Lipopolysaccharide enhances the production of vascular endothelial growth factor by human pulp cells in culture.
We investigated whether vascular endothelial growth factor (VEGF) production by human pulp cells (HPC) is regulated by lipopolysaccharide (LPS) in relation to the pathogenesis of pulpitis. Although HPC incubated with medium alone only marginally expressed VEGF mRNA and produced a low level of VEGF as detected by enzyme-linked immunosorbent assay, the VEGF mRNA expression and VEGF production were markedly enhanced upon stimulation with LPS from Escherichia coli. Prevotella intermedia LPS, phorbol 12-myristate 13-acetate, and interleukin-6 also induced VEGF mRNA expression in HPC. A simian virus 40-infected HPC line also exhibited increased VEGF mRNA expression in response to E. coli LPS, but lung and skin fibroblasts did not. Fetal bovine serum (FBS) increased the sensitivity of HPC to LPS in a dose-dependent manner. HPC did not express membrane CD14 on their surfaces. However, the anti-CD14 monoclonal antibody MY4 inhibited VEGF induction upon stimulation with LPS in HPC cultures in the presence of 10% FBS but not in the absence of FBS. LPS augmented the VEGF production in HPC cultures in the presence of recombinant human soluble CD14 (sCD14). To clarify the mechanisms of VEGF induction by LPS, we examined the possible activation of the transcription factor AP-1 in HPC stimulated with LPS, by a gel mobility shift assay. AP-1 activation in HPC was clearly observed, whereas that in skin fibroblasts was not. The AP-1 inhibitor curcumin strongly inhibited LPS-induced VEGF production in HPC cultures. In addition, a protein synthesis inhibitor, cycloheximide, inhibited VEGF mRNA accumulation in response to LPS. These results suggest that the enhanced production of VEGF in HPC induced by LPS takes place via an sCD14-dependent pathway which requires new protein synthesis and is mediated in part through AP-1 activation. (+info)
Thermal image analysis of electrothermal debonding of ceramic brackets: an in vitro study.
This study used modern thermal imaging techniques to investigate the temperature rise induced at the pulpal well during thermal debonding of ceramic brackets. Ceramic brackets were debonded from vertically sectioned premolar teeth using an electrothermal debonding unit. Ten teeth were debonded at the end of a single 3-second heating cycle. For a further group of 10 teeth, the bracket and heating element were left in contact with the tooth during the 3-second heating cycle and the 6-second cooling cycle. The average pulpal wall temperature increase for the teeth debonded at the end of the 3-second heating cycle was 16.8 degrees C. When the heating element and bracket remained in contact with the tooth during the 6-second cooling cycle an average temperature increase of 45.6 degrees C was recorded. (+info)
Super pulse CO2 laser for bracket bonding and debonding.
A super pulse and a normal pulse CO2 laser were used to carry out enamel etching and bracket debonding in vitro and in vivo. The shear bond strength of the orthodontic brackets attached to laser-etched and conventional chemically-etched extracted premolars was measured. The pulp cavity temperature was also measured using the same laser irradiation conditions as the shear test. Both super pulse and normal pulse CO2 laser etching resulted in a lower shear bond strength (super pulse: 6.9 +/- 3.4 kg, normal pulse: 9.7 +/- 5.2 kg) than that of chemical etching (15.3 +/- 2.8 kg). Furthermore, the super pulse CO2 laser was able to create debonding at 2 watts within a period of less than 4 seconds (2.9 +/- 0.9 seconds). The super pulse, when irradiating the ceramic brackets from above, during debonding showed a 1.4 degrees C temperature increase in the dental pulp at 2 watts and an increase of 2.1 degrees C at 3 watts. While etching, directly irradiating the enamel surface at 3 watts, the dental pulp showed a temperature increase of 3.5 degrees C. These temperature increases were within the physiologically acceptable limits of the pulp. These results indicate that, in orthodontic treatments, super pulse CO2 laser debonding is more useful than laser etching. (+info)
An evaluation of the changes in maxillary pulpal blood flow associated with orthognathic surgery.
