Human Masseter Muscle Research Articles

Location of the Neuromuscular Junction of the Human Masseter Muscle Estimated from the Low Frequency Component of the Surface Electromyogram

The position of the neuromuscular junction of the human masseter muscle has estimated from the low frequency component of the surface electromyogram. Monopolar surface electromyograms were recorded in response to clenching from eight sites with the reference electrode placed on the tip of the nose in six healthy male subjects. Component of the slow wave was separated from the raw recordings using digital filter, and the difference of the polarity and magnitude with the sites was examined. The base line of the recordings deflected either negatively or positively depending on the recording sites. These deflections coincided with bursts of muscular action potentials. Deflection of the slow wave component was largely negative over the inferior masseter close to the mandibular ramus but shifted to positive over the superior part. The greatest magnitude of the muscular action potential coincided with the most negative deflection of the slow wave. The phase of the muscular action potential burst also reversed near the site of the polarity change of the slow wave. These findings suggest that the slow wave, as detected by this method, originates mainly from the synaptic potential at the meuromuscular junction and that this is located on the inferior part of the muscle close to the mandibular ramus.

MULTIDISCIPLINARY PAIN ABSTRACTS: 16 . Clinical Science (16)

The present double‐blind, placebo‐controlled study was designed to test quantitatively the effect and of nerve growth factor (NGF) injected into the masseter muscle. Pressure pain thresholds (PPT) and pressure tolerance thresholds (PTOL) were used as indices of mechanical allodynia and hyperalgesia in the jaw‐closing muscles. In addition, perceived pain intensity was assessed by the subjects on a 0 to 10 numerical rating scale (NRS) with the jaw at rest and in relation to various oral functions (chewing, yawning, talking, swallowing, drinking and smiling). Repeated measures analysis of variance (ANOVA) was used to test for significant effects. Injection of NGF into the masseter muscle was associated with significantly reduced PPT for 7 days and PTOL for 1 day. Buffered isotonic saline injections into the masseter muscle also significantly lowered the PPT after 1 day and isotonic saline had no significant effect on PTOL. In contrast, assessment of PPT and PTOL in the noninjected temporalis muscles demonstrated a significant increase after 14 to 28 days, which may have reflected an adaptation to the test procedure. NRS scores of chewing and yawning were significantly increased for 7 days following NGF injection. Systemic adverse effects were noted in one subject who reported fever and slight discomfort about 8 hours after the NGF injection. In conclusion, this is the first study to show that injection of NGF into the human masseter muscle causes local signs of mechanical allodynia and hyperalgesia that persist for at least 7 days as well as pain during strenuous jaw movement. The present pain model is safe and may be used to gain further insight into the neurobiological mechanisms of muscle pain and sensitization.

Mental stress-induced physiological changes in the human masseter muscle.

The effect of a long mental stress on the hemodynamics of masticatory muscles has not been investigated to date. We hypothesized some hemodynamic and electromyographic changes in jaw-closure muscles related to sympathetic nervous system activity. While healthy adult female volunteers performed a two-hour mental stress task, electromyographic activity of the temporal and masseteric muscles was recorded, and hemodynamic changes of the masseter muscle were measured non-invasively. Autonomic function was assessed by heart rate spectral analysis. Integrated electromyographic activity of the temporalis muscle, but not the masseter muscle, showed an increase that coincided with the increase in sympathetic nervous activity. In the masseter muscle, despite little change in integrated electromyographic activity, notable changes were found in hemodynamic parameters. These results suggest that hemodynamics of jaw muscles is susceptible to mental stress, implying a potential role in the etiology of jaw muscle dysfunction associated with mental stress.

