It has been difficult for investigators to simultaneously and reliably evaluate bite force in the intercuspal position with the area and location of occlusal contacts. This study was designed to investigate the variations in these parameters with respect to two factors: three levels of clenching and the preferred chewing side. Human subjects with normal occlusion were examined with a recently developed system (Dental Prescale Occluzer, Fuji Film, Tokyo, Japan). The three levels of clenching intensity were assessed by masseteric EMG activity and included the maximum voluntary contraction, and 30% and 60% of the maximum. The results indicated that the bite force and occlusal contact area on the whole dental arch increased with clenching intensity. In contrast, the average bite pressure, obtained by dividing the bite force by the contact area, remained unchanged regardless of the clenching intensity. As the clenching intensity increased, the medio-lateral position of the bite force balancing point shifted significantly (P<0.01) from the preferred chewing side toward the midline. The antero-posterior position remained stable in a range between the distal third of the first molar and the mesial third of the second molar. The bite force and occlusal contact area, which were mainly on the molars, increased with the clenching intensity, whereas the proportions of these two variables on each upper tooth usually did not change significantly. The exception was the second molar on the non-preferred chewing side. When comparisons were made between pairs of specific upper teeth of same name, usually no significant difference was found in bite force or occlusal contact area, regardless of the clenching level. Again, the exception to this observation was the second molar on the preferred chewing side, which had a larger area at the 30% clenching level. The results in normal subjects suggest that as the clenching intensity increases in the intercuspal position, the bite force adjusts to a position where it is well-balanced. This adjustment may prevent damage and overload to the teeth and temporomandibular joints.

To examine the relationships between masticatory force, electromyogram (EMG) of masticatory muscles, and jaw movement pattern, we quantitatively evaluated the effects of changing hardness of a chewing substance on these three variables. Cortically induced rhythmic jaw movements of a crescent-shaped pattern were induced by electrical stimulation of the cerebral cortical masticatory area in the anesthetized rabbit. The axially directed masticatory force was recorded with a small force-displacement transducer mounted on the ground surface of the lower molars. EMGs were recorded from the masseter and digastric muscles simultaneously with jaw movements. Five test strips of polyurethane foam of different hardness were prepared and inserted between the upper molar and the transducer during the movements. The peak, impulse, and buildup speed of the masticatory force increased with strip hardness, whereas duration of the exerted force did not vary with strip hardness. The integrated activity and duration of the masseteric EMG bursts also increased with strip hardness. The integrated EMG activity of the digastric bursts was weakly related to strip hardness, whereas the duration was not. The minimum gape increased with strip hardness, but the maximum gape did not. The horizontal excursion of the jaw did not vary in a hardness-dependent manner, although it was greater in the cycles with strip application than in the cycles without strip application. Deprivation of periodontal sensation by cutting the nerves to the teeth reduced the buildup speed of the force, maximum gape, net gape, and horizontal jaw movements. The denervation also elongated the force duration and that of masseteric EMG bursts. However, the rate of the hardness-dependent changes in the above parameters did not alter after denervation. The latency of the masseteric EMG response to strip application was evaluated before and after denervation. In both conditions, it was > or = 6 ms in approximately 70% of the cycles and <6 ms in the remaining approximately 30%, which cannot be explained by a simple reflex mechanism. On the basis of the analysis of correlation coefficients, the masseteric integrated EMG seemed to be a good indicator of the peak and impulse of the masticatory force both before and after denervation. We conclude that periodontal afferents would be responsible for a quick buildup of masticatory force and that afferents other than those from periodontal tissue would contribute to the hardness-dependent change of masticatory force during cortically induced rhythmic jaw movements.

