A series of preventive management, consisting of the caries prevention program, treatment, and regular check-up for 208 adult patients, was practiced, and evaluated to clarify the effect of the prevention program. As a result, the plaque control record (PCR) has been significantly improved by the preventive program. The risk of saliva buffer (BF), the amount of saliva secretion and lactobacilli (LB) have been significantly improved by treatment. But mutans streptococci (SM) showed no difference significantly. Compared to before starting the preventive treatment, the group that was continuing for three years of check-ups after treatment showed a significantly improved the risk of BF and PCR. After three years of regular check-ups, SM and LB in the caries group were significantly higher than those in the non-caries group, though the two groups showed no difference before starting the preventive program. Individual patients' risk is understood by using the risk test according to these effects. It was suggested that the monitoring of the results of the risk test after treatment as well as in the regular check-up and before the preventive program are needed for the possibility of contributing to adults' caries preventive management.
We have shown that conditioning electrical stimulation of the amygdala has an inhibitory effect on the nociceptive neurons in the medullary dorsal horn of the rat. The purpose of this study is to investigate whether the inhibitory effect depends on the activation of cell bodies or passing fibers by the glutamate microinjection into the amygdala. The animals were anesthetized with N_2O-O_2 (2:1) and 0.5%-halothane, and immobilized with pancuronium bromide. The peripheral test stimulus (a single rectangular pulse of 2.0 msec in duration) was applied to the facial skin in the receptive field of nociceptive neurons, and the ipsilateral amygdaloid conditioning stimuli to the recording site were trains of 33 pulses (0.5 msec in duration, 100-300μA) delivered at 330Hz. Thirty-five wide dynamic range (WDR) neurons and 11 nociceptive specific (NS) neurons were recorded. Both neurons were distributed in the superficial layers of the caudal nucleus and diffusely throughout the dorsal part of the reticular subnucleus. The conditioning stimulation in the central nucleus, basomedial and basolateral nuclei markedly inhibited the activities in 13 of 17 nociceptive neurons (10 WDR and 3 NS neurons). The inhibitory effect was 68.0±15.3% (mean±S.D.) at maximum. Microinjection of 0.5M monosodium glutamate (5μl) into the amygdala resulted in inhibition of medullary nociceptive neurons (5 WDR and 2 NS neurons). These findings suggest that the excitation of cell bodies in the amygdala contribute to the inhibitory effects on the 2nd order nociceptive neurons. Because it has been known that the amygdala is a key structure for mediating stress responses, the antinociceptive effect may provide one of the neurophysiological basis for the stress-induced analgesia (SIA).
Both voluntary and reflex components are involved in normal swallowing. Swallowing depends on the bulbar central pattern generator (CPG). Therefore, the relationship between the voluntary component (central input) and reflex component (sensory input) may be important to understand the central mechanisms for deglutition. There are water receptors, mechanoreceptors (tactile receptors and deep mechanoreceptors) and taste receptors in the oral mucosa. In this study, the role of sensory receptors in voluntary swallowing was investigated. Twenty healthy volunteers (mean±SD, 28.9±9.7 years) were enrolled in this study. A fine tube was inserted into the pharyngolaryngeal region (PL) or the tongue base (TB). Stimulating solution at room temperature was delivered into the PL or the TB through this tube. Each subject was instructed to repeat swallowing as fast as possible. EMG activity was recorded from suprahyoid muscles during swallowing. The swallowing interval (SI) between two consecutive swallows in each infusion was measured. SIs were shorter in the case of water infusion into the PL than in the case of water infusion into the TB, suggesting that water receptors are localized in the PL. Infusion of 0.15M NaCl into the PL prolonged SI, because 0.15M NaCl inhibits water receptors. However, infusion of 0.15M NaCl into the TB shortened SI, suggesting that excitation of Na^+taste receptors can facilitate voluntarily swallowing. SI with resting saliva infusion into the PL was almost the same as that with water infusion, suggesting that resting saliva can excite water receptors. In the weak mechanical stimulation (infusion rate of 0.2ml/min), SIs varied greatly from subject to subject. Therefore, the variation in SI cannot be explained by difference in sensitivity of the mucosal receptors among subjects. It appears that the ability of CPG to perform repetitive voluntary swallowing varies greatly in subjects. The strong mechanical stimulation (infusion rate of 5.0ml/min) did not influence SI in a subject showing short SI with the weak stimulation, but it shortened SI in a subject showing long SI. This suggests that excitation of oral mucosal receptors strongly compensates for difficulty in swallowing in subjects showing a long SI.
The frog glossopharyngeal nerve elicits phasic responses to various taste stimuli applied to the tongue after a rinse of 1mM NaCl. The difference in the receptor sites for various taste stimuli eliciting phasic responses in the frog glossopharyngeal nerve was investigated by using a cross-adaptation method. Cross-adaptation experiments were carried out as follows. First, one stimulus was applied to the tongue and was followed by another stimulus after the response to the first stimulus had declined. The cross-adaptation experiments were carried out between pairs of four basic taste substances, four bitter substances and three chloride-salts. The results obtained suggest that four basic taste substances (quinine-HCl, NaCl, saccharin and acetic acid) stimulate different receptor sites. The response to one of the bitter substances (quinine-HCl, denatonium, caffeine and theophylline) applied secondarily was decreased by another bitter substance applied first, but reduction in the response to the second stimulus depended on the types of bitter substances applied first. This was also true in cross-adaptation experiments between pairs of three salts (NaCl, KCl and NH_4Cl). However, quinine-HCl and salts did not share a receptor mechanism with each other. The present results suggest that there are different receptor sites responsible for phasic responses to various taste substances and that some receptors interact with other receptors. The sites responsible for adaptation to taste stimulation are discussed.
A high dose local anesthetic, 5% lidocaine, and a semi-permanent neurolytic agent, 99% alcohol, were infused at the infraorbital foramen. The purpose of the paper is the progression in morphological change was observed light microscopically and electron, from nerve injury to regeneration. Immediately after drug injection, there were no significant changes seen in either the alcohol or lidocaine treated groups. One day after drug injection, both the alcohol treated group and the lidocaine treated group showed almost complete destruction of the myelinated nerve fibers within the fascicle. In the alcohol treated group, this damaged state persisted for 1 month post-injection. In the lidocaine treated group, however, there was a 50% reduction in the number of damaged myelinated fibres by the 3 day post-injection. In the alcohol treated group, it was observed that between 2 months and 3 months post-injection. 75% of the myelinated nerve fibers were less than 5μm in diameter, while 20% were thick myelinated nerve fibers greater than 5μm. 6 months after the injection, it was observed that 70% of myelinated nerve fibers were of thick diameter, whilst 30% were thin. These values were very similar to those seen in the control group. In the lidocaine treated group, it was observed that from 1 week to 6 months post-injection, the percentage of myelinated nerve fibers less than 5μm gradually decreased, while the percentage of fibers greater than 5μm increased. Approximately 5% of the fibres remained damaged. Our results demonstrate that the percentage of thick myelinated nerve fibers increased between 3 months and 6 months post-injection. This period correlates well with the period of time taken for clinical re-block administration. This correlation suggests that it takes a set amount of time for regenerative nerve fibers within the fascicle to grow to a length exceeding 5μm and become functional. This further suggests that sensory function is regained even before the ratio of thick and thin myelinated nerve fibers returns to normal levels.