Effects of experimental muscle pain on mechanical properties of single motor units in human masseter

Muscle pain is known to influence muscle activity but the details of its effects on the mechanical properties of single motor units (SMU) have not been described. We have recently reported a decreased firing rate of SMU in the human masseter muscle during painful contractions with a constant force output. Force output can be modulated by the SMU discharge rate in relation to the contractile properties of SMU. Therefore, the objective of the present study was to measure the mechanical properties of SMU in the masseter to clarify the mechanism which underlies the decrease in SMU firing rate during jaw-muscle pain. A spike-triggered averaging (STA) technique was used to determine the mechanical properties of low-threshold SMU in the masseter muscle recorded with fine wire electrodes during a voluntary isometric contraction. The twitch amplitude, contraction time, and half-relaxation time were determined from the averaged force records before and during experimental jaw-muscle pain induced by injection of 0.2 ml (100 microg/ml) capsaicin in 8 healthy subjects. Injections of 0.2 ml isotonic saline served as a non-painful control in 11 healthy subjects. The twitch amplitude was significantly increased during capsaicin-evoked muscle pain (P<0.001) without significant changes of half-relaxation time and contraction time. No significant changes in SMU twitch properties were observed during the control injections. Potentiation of twitch force could be a possible compensatory mechanism to maintain a constant force output during painful isometric contractions when SMU firing decreases. This finding therefore provides new information on the adaptation of motor function by muscle pain.

Is the long-latency stretch reflex in human masseter transcortical?

A long-latency stretch reflex (LLSR) has been described in the human masseter muscle, but its pathway remains uncertain. To investigate this, the excitability of corticomotoneuronal (CM) cells projecting to masseter motoneurons during the LLSR was assessed with transcranial magnetic stimulation (TMS). A facilitated response to TMS would be evidence of a LLSR pathway that traverses the motor cortex. Surface electromyogram electrodes were placed over the left or right masseter, and subjects ( n=10) bit on bars with their incisor teeth at 10% of maximal electromyographic activity (EMG). Servo-controlled displacements were imposed on the lower jaw to evoke a short- and long-latency stretch reflex in masseter. TMS intensity was just suprathreshold for a response in contralateral masseter. Trials consisted of: (1) stretch alone, (2) TMS alone, and (3) TMS with a preceding conditioning stretch at varied conditioning-testing (C-T) intervals chosen to combine TMS with the short-latency stretch reflex (3 ms, 5 ms) and the LLSR (23-41 ms). Masseter EMG was rectified and averaged. With TMS alone, mean (+/- SE) MEP area above baseline was 56+/-9%. The area of masseter MEPs above baseline in the C-T trials was calculated from each EMG average following subtraction of the response to stretch alone. Conditioning muscle stretch had no significant effect on masseter MEPs evoked by TMS with any C-T interval (ANOVA; P=0.90). In addition, subjects were unable to modify the SLSR or LLSR by voluntary command. It is concluded that the long-latency stretch reflex in the masseter does not involve the motor cortex and is not influenced by "motor set".

Injection of nerve growth factor into human masseter muscle evokes long-lasting mechanical allodynia and hyperalgesia

Nerve growth factor (NGF) is a neurotrophic protein with a pivotal role in development and maintenance of the nervous system on one side and inflammatory and neuropathic pain states on the other. NGF causes clear signs of behavioral hyperalgesia in animal models and following intradermal and systemic administration in humans. The present double-blinded, placebo-controlled study was designed to test quantitatively the effect and duration (1 h, 1, 7, 14, 21 and 28 days) of NGF (5 μg in 0.2 ml) injected into the masseter muscle. Pressure pain thresholds (PPT) and pressure tolerance thresholds (PTOL) were used as indices of mechanical allodynia and hyperalgesia in the jaw-closing muscles. In addition, perceived pain intensity was assessed by the subjects on a 0–10 numerical rating scale (NRS) with the jaw at rest and in relation to various oral functions (chewing, yawning, talking, swallowing, drinking and smiling). Repeated measures analysis of variance (ANOVA) was used to test for significant effects. Injection of NGF into the masseter muscle was associated with significantly reduced PPT for 7 days (ANOVA: P<0.001) and PTOL for 1 day ( P<0.001). Buffered isotonic saline injections into the masseter muscle also significantly lowered the PPT after 1 day but to a significantly smaller extent than the NGF injections ( P<0.001) and isotonic saline had no significant effects on PTOL. In contrast, assessment of PPT and PTOL in the non-injected temporalis muscles demonstrated a significant increase after 14–28 days ( P<0.001), which may have reflected an adaptation to the test procedure. NRS scores of chewing and yawning were significantly increased for 7 days following NGF injection ( P<0.001). Systemic adverse effects were noted in one subject who reported fever and slight discomfort about 8 h after the NGF injection. In conclusion, this is the first study to show that injection of NGF into the human masseter muscle causes local signs of mechanical allodynia and hyperalgesia that persist for at least 7 days as well as pain during strenuous jaw movement. The present pain model is safe and may be used to gain further insight into the neurobiological mechanisms of muscle pain and sensitization.

