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.

The role of oral and facial sensory receptors in the control of masticatory muscle activities was assessed from the effect of acute deafferentiation on cortically induced rhythmic jaw movements (CRJMs) in anesthetized rabbits. When a thin polyurethane-foam strip (1.5, 2.5 or 3.5 mm thick) was placed between opposing molars during CRJMs, masseteric activities were facilitated in association with an increase in the medial excursion of the mandible during the power phase. The effects varied with the pattern of CRJMs, and the rate of facilitation was greater for small circular movements than for the crescent-shaped movements. Furthermore, the response of the masseter muscle was greater in the anterior half of the muscle, where muscle spindles are most dense, than in its posterior half. It was also demonstrated that the response increased with an increase in the thickness of the test strip. In contrast, the activities of the jaw-opening muscle were not affected significantly. The duration of masseteric bursts increased during application of the test strip and the chewing rhythm tended to slow down. However, the latter effect was not significant. After locally anesthetizing the maxillary and inferior alveolar nerves, the facilitative responses of the masseter muscle to the test strip was greatly reduced but not completely abolished. Lesioning of the mesencephalic trigeminal nucleus (Mes V) where the primary ganglion cells of muscle spindle afferents from jaw-closing muscles and some periodontal afferents are located, also reduced the facilitative effects. Similar results were obtained in the animals with the kainic acid injections into the Mes V 1 week before electrical lesioning of this nucleus. In these animals the effects of electrical lesioning of the Mes V could be attributed to the loss of muscle receptor afferents since the neurons in the vicinity of the Mes V were destroyed and replaced by glial cells, whereas the Mes V neurons are resistant to kainic acid. When electrical lesioning of the Mes V and sectioning of the maxillary and inferior alveolar nerves were combined in animals with a kainic acid injection into the Mes V, the response of the masseter muscle to application of the strip was almost completely abolished. From these findings, we conclude that both periodontal receptors and muscle spindles are primarily responsible for the facilitation of jaw-closing muscle activities.(ABSTRACT TRUNCATED AT 400 WORDS)

The effects of inferior alveolar nerve (IAN) transection on escape behavior and MDH neuronal activity to noxious and nonnoxious stimulation of the face were precisely analyzed. Relative thresholds for escape from mechanical stimulation applied to the whisker pad area ipsilateral to the transection were significantly lower than that for the contralateral and sham-operated whisker pad until 28 days after the transection, then returned to the preoperative level at 40 days after transection. A total of 540 neurons were recorded from the medullary dorsal horn (MDH) of the nontreated naive rats [low-threshold mechanoreceptive (LTM), 27; wide dynamic range (WDR), 31; nociceptive specific (NS), 11] and sham-operated rats with skin incision (LTM, 34; WDR, 30; NS, 23) and from the ipsilateral (LTM, 82; WDR, 82; NS, 31) and contralateral MDH relative to the IAN transection (LTM, 77; WDR, 82; NS, 33). The electrophysiological properties of these neurons were precisely analyzed. Background activity of WDR neurons on the ipsilateral side relative to the transection was significantly increased at 2-14 days after the operation as compared with that of naive rats. Innocuous and noxious mechanical-evoked responses of LTM and WDR neurons were significantly enhanced at 2-14 days after IAN transection. The mean area of the receptive fields of WDR neurons was significantly larger on the ipsilateral MDH at 2-7 days after transection than that of naive rats. We could not observe any modulation of thermal responses of WDR and NS neurons following IAN transection. Also, no MDH neurons were significantly affected in the rats with sham operations. The present findings suggest that the increment of neuronal activity of WDR neurons in the MDH following IAN transection may play an important role in the development of the mechano-allodynia induced in the area adjacent to the area innervated by the injured nerve.

