Dentine sensitivity caused by illumination of intraoral scanner and light curing unit.

Background: Patients often compliant sensitivity to high-intensity light irradiated application during dental procedures. This study aims to investigate tooth sensitivity caused by high-intensity light irradiated from an intraoral scanner (IOS) and a light-curing unit (LCU). Material and Methods: Forty-five teeth from 45 healthy volunteers were included. These were equally classified into three groups using the cold test (4 ± 1 °C) and NRS pain assessment; A=control, B=cavity without sensitivity, and C=cavity with sensitivity. Two thermocouple probes were attached to the cervical area of the experimental and control tooth with a composite resin. Tooth sensitivity response by participant grip force was monitored. The digital oscilloscope was used to record two surface temperatures and a pain response during an IOS or a LCU irradiation. The high-intensity light from a LCU and an IOS was randomly applied at 2 mm above the cervical area for 20s. The data were compared statistical with two-way repeated measures ANOVA and Pearson's correlation. Results: The illumination caused increasing surface temperatures of about 22.98 ± 3.20 °C for a LCU and 5.86 ± 1.46 °C for an IOS from a 29.5 °C baseline. As the light intensity from the LCU generated more heat, participants reported more tooth sensitivity with a shorter response time (2.10s to 18.70s). There was a positive correlation between surface temperature and pain response (R2 = 0.232; p<0.01). Conclusions: The heat from high-intensity light from a LCU and an IOS can cause tooth sensitivity in some individuals especially those who had a cervical cavity with dentine sensitivity. The higher light intensity would raise the surface temperature and cause a higher sensitivity response. Key words:Light curing unit, intraoral scanner, tooth temperature, dentine sensitivity.

Observations on fluid flow from exposed dentine in primary teeth: An in vitro study.

OBJECTIVE: To investigate fluid flow through dentine in primary teeth in vitro using the replica technique, and to compare the results with those obtained from permanent dentine. DESIGN: The experiments were carried out on 22 extracted, mandibular, primary, incisor teeth. The incisal edge was removed to 1mm below the dentino-enamel junction and half the exposed surface etched with phosphoric acid. The exposed dentine was blotted dry and the pressure in the pulp cavity held at 0, 15, 30 or 45cm H2O above atmospheric for 30s. Fluid that accumulated on the dentine surface was recorded with impression material and a replica made with epoxy resin which was examined in a scanning electron microscope. RESULTS: Structures resembling fluid droplets were present in the replicas of unetched dentine in all 22 teeth, and at all the pulpal pressures tested. The droplets formed at 45cm H2O were significantly larger (median diam., 5.14mm; interquartile range, 3.26mm; Friedman repeated measures analysis of variance on ranks (RMAVR) and Tukey test) than those formed at other pressures. There was no evidence of droplets in the replicas of etched dentine with any of the pulpal pressures. CONCLUSIONS: These results demonstrate that fluid will tend to flow from dentine in deciduous teeth when it is exposed. They are similar to those obtained in a previous study in this laboratory on permanent teeth. The fact that fluid droplets were absent from etched dentine suggests that, after being blotted, the etched dentine matrix absorbed fluid that tended to flow out through the dentinal tubules.

Effect of full crown preparation on pulpal blood flow in man.

OBJECTIVE: To determine if full crown preparation causes an increase in pulpal blood flow (PBF), indicating inflammation, in human subjects. DESIGN: The experiments were carried out on 35 intact, mandibular posterior teeth in 13 subjects: 32 were abutments for 16 fixed bridges that replaced first molars; the other 3 were first premolars adjacent to abutment teeth that served as un-operated controls. Crown preparations were made using an air-rotor with water-spray under regional block anaesthesia (4% articaine with epinephrine 1:100,000). PBF was recorded with a laser Doppler flow meter (LDF) before and after administering the anaesthetic, with the LDF probe on the buccal enamel. PBF was then recorded from the abutment teeth with the probe on buccal dentine after preparing the buccal surfaces of both teeth, after completing the crown preparations, and after 1 and 7days. PBF was also recorded from the buccal enamel of the control teeth on each occasion. RESULTS: The mean±S.D. PBF values before and after anaesthesia were 2.63±2.13 and 2.42±2.38P.U. respectively, which were not significantly different (Paired t-test). The mean values for the abutment teeth after buccal preparation, after complete crown preparation, and after 1 and 7days were 5.20±2.49, 4.53±2.52, 4.92±2.98 and 5.48±2.65P.U. respectively. The 4 values for each tooth were not significantly different (two-way RM ANOVA). In the control group, the values under all six conditions were not significantly different. CONCLUSIONS: Regional block anaesthesia produced no change in PBF, nor did full-crown preparation, neither immediately after the procedure nor 1 and 7days later.

Effect of cavity depth on dentine sensitivity in man.

OBJECTIVE: To determine if dentine at the enamel-dentine junction (EDJ) in man is more sensitive to hydrostatic pressure stimuli then deeper dentine. DESIGN: Cavities (1mm diam.) were cut at the tips of the buccal and lingual cusps of 8 premolars in 3 subjects (ages: 22-25 years). Both cavities were initially deepened to expose the EDJ then one (the test cavity) was deepened in steps of 0.5mm to a maximum of 2.0 mm below the EDJ. The cavities were tested at each stage, before and after etching, with 5s, hydrostatic pressure stimuli between 400 mm above, and 400 mm below atmospheric. The intensity of any pain produced was recorded on a VAS scale and electrodes were placed in both cavities in an attempt to monitor any action potentials evoked in intradental nerves. RESULTS: In all the teeth, the intensity of the pain produced by a stimulus tended to increase as the cavity was deepened, as did the number of action potentials recorded (in 6 of the 8 teeth). The responses were greater from etched than unetched dentine, and negative pressures evoked greater responses than the corresponding positive pressures. CONCLUSION: There was no evidence that dentine close to the EDJ was more sensitive to hydrostatic pressure stimuli than deeper dentine. It may however be more sensitive to mechanical stimuli as it is more compliant.