Intracellular recordings were obtained from rat trigeminal motoneurons in slice preparations to investigate the role of calcium conductances in the depolarizing and hyperpolarizing spike afterpotential (ADP and mAHP, respectively). The mAHP was suppressed by bath application of 1 microM apamin, 2 mM Mn2+, and 2 mM Co2+, and also by intracellular injection of ethylene glycol-bis(b-aminoethylenether)-N,N,N',N'-tetraacetic acid (EGTA), suggesting that the potassium conductance generating the mAHP is activated by Ca2+ influx. Mn2+ (2 mM) or Cd2+ (500 microM) reduced the ADP, whereas the ADP amplitude was increased by raising extracellular Ca2+ concentration from 2 to 8 mM by bath application of Ba2+ (0.5-5 mM) and by intracellular injection of EGTA. This would suggest that Ca2+ itself is likely to be the charge carrier generating the ADP. Focal application of omega-conotoxin GVIA (10-30 microM) suppressed the mAHP and enhanced the ADP, whereas focal application of omega-agatoxin IVA (10-100 microM) reduced the ADP amplitude without apparent effects on the mAHP. We conclude that Ca2+ influx through omega-agatoxin IVA-sensitive calcium channels is at least in part responsible for the generation of the ADP and that Ca2+ influx through omega-conotoxin GVIA-sensitive calcium channels contributes to the generation of the mAHP. Because of the selective suppression of the ADP and mAHP by omega-agatoxin IVA and omega-conotoxin GVIA, respectively, it is suggested that both calcium channels are separated geometrically in rat trigeminal motoneurons.

It has been demonstrated that the vertical jaw movement trajectories during gum-chewing can be explained by jerk-cost minimization. However, it is uncertain whether the masticatory jaw movement in space can be predicted by the minimum-jerk model. The aims of the present study were to develop minimum-jerk models that would explain 3D masticatory jaw movements with different hardnesses of foods, and to evaluate if the models can predict the movements accurately. The 3D masticatory jaw movement during food breakage was formulated for two types of test foods. The coefficients of determination (R2) between the measured and model-based values ranged from 0.846 to 0.882. Differences were found in the kinematic parameters between the test foods. The results suggest that the models predict the 3D jaw movements during food breakage and are effective in differentiating among the kinematic features of masticatory jaw movements that are peculiar to the mechanical properties of foodstuffs.

When a thin plastic test strip of various hardness is placed between the upper and lower teeth during rhythmical jaw movements induced by electrical stimulation of the cortical masticatory area (CMA) in anesthetized rabbits, electromyographic (EMG) activity of the masseter muscle is facilitated in a hardness-dependent manner. This facilitatory masseteric response (FMR) often occurred prior to contact of the teeth to the strip, and thus preceded the onset of the masticatory force. Since this finding suggests involvement of a feed-forward mechanism in the induction of the FMR, the temporal relationship between the onset of the FMR and that of the masticatory force was analyzed in five sequential masticatory cycles after application of the strip. The FMR was found to precede the onset of masticatory force from the second masticatory cycle after application of the strip, but never did in the first cycle. This finding supports the concept of a feed-forward control mechanism that modulates FMR timing. Furthermore, the FMR preceding the force onset disappeared after making a lesion of the mesencephalic trigeminal nucleus (MesV) where the ganglion cells of the muscle spindle afferents from the jaw-closing muscles are located. In contrast, no such change occurred after blocking periodontal afferents by transection of both the maxillary and the inferior alveolar nerves. The putative feed-forward control of the FMR is therefore dependent mainly on sensory inputs from the muscle spindles, but little on those from the periodontal receptors, if any. We further examined the involvement of the CMA with the putative feed-forward control of the FMR via the transcortical loop. For this purpose, rhythmical jaw movements were induced by stimulation of the pyramidal tract. No significant change in the timing of the FMR occurred after the CMA ablation, which strongly suggests that the CMA is not involved in the putative feed-forward control of the FMR. The FMR was also noted to increase significantly in a hardness-dependent manner even after the MesV lesion, although the rate of increment decreased significantly. Contribution of muscle spindles and periodontal receptors to the hardness-dependent change of the FMR is discussed.