Reperfusion response changes induced by repeated, sustained contractions in normal human masseter muscle

The purpose was to evaluate the intramuscular reperfusion response characteristics associated with repeated isometric contractions in normal human masseter. Intramuscular blood volume was quantified with a near-infrared spectroscopic device that measured the total haemoglobin (Hb) concentration in the muscle. Electromyographic (EMG) activity from the masseter and total bite forces were also recorded. Sixteen healthy volunteers, eight females and eight males, without masticatory muscle pain participated. They were asked first to clench their teeth for as long as possible at 50% of their maximum voluntary contraction (MVC). This was followed by a 60 s rest and then immediately by a standard clenching task (50% MVC for 30 s) and a 60 s recovery period, immediately after which they were asked to repeat exactly the same procedure, with a final 5 min recovery period after the second 30 s contraction. Bite force, EMG and Hb concentration were measured continuously and the duration of the two endurance tasks and the amplitudes of all recorded signals were compared (first trial versus second trial). Specifically, the difference between the lowest Hb (trough) seen during the standardised 30 s contractions and the highest (peak) seen just after them was assessed. The trough-to-peak difference in Hb concentration of the second standard contraction task was significantly smaller than that of the first standard task ( P<0.05, paired t-test). These data show that with sustained effort the post-contraction vasodilatory reperfusion responses of the human masseter are diminished, suggesting a progressive desensitisation of the vasodilatory system.

Glutamate-evoked pain and mechanical allodynia in the human masseter muscle

The present study examined the effect of peripheral administration of the excitatory amino acid (EAA) glutamate on the intensity of perceived pain and pressure pain thresholds (PPTs) in healthy young women ( n=17) and men ( n=18). Two injections separated by 25 min of 0.2 ml, 1.0 M glutamate into the masseter muscle produced significantly higher scores of pain on 0–10 cm visual analogue scales (VAS) in women than in men (analysis of variance, ANOVA: P<0.001). There was no significant difference between the VAS scores for the first and the second injections in either men or women. The PPTs determined in the masseter muscle were significantly reduced following the first injection and further significantly reduced after the second injection (ANOVA: P<0.001). Furthermore, the PPTs were reduced to a similar extent in both women and men (maximum 44–56%), suggesting that gender did not influence the process of sensitization. There were no significant difference in VAS scores or PPTs between women taking oral contraceptives ( n=9) and those who did not ( n=8) (ANOVAs: P=0.709, P=0.153). It is concluded that the VAS scores produced by intramuscular administration of 1.0 M glutamate may reflect a gender-dependent activation of nociceptive pathways which, in part, may be mediated through peripheral EAA receptors. The reduction of PPTs in the masseter muscle following administration of glutamate in a concentration of 1.0 M may reflect allodynia to mechanical stimuli. This process of sensitization was not gender-dependent. The present results suggest that injection of 1.0 M glutamate into the masseter muscle may provide a useful experimental method to test sensitization and efficacy of peripheral EAA receptor antagonists in human subjects.

Functional anatomy of the human temporal muscle

The authors carried out an anatomical and magnetic resonance imaging study on the architecture of the mandibular elevator muscles of 169 cadavers. The aim of the study was to define the organisational architecture of the human masseter, temporal and pterygoid muscles. Layer by layer dissection and anatomical cuts in different spatial planes showed that the temporal muscle has a different architecture to the other mandibular elevator muscles. Indeed this muscle does not have the pennate structure of the masseter and pterygoid muscles. Through electromyographic study the behavior of this muscle allowed the establishment of its functional segmentation during the masticatory cycle. Our study showed three distinct anatomical portions in the middle of the temporal muscle which correspond to this functional classification. The MRI study confirmed the results of our anatomical study.

Non-nociceptive upper limb afferents modulate masseter muscle EMG activity in man.