The objective of this study was to evaluate the use of the Laser Doppler Flowmeter (LDF) in the measurement of pulpal blood flow following orthognathic surgery and to conduct an initial study of the effects of a Le Fort I osteotomy on the pulpal blood flow of the maxillary central incisors. The design consisted of a preliminary prospective controlled consecutive clinical trial undertaken at the Orthodontic Clinic, University Dental Hospital NHS Trust, Wales, 1994. The study group consisted of 15 consecutive patients who were to receive a standard advancement Le Fort I osteotomy. Seven patients who were to undergo a mandibular advancement only acted as a control. A further 20 separate patients participated in a study for the assessment of measurement error. The blood flow in relative perfusion unit v. time, was measured using a Laser Doppler Flowmeter. Measurement error for flowmeter recordings with hand-held application and custom-made splint support showed no consistent difference or significant random variation between the two methods for holding the probe against the teeth (pooled S.D. of reproducibility 1/1 = 1.91/1.39 for custom splint location as opposed to 0.96/1.07 for hand-held/fixed bracket location). For the surgical patients under investigation no significant differences for maxillary pulpal blood flow were found in the control group (mandibular osteotomy) over time. However, in the maxillary osteotomy patients there was a tendency for an initial rise in the maxillary perfusion post-surgery as measured at the central incisor pulps, followed by an overall reduction at 6 months. As an example, the mean value for the upper right central showed a significant increase in blood flow during the immediate post-operative period (P < 0.05), but at 6 months after surgery demonstrated a statistically significant overall reduction in comparison with the presurgical reading (P < 0.001). The laser Doppler flowmeter is not an easy instrument to use in the clinical assessment of pulpal blood flow. However, it would appear from these longitudinal series of readings, taken over a 6-month period on 15 patients, that the maxillary perfusion recorded at the central incisor pulps may be permanently affected in many Le Fort I osteotomy patients. For patients that already have a prejudiced blood supply this could lead to devitalization and discoloration of incisors. It is not known if this affect on the perfusion of the pulp continues beyond 6 months post-surgery. (+info)
Neural modulation of inflammatory reactions in dental tissues incident to orthodontic tooth movement. A review of the literature.
This article reviews the current knowledge of the biological aspects of dental tissue changes incident to orthodontic tooth movement. The inflammatory nature of these tissue changes was first recognized in the early 1970s, and since then a number of morphological and quantitative investigations have been published in support of this view. The studies dealing with vascular and cellular dental tissue changes, as well as those concerned with inflammatory mediators present at sites of orthodontic tooth movement are systematized and presented accordingly. Special emphasis is placed upon the role of the sensory nerve fibres and their neuropeptides in the control, and development of an inflammatory process, i.e. their role in tooth movement. (+info)
Tooth pulp- and facial hair mechanoreceptor-evoked responses of trigeminal sensory neurons are attenuated during ketamine anesthesia.
BACKGROUND: Evidence exists that ketamine, administered systemically using a dose required for inducing a state of anesthesia, may antagonize nociceptive but not innocuous input to lumbar dorsal horn neurons. However, it is unclear whether ketamine exerts this selective action on sensory inputs to trigeminal sensory neurons. The current study was undertaken to compare the responses evoked in trigeminal sensory neurons by electrical stimuli applied to the tooth pulp versus air-puff stimuli applied to facial hair mechanoreceptors (FHMs) during quiet wakefulness versus ketamine anesthesia. METHODS: Accordingly, responses of rostral trigeminal sensory nuclear complex (TSNC) and trigeminothalamic tract neurons evoked by tooth pulp (a source of small-diameter fiber input) and FHMs (a source of larger-diameter fiber input) were recorded extracellularly from chronically instrumented cats before, during, and after recovery from the anesthetic state induced by a single (2.2 mg/kg) intravenous injection of ketamine. RESULTS: Overall, tooth pulp-evoked responses of TSNC neurons were maximally suppressed by 50% within 5 min after the intravenous administration of ketamine. Ketamine also suppressed the FHM-evoked responses of TSNC and trigeminothalamic neurons by 45%. The time course of ketamine's suppressive action was equivalent for tooth pulp- and FHM-evoked responses. However, the recovery of tooth pulp-evoked TSNC neuronal responses at suprathreshold intensities was markedly prolonged compared with neuronal responses driven by threshold stimuli or FHM. CONCLUSIONS: These electrophysiologic results in the chronically instrumented cat preparation indicate that a nonselective suppression of orofacial somatosensory information occurs during ketamine anesthesia. The prolonged recovery of suprathreshold responses of TSNC neurons mediated by small-diameter afferent fiber input may partly underlie the analgesic action of ketamine that is clinically relevant at subanesthetic doses. (+info)
Interleukin-1 and tumor necrosis factor receptor signaling is not required for bacteria-induced osteoclastogenesis and bone loss but is essential for protecting the host from a mixed anaerobic infection.