The effect of applying potassium chloride solutions at atmospheric pressure on the sensitivity of dentine in man.

OBJECTIVE: To determine the effects of applying KCl solutions to exposed dentine at atmospheric pressure on pain evoked by probing and air blast stimuli in human subjects. DESIGN: The experiments were carried out on 24 premolars in 16 subjects (aged 16-30 years). A cavity (diameter 3mm, depth 3mm) was cut at the tip of the buccal cusp and etched with 35% orthophosphoric acid. The cavity was filled with 500, 250 mmol/l KCl or 500 mmol/l NaCl for 10 min, after which it was rinsed with normal saline. Each solution was tested in 8 teeth. Air blast and probing stimuli were applied to the exposed dentine prior to dentine treatment and at 0, 2, 5, 10, and 20 min after treatment. After each stimulus the subject indicated the intensity of the pain evoked on a visual analogue scale (VAS). RESULTS: In teeth treated with 250 or 500 mmol/l KCl, the mean VAS response to air blast stimuli was significantly decreased at 5 and 10 min after treatment. The mean VAS response to probing was significantly decreased 10 min after treatment with 500 mmol/l KCl. Otherwise there were no significant changes. CONCLUSION: Topical application to exposed dentine of solutions containing a high concentration of potassium ions at atmospheric pressure produce a temporary reduction in the sensitivity of dentine to air blast and probing stimuli.

Effects of potassium ions on dentine sensitivity in man.

OBJECTIVE: To determine the effect of applying 500 mmol/l KCl at a pressure of 150 mm Hg above atmospheric to exposed dentine on pain sensation evoked by probing and air blast stimuli in human subjects. DESIGN: The experiments were carried out on 14 pairs of premolars in 14 human subjects (aged 17-30 years). Dentine was exposed at the tip of the buccal cusp, etched with acid and covered with saline, then 500 mmol/l KCl in Ringer's was applied at a pressure of 150 mm Hg for 4 min. Mechanical probing and air-drying stimuli were performed before and 2, 10, 20, 30 min after applying the KCl solution. The subject indicated the intensity of any pain produced on a visual analogue scale (VAS). Pulpal blood flow was recorded with a laser Doppler flow meter. Exactly the same procedure was carried out on the contralateral tooth except that 500 mmol/l NaCl in Ringer's was used in place of the KCl solution. RESULTS: The pain responses to mechanical probing and air blast stimuli were significantly reduced during the first 10 min after applying the KCl but not the NaCl solution. Pulpal blood flow did not change significantly after either treatment. CONCLUSION: Potassium ions, when applied to exposed dentine at a pressure of 150 mm Hg above atmospheric, produced temporary block of impulse conduction in sensory nerve endings in the dentine or pulp.

Pain and the rate of dentinal fluid flow produced by hydrostatic pressure stimulation of exposed dentine in man.

OBJECTIVE: To determine the relationship between pain intensity and the rate of fluid flow through dentine in human subjects. DESIGN: The experiments were carried out on 16 premolars in 13 human subjects (aged 15-25 years). Dentine was exposed at the tip of the buccal cusp, etched with acid and covered with saline. A series of 5 s hydrostatic pressure stimuli between 400 mmHg above and 400 mmHg below atmospheric were applied to the dentine, in steps of 50 mmHg. The subject indicated the intensity of any pain produced on a visual analogue scale (VAS). The fluid flow through dentine during application of the same stimuli was measured in vitro within 3 h after tooth extraction. RESULTS: The median pain threshold with negative (subatmospheric) stimuli was -125 mmHg and, with positive pressure stimuli, 200 mmHg, which corresponded to dentinal fluid flow rates of 3.29 nL/(s mm(2)) exposed dentine and 5.75 nL/(s mm(2)), respectively. Both the median pressure and the mean rate of flow at threshold with negative pressures were significantly lower than with positive pressures. The curves relating VAS score to stimulus intensity were similar with both negative and positive pressures. CONCLUSION: The sensory transduction mechanism for pain in human teeth is more sensitive to outward than inward flow through dentinal tubules. The difference in sensitivity was however much less than that of the hydrodynamic receptors in the cat, which respond very much more strongly to negative than positive pressure stimuli.

Increase of mast cells and tumor angiogenesis in oral squamous cell carcinoma.

BACKGROUND: Although mast cells (MCs) have been implicated in promoting angiogenesis in some malignant tumors, especially of the aerodigestive tract, little is known in oral squamous cell carcinoma (SCC). METHODS: A retrospective study was conducted to elaborate upon the correlation between MCs and tumor angiogenesis in 26 cases of oral SCC, six cases of oral pre-malignant dysplasia, 10 cases of oral hyperkeratosis, and six cases of normal oral mucosa by means of immunohistochemical technique. RESULTS: The MCs in all lesions and normal oral mucosa strongly expressed tryptase. The densities of MCs and microvessels appeared to increase with disease progression. The MC and microvascular counts were significantly higher in oral SCC than in hyperkeratosis and normal oral mucosa (P < 0.05). A significant correlation between MC and microvascular densities was observed in oral SCC (r = 0.5; P = 0.012). CONCLUSIONS: These findings suggest that MCs may upregulate tumor angiogenesis in oral SCC, perhaps via MC tryptase.