Recent electrophysiological data obtained in anaesthetized rats evidenced jaw muscle excitatory responses to the electrical stimulation of type II limb somatosensory afferents. In the present work, we describe an inhibitory reflex evoked in human masseter muscles by stimulation of non-nociceptive fibres travelling in the median and radial nerves (MED and RAD, respectively). Eighteen healthy volunteers participated in the study. Subjects were seated on a comfortable chair, with the complex head-mandible-neck-trunk and the limbs securely fixed to the chair. Attempts were made to minimize possible interferences due to the activation of afferents other than the stimulated ones. The subjects were instructed to contract masseter muscles at a submaximal level and to maintain a stable level of muscle contraction during all trials. EMG voluntary activity was recorded from both masseter muscles by means of coaxial needle electrodes before and after the electrical stimulation of MED and/or RAD at intensities below pain threshold. In all subjects, MED stimulation induced bilaterally a marked depression of masseter EMG activity, which occurred at a latency of 23.6 +/- 2.1 ms and lasted 27.8 +/- 6.6 ms. RAD stimulation also induced a marked reduction in masseter EMG activity, but this effect was clearly observed in 9 out of 18 subjects, and it showed latency (30.2 +/- 7.5 ms) and duration (44.9 +/- 5.4 ms) significantly longer in comparison with the MED-induced effect. All subjects exhibited the inhibitory period in masseter EMG following the simultaneous stimulation of both nerves; this one appeared at a latency not significantly different (25.3 +/- 5.9 ms) and lasted much more (37.4 +/ - 8.2 ms) than EMG depression evoked by MED stimulation. The duration of masseter muscle inhibition, induced by MED and/or RAD stimulation, was inversely related to the level of EMG activity, while latency was not related to it. Significant increases in the inhibitory period duration were also observed by increasing stimulus intensity, within a subthreshold range for the activation of nociceptive fibres. In all cases, the inhibitory period was followed by a later excitatory rebound activity, whose latency and duration depended on the duration of the preceding EMG inhibition and on the background level of masseter activation. In conclusion, results evidenced that the activation of arm somatosensory fibres modulates masseter muscle activity in normal man. This might lead to a coordination between limb and masticatory muscle activity, which is required in several complex motor acts.

Task-related electromyographic spectral changes in the human masseter and temporalis muscles.

The masticatory muscles differ in their fiber type composition. It can therefore be expected that their electromyographic (EMG) power spectra will differ during the performance of different bite force tasks. In the present study, surface EMG activity was picked up from the masseter and from the anterior and posterior temporalis muscles of nine adult subjects. At a bite force level as low as 25 N, the mean power frequency (MPF) values of the posterior temporalis were significantly lower than those of the masseter and anterior temporalis. The MPF values of the masseter muscles decreased with an increase of bite force magnitude, whereas the MPF values of the anterior and posterior temporalis did not change significantly. The MPF values were significantly influenced by the direction of bite force. The observed changes of MPF are possibly related to the recruitment of different fiber types, and support the concept that the masticatory muscles behave heterogeneously.

Human single masseter muscle fibers contain unique combinations of myosin and myosin binding protein C isoforms.

Striated craniofacial and limb muscles differ in their embryological origin, regulatory program during myogenesis, and innervation. In an attempt to explore the effects of these differences on the striated muscle phenotype in humans, the expression of myosin and myosin-associated thick filament proteins were studied at the single fiber level both in the human jaw-closing masseter muscle and in two limb muscles (biceps brachii and quadriceps femoris muscles). In the masseter, unique combinations of myosin heavy chain (MyHC) and myosin binding protein C (MyBP-C) isoforms were observed at the single fiber level. Compared to the limb muscles, the MyHC isoform expression was more complex in the masseter while the opposite was observed for MyBP-C. In limb muscles, a coordinated expression of three MyHC and three MyBP-C isoforms were observed, i.e., single fibers contained one or two MyHC isoforms, and up to three MyBP-C isoforms. Also, the relative content of the different MyBP-C isoforms correlated with the MyHC isoform expression. In the masseter, on the other hand, up to five different MyHC isoforms could be observed in the same fiber, but only one MyBP-C isoform was identified irrespective MyHC isoform expression. This MyBP-C isoform had a migration rate similar to the slow MyBP-C isoform in limb muscle fibers. In conclusion, a unique myofibrillar protein isoform expression was observed in the human masseter muscle fibers, suggesting significant differences in structural and functional properties between muscle fibers from human masseter and limb muscles.

