene glycol dimethacrylate (TEGDMA) and 2-hydroxyethyl methacrylate (HEMA) were identified in samples from the pulp space. In the current study, we examined the effects of two levels of positive hydrostatic pressure on the passage of resin monomers through dentin in vitro from a composite-resin/bonding-resin combination to test the hypothesis that monomer diffusion is prevented by such pressure. An occlusal cavity prepared in the tooth crown was restored with the resins. Distilled water samples from the pulpal space were removed over time and analyzed for monomer content by high-performance liquid chromatography and mass spectrometry. Positive pulpal pressure reduced but did not prevent pulpward movement of diluent monomers that leach from bonding agents and from resin composites through dentin in vitro. The degree of reduction of diffusion was greater with TEGDMA than with the lower-molecular-weight monomer HEMA.
Neuroplastic changes are known to occur in the CNS in response to injury of peripheral nerves. Previous investigation has demonstrated neuroplasticity in second-order neurons of the subnucleus oralis (SO) of the trigeminal (V) nuclear complex in association with aseptic injury to the tooth pulp. A question arises, therefore, as to whether similar changes occur in response to injury associated with inflammation induced by tooth pulp infection. The effects of tooth pulp infection on the mechanoreceptive fields (RFs) of SO neurons were examined in rats. Infection was established by exposure and removal of the coronal pulp of the mandibular first molar, which was left open to the oral environment for 7 (n = 5) or 28 (n = 6) days. Neurons in SO were then electrophysiologically characterized in chloralose/urethane-anesthetized rats. The RF and the response properties of 118 low-threshold mechanoreceptive (LTM) neurons from seven-day-old rats and 149 LTM neurons from 28-day-old rats were compared with those of 204 LTM neurons tested in 11 untreated (control) rats. Significant differences were noted in RF size and location when control, seven-day-old, and 28-day-old groups were compared. Radiographic examination revealed inconsistencies among examiners in the interpretation of periapical lesions < 2 mm in diameter and general agreement in the identification of periapical lesions > 2 mm in diameter. Histological examination of teeth with pulp exposure revealed superficial necrosis and inflammation without periapical extension in the seven-day-old animals and total pulp necrosis with periapical inflammation, abscess formation, and alveolar bone resorption in the 28-day-old animals. The results indicate that neuroplastic changes in LTM oralis neurons can develop subsequent to tooth pulp infection and that there may be a correlation between the incidence of these changes and the extension of the attending inflammation from the pulp to the dental supporting tissues.
Inflammatory changes in the dental pulp are accompanied by release of a wide variety of chemical mediators. Nitric oxide, an oxidative free radical produced by the enzyme nitric oxide synthase (NOS), has been implicated in multiple inflammatory processes, which makes it a suitable marker for changes which likely occur following tooth pulp insult. Since limited information on nitric oxide in the pulp is available, it is necessary first to examine relative distributions of NOS in uninflamed and inflamed rat pulp. We accomplished this by characterizing regions of nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) activity and the distribution of both macrophage NOS (macNOS) and neuronal NOS (nNOS) immunoreactivity in normal and inflamed rat molar pulp at multiple time points. The results showed that: (1) deep cavity preparation on the mesial surface of the molar produced a time-dependent inflammation, with acute inflammation early progressing to chronic, granulomatous inflammation with necrosis later that spread preferentially down the mesial root; (2) control (non-prepared) teeth showed a relatively faint and homogeneous distribution of NADPH-d and macNOS reactivity but no discernible nNOS reactivity; (3) inflamed teeth displayed localized increased intensity of NADPH-d and macNOS reactivity surrounding the inflamed area of pulp, but no increased nNOS activity; (4) pulp vessels supplying the inflamed area showed increased NADPH-d reactivity, but no increased macNOS or nNOS reactivity; and (5) neither NADPH-d, macNOS, nor nNOS reactivity was observed in pulpal nerves. Therefore, nitric oxide may mediate the pulpal inflammatory response through its effects on the paralesional pulp tissue and surrounding endothelial/vascular structures.
The aim of this study was to explore pulp healing and reparative dentinogenesis following pulp-capping by using recombinant human insulin-like growth factor I (rhIGF-I). Exposures were made through the mesial pulp horn in first upper molars in two-month-old Wistar rats. The pulp was covered with one dose of sterile 4% methylcellulose gel containing either 400 ng rhIGF-I or saline in contralateral controls. The exposure site was closed with sterile Teflon membrane, and the cavity was filled with IRM cement. Additional molars were capped with Dycal as controls. After 3, 7, or 28 days, animals were anesthetized and fixed by intravascular glutaraldehyde perfusion. Molars were decalcified and processed for histological analysis and cut with membrane and residual methacrylate from IRM in situ. Only specimens with acceptable pulp sealing according to blinded microscopy control were included. On day 3, identical inflammatory responses in the upper pulp were observed in molars with rhIGF-I gel or control gel. On day 7, granulation tissue ingrowth had partly replaced inflammatory infiltration in both groups. After 28 days, complete dentin bridging and tubular dentin formation were observed more frequently and closer to the test substance containing rhIGF-I. The reparative dentin response to capping with rhIGF-I was similar to that after the use of Dycal. In conclusion, microscopic control of membrane sealing in situ gives valid information on the more subtle pulp effects of growth factors. The observations suggest that pulp-capping of rat molars by means of rhIGF-I enhances reparative dentinogenesis in comparison with vehicle controls.
The structure of reparative tertiary dentin in human deciduous teeth has been studied. Reparative dentin is secreted by a new generation of odontoblast-like cells which have been subject to strong stimuli, e.g., trauma or deep active caries lesions with associated pulp inflammation. Ground sections of 25 teeth were prepared, and contact microradiographs were produced. Another 30 teeth were demineralized, embedded in paraffin, sectioned, and stained with hematoxylin and eosin. Some demineralized sections from each tooth were also studied in the scanning electron microscope. Most of the teeth showed some type of tertiary dentin formation. Mineralized tissue with a varied morphology was observed. In teeth which had been subject to trauma, the entire pulp chamber was sometimes obliterated. Mineralization seemed to start in the incisal region, and the central part of the pulp was the last part to be obliterated. Radiolucent voids and canals were seen. The organic matrix was dense and fibrous. In the pulp chamber and especially in the root canals, resorption had often occurred, indicating that signals giving rise to odontoclasts were also present. Resorption was often followed by deposition of various amounts of cementum-like repair tissue. The cells responsible for the formation of reparative dentin are believed to be subodontoblasts or undifferentiated ectomesenchymal cells. The varied morphology of the reparative dentin, observed in the pulp of the teeth examined, indicates that different stimuli lead to induction of hard-tissue-forming cells which produce different types of hard tissue.