Bacterial infection causes significant morbidity, mediated in part by the up-regulation of inflammatory cytokines. Cytokine induction is thought to stimulate osteolysis in conditions such as periodontal disease and otitis media. To establish the relative importance of interleukin-1 (IL-1) and tumor necrosis factor (TNF) in mediating the response to a mixed anaerobic infection, we used an in vivo model in which the dental pulp was inoculated with six anaerobic pathogens, in mice with functional deletions of receptors to IL-1 (IL-1RI(-/-)), TNF (TNFRp55(-/-)-p75(-/-)), or both (TNFRp55(-/-)-IL-1RI(-/-)). Polymorphonuclear and mononuclear phagocyte recruitment occurred to the greatest extent in TNFRp55(-/-)-IL-1RI(-/-) mice, and to a lesser extent in IL-1RI(-/-) or TNFRp55(-/-)-p75(-/-) mice, and the least in wild-type mice, demonstrating that recruitment of these phagocytes is not dependent on IL-1 or TNF receptor signaling. A similar pattern was observed for bacterial penetration into host tissue. Because it had recently been reported that TNF played a critical role in mediating lipopolysaccharide-induced bone loss, we anticipated that mice with targeted deletions of TNFRp55(-/-) would have reduced osteoclastogenesis. Surprisingly, osteolytic lesion formation was greatest in animals lacking TNF and/or IL-1 receptors. These results indicate that IL-1 or TNF receptor signaling is not required for bacteria-induced osteoclastogenesis and bone loss, but does play a critical role in protecting the host against mixed anaerobic infections. (+info)
Effects of capsaicin-induced sensory denervation on osteoclastic resorption in adult rats.
Many recent findings suggest that the nervous system has efferent effects on bone. A putative role of the sensory innervation has been assessed by using a synchronised rat model of bone resorption after treating adult animals with the neurotoxin capsaicin. Fourteen days after capsaicin treatment (50 mg kg-1) the right maxillary molars were extracted to activate a wave of resorption along the mandibular cortex. The rats were killed 4 days later (i.e. at the peak of resorption in this model), and their right mandibles were processed for histometric evaluation of resorption along the cortex and of calcitonin gene-related peptide (CGRP)- and substance P (SP)-immunoreactive (IR) fibres in the dental pulp. CGRP-IR and SP-IR fibres were significantly reduced in numbers by the capsaicin treatment (by 58 and 49%, respectively), confirming the success of sensory denervation. The resorption surface was significantly reduced (P < 0.005) versus the sham-treated animals. Although the size of the osteoclast population recruited in the site was not modified, the number of actively resorbing osteoclasts was significantly reduced (P < 0.03). However, the activity of the resorbing cells was not modified. Non-specific esterase-positive osteoclast precursors were also significantly few after capsaicin treatment. These data show that the sensory nervous system is involved in the control of bone resorption at two different levels: (1) in the recruitment of osteoclast precursors, and (2) in regulating the access of recruited cells to the bone surface. (+info)