Effects of sleep bruxism on periodontal sensation and tooth displacement in the molar region.

The purpose of this study was to investigate the effects of sleep bruxism on periodontal sensation and tooth displacement in the molar region. Twenty-eight (28) subjects lacking objective or subjective abnormalities in stomatognathic function were divided into two groups representing bruxers (n=14) and controls (n=14). Sleep bruxism was confirmed based on the nocturnal electromyography activity of the masseter muscle. Periodontal sensation was assessed based on interocclusal tactile threshold (ITT), which refers to the minimal thickness that can be detected between the occlusal surfaces of the teeth. ITT was measured in the first molar region. Displacement of teeth during clenching was measured using a two-dimensional tooth displacement transducer. Statistical analysis of the differences in ITT and tooth displacement between the bruxers and controls was performed by Mann Whitney U-test (p < 0.05). Mean ITT for bruxers was significantly lower than that for controls (p < 0.01). The mean displacement of both the maxillary and mandibular first molar for the bruxers was significantly larger than that for the controls (p < 0.05). The results of this study suggest that sleep bruxism affects both periodontal sensation and tooth displacement.

The effect of bruxism on periodontal sensation in the molar region: A pilot study.

STATEMENT OF PROBLEM: Periodontal sensation in individuals with bruxism may differ from that in nonbruxers, as excessive amounts of occlusal force may be applied to the teeth during the night. However, this concept is not adequately addressed in the literature. PURPOSE: The purpose of this study was to investigate the effects of bruxism on periodontal sensation in the molar region. MATERIAL AND METHODS: Fourteen dental school faculty and students lacking objective or subjective abnormalities of stomatognathic function were divided into 2 groups representing nonbruxers (n=7) and bruxers (n=7). Bruxism was confirmed based on the nocturnal electromyography activities of the masseter muscle. Periodontal sensation was assessed based on interocclusal tactile threshold, which refers to the minimal thickness that can be detected between the occlusal surfaces of the teeth. Interocclusal tactile threshold was measured in the first molar region each for the left and right sides by placing variable thicknesses of metal foil and recording the threshold twice daily (morning and afternoon) on 3 separate days. Multivariate ANOVA was performed for bruxism (with or without) as a between-subjects effect, and time of day (morning and afternoon) and side (left and right) as within-subjects effects (alpha=.05) RESULTS: Multivariate ANOVA revealed no significant differences in interocclusal tactile threshold between morning and afternoon or between the left and right sides in either group. The mean (SD) interocclusal tactile threshold for the bruxers was 17.1 (3.9) microm, while that for the nonbruxers was significantly greater at 29.9(5.6) microm (P<.001). CONCLUSIONS: The periodontal sensation in bruxers was increased compared to nonbruxers.

Involvement of reticular neurons located dorsal to the facial nucleus in activation of the jaw-closing muscle in rats.

The location of excitatory premotor neurons for jaw-closing motoneurons was examined by the use of electrical and chemical stimulation and extracellular single-unit recording techniques in the anesthetized rat. Single-pulse electrical stimulation of the supratrigeminal region (SupV) and the reticular formation dorsal to the facial nucleus (RdVII) elicited masseter EMG response at mean (+/-SD) latencies of 2.22 +/- 0.59 ms and 3.10 +/- 1.14 ms, respectively. Microinjection (0.1-0.3 microl) of glutamate (50 mM) or kainate (0.5-100 microM) into RdVII increased masseter nerve activity in artificially ventilated and immobilized rats by 30.2 +/- 40.5% and 50.7 +/- 46.8% compared to baseline values, respectively. Forty reticular neurons were antidromically activated by stimulation of the ipsilateral trigeminal motor nucleus (MoV). Twenty neurons were found in RdVII, and the remaining 20 neurons were located in SupV, or areas adjacent to SupV or RdVII. Eleven neurons in RdVII responded to at least either passive jaw opening or light pressure applied to the teeth or tongue. Nine neurons responded to passive jaw opening. Five of the nine neurons responded to multiple stimulus categories. A monosynaptic excitatory projection from one neuron in RdVII was detected by spike-triggered averaging of the rectified masseter nerve activity. We suggest that reticular neurons in RdVII are involved in increasing masseter muscle activity and that excitatory premotor neurons for masseter motoneurons are likely located in this area. RdVII could be an important candidate for controlling activity of jaw-closing muscles via peripheral inputs.

Coeruleotrigeminal suppression of nociceptive sensorimotor function during inflammation in the craniofacial region of the rat.

Descending action from the locus coeruleus (LC) on the trigeminal sensorimotor function was evaluated in a rat model of oral-facial inflammation. For the induction of oral-facial inflammation, mustard oil (20% solution in 20microl mineral oil) was injected into the region of the temporomandibular joint (TMJ). One week before testing, rats received bilateral lesions of the LC using a cathodal current. The electromyogram (EMG) threshold, which is the threshold intensity for the onset of EMG activity of the masseter muscle evoked by pressure on the TMJ region, was used in the present study as an indicator of the trigeminal sensorimotor function. Following mustard oil injection, in the LC-lesioned rats, EMG thresholds significantly decreased at 30min, which lasted up to 240min. In contrast, EMG thresholds in the LC-intact rats returned to the level before injection after 180min. Systemic naloxone (1.3mg/kg, i.v.) produced a further decrease of EMG thresholds in both the LC-intact and LC-lesioned rats. Under the existence of naloxone, EMG thresholds in the LC-lesioned rats were significantly lower than those of the LC-intact rats. These results suggest that oral-facial inflammation activates the coeruleotrigeminal modulating system and that an action of this system is independent of the opioid depressive mechanism.