Studies at spinal levels indicate that peripheral tissue or nerve injury induces a state of hyperexcitability of spinal dorsal horn neurons that participates in the development of persistent pain and hyperalgesia. It has not been demonstrated that persistent injury in the orofacial region leads to a similar state of central hyperexcitability in the trigeminal system. The purpose of the present study was to conduct a parametric analysis of the response properties of nociceptive and nonnociceptive neurons in trigeminal nucleus caudalis (medullary dorsal horn, MDH) in a rat model of persistent orofacial inflammation. Neurons were recorded extracellularly and classified as low-threshold mechanoreceptive (LTM, n = 49), wide dynamic range (WDR, n = 82), and nociceptive-specific (NS, n = 11) neurons according to their response properties to mechanical stimuli applied to their cutaneous receptive fields (RFs). The inflammation was induced 24 h before the recordings by injecting complete Freund's adjuvant (CFA) into the temporomandibular joint (TMJ) capsule or the perioral (PO) skin. The mean areas of the high-threshold RFs of WDR neurons in TMJ (8.66 +/- 0.61 cm(2), n = 25) and PO (5.61 +/- 2.07 cm(2), n = 25) inflamed rats were significantly larger than those in naive rats (1.10 +/- 0. 16 cm(2), n = 32). The mean RF size in TMJ-inflamed rats also was significantly larger than that in PO-inflamed rats (P < 0.01). Furthermore the mean area of the RFs of NS neurons (3.74 +/- 1.44 cm(2), n = 5) was significantly larger in TMJ inflamed rats as compared with naive rats (0.4 +/- 0.09 cm(2), n = 3) (P < 0.05). The background activity in the TMJ- and PO-inflamed rats was generally greater in WDR and NS neurons, but less in LTM neurons, when compared with naive rats. The responses of WDR neurons to noxious mechanical stimuli were increased significantly in TMJ-inflamed rats (P < 0.05) as compared with naive rats. WDR neuronal responses to mechanical stimulation also were increased in PO-inflamed rats but to a lesser extent than in TMJ-inflamed rats. The injection of CFA into the TMJ or PO skin resulted in reduced responses of LTM neurons to mechanical stimuli. The responses of MDH nociceptive neurons to 48-55 degrees C heating were greater in inflamed rats as compared with naive rats. A subpopulation of WDR neurons recorded from TMJ (n = 4 of 10)- or PO (n = 3 of 13)-injected rats responded to cooling in addition to heating of the RFs but did not grade their responses with changes in stimulus intensity. These results indicate that persistent orofacial inflammation produced hyperexcitability of MDH nociceptive neurons. TMJ inflammation resulted in more robust changes in MDH nociceptive neurons as compared with PO inflammation, consistent with previous studies of increased inflammation, increased MDH Fos-protein expression, and increased MDH preprodynorphin mRNA expression in this deep tissue orofacial model of pain and hyperalgesia. The inflammation-induced MDH hyperexcitability may contribute to mechanisms of persistent pain asso...

Bilateral trigeminal deafferentation was performed in the rabbit in order to assess the role of orofacial inputs in regulation of the pattern of jaw movements during chewing. After bilateral combined section of the maxillary and inferior alveolar nerves, the animals did not eat food by themselves in the first postoperative week. However, they could chew and swallow when food was inserted into the mouth by an experimenter. The pattern of jaw movements and associated EMG activities of masticatory muscles during chewing were modulated remarkably by deafferentation. These modifications include 1) decrease in the horizontal excursions of the mandible at the power phase, 2) decrease in the maximum gape, 3) insufficient occlusion at the power phase (or increase in the minimum gape), 4) irregular patterns of jaw movements, 5) facilitation of the chewing rate, 6) increase in the number of chewing cycles in a masticatory sequence (the process from acceptance of food to swallowing), and 7) decrease in jaw-closing muscle activities. The findings indicate that deafferentation of the trigeminal sensory branches reduced masticatory force. On the other hand, no significant change was seen in the animals with disruption of cutaneous sensations of the face due to bilateral section of the infraorbital and mental nerves. Intraoral sensations rather than extraoral sensations may thus be important for regulation of masticatory force and jaw movements during chewing. Jaw movements during chewing were also analyzed in the animals with either bilateral ablation of the cortical masticatory area (CMA) or bilateral lesion of the ventral posteromedial nucleus (VPM) of the thalamus in order to examine whether profound effects of trigeminal deafferentation are produced via the transcortical loop. The animals with lesion of either the CMA or VPM demonstrated disturbances in feeding behavior, including the dropping of ingested food from the mouth, elongation of a masticatory process, reduction in the chewing efficiency, etc. However, the pattern of jaw movements during chewing were essentially similar to that in the preoperative period. These results do not necessarily deny a contribution of the CMA to regulation of jaw movements but suggest that the transcortical feedback loop via the CMA and thalamic VPM nucleus would not primarily be responsible for pattern formation of jaw movements during chewing in the rabbit. Probably, the sensory feedback via the transcortical loop may indirectly facilitate activities of the brain stem CPG, which facilitates the chewing rhythm or enables masticatory sequences to be conducted smoothly.

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.

The electromyographic (EMG) activity of the human genioglossus (GG) muscle during chewing efforts is not fully understood. In this study, the EMG activity of the human GG muscle during unilateral gum chewing was illustrated and correlated with the activities in the anterior temporalis (AT), the anterior digastric (DG), and the inferior orbicularis oris (OI) muscles. GG muscle activity was measured with customized surface electrodes, while other muscles were recorded with conventional surface electrodes. EMG activities during tongue displacement and the articulation of long vowels, recorded by the customized electrodes, were consistent with the recordings obtained by fine wire electrodes placed in the GG muscle. Jaw displacement was monitored by means of a kinesiograph with a transducer attached to the mandibular central incisors. Mean normalized GG muscle activity showed an onset in the last one-fifth of the intercuspal phase, gradually increasing during jaw-opening, and at its greatest immediately before the maximum jaw-opening position. It then decreased during jaw-closing and ceased in intercuspation but showed a small rebound in the third fifth of the intercuspal phase. The GG muscle burst showed phase lags with the DG and OI muscles and an opposite phase with the AT muscle (all P < 0.0001). All correlations were statistically significant (all P < 0.0001, r values between 0.88 and 0.97). The results suggest central coordination of the timing of the activities of the jaw, lip, and tongue muscles in chewing.

Maximum occlusal force tended to increase with age. There was a gender difference in the maximum occlusal force at all age groups, values being larger in the males. In the males, the maximum occlusal force continued to increase until their 20s, while in the females, this increase almost terminated at the age of 17.