Effect on prostaglandin E2 and leukotriene B4 levels by local administration of glucocorticoid in human masseter muscle myalgia

Our aim was to determine whether masseter muscle (M) and plasma (P) levels of prostaglandin E2 (PGE2) or leukotriene B4 (LTB4) are influenced by local glucocorticoid administration and whether such changes would be associated with corresponding changes in local pain or hyperalgesia. Eighteen patients with fibromyalgia and 15 with local masseter myalgia were examined immediately before and 2 weeks after intramuscular administration of glucocorticoid with regard to masseter muscle resting pain and tenderness to palpation, pressure pain threshold, maximum voluntary mouth opening (MVM), and pain on maximum voluntary mouth opening. The primary criteria for inclusion were presence of pain for a period of at least 3 months and tenderness to digital palpation in the masseter muscle region. At both visits microdialysis samples were obtained from the masseter muscle, and venous blood was collected for analysis of PGE2 and LTB4. Dialysate levels of M-PGE2 did not change significantly after glucocorticoid administration, but reduction of masseter resting pain and increase of MVM were associated with decrease of M-PGE2 in the patients with fibromyalgia. Dialysate levels of M-LTB4 increased in both groups. In the patients with local myalgia the plasma level of LTB4 also increased, and this increase was associated with a decrease of pain and masseter tenderness. In conclusion, this study shows that reduction of masseter level of PGE2 after intramuscular glucocorticoid administration is associated with a decrease of resting pain in patients with fibromyalgia. In addition, the masseter muscle level of LTB4 increases in patients with fibromyalgia and local myalgia.

Comparison of phosphocreatine concentration in the human masseter and medial pterygoid muscles by 31P‐CSI

The aim of this study is to compare phosphocreatine (PCr) concentrations of human masseter and medial pterygoid muscles by a recently developed localized magnetic resonance spectroscopy (MRS) method, chemical shift imaging (CSI). The characteristic spectra of phosphorous metabolites including PCr and β‐ATP from the superficial part of the masseter (SM) and the deep part of the masseter (DM) and the medial pterygoid muscles (MPt) from 11 volunteers, 20–27‐year‐old were obtained. The study clearly demonstrated higher PCr/β‐ATP in the SM and MPt than in the DM both in mean values (P &lt; 0·01) and in individual subjects. The results indicate that SM and MPt are power producers. There were no significant differences in the mean values of the PCr/β‐ATP ratios in SM and MPt, however, the PCr/β‐ATP ratios varied individually and the subjects could be divided into three distinct groups: values of MPt higher than SM (group A, 4 subjects); values of MPt almost equal to SM (group B, 3 subjects); and values of MPt lower than SM (group C, 4 subjects). There appears to be a close relationship between the PCr content as determined in the groups here and occlusal guidance.

Maximum Shortening Velocity and Myosin Heavy-chain Isoform Expression in Human Masseter Muscle Fibers

While human masseter muscle is known to have unusual co-expression of myosin heavy-chain proteins, cellular kinetics of individual fibers has not yet been tested. Here we examine if myosin heavy-chain protein content is closely correlated to fiber-shortening speed, as previously reported in other human muscles, or if these proteins do not correlate well to shortening speeds, as has been demonstrated previously in rat muscle. Slack-test recordings of single, skinned human masseter fibers at 15 degrees C revealed maximum shortening velocities generally slower and much more variable than those recorded in human limb muscle. The slowest fiber recorded had a maximum shortening velocity (V0) value of 0.027 muscle lengths x s(-1), several times slower than the slowest type I fibers previously measured in humans. By contrast, human limb muscle controls produced V0 measurements comparable with previously published results. Analysis by gel electrophoresis found 63% of masseter fibers to contain pure type I MyHC and the remainder to co-express mostly type I in various combinations with IIA and IIX isoforms. V0 in masseter fibers forms a continuum in which no clear relationship to MyHC isoform content is apparent.

Abundant expression of myosin heavy-chain IIB RNA in a subset of human masseter muscle fibres

Type IIB fast fibres are typically demonstrated in human skeletal muscle by histochemical staining for the ATPase activity of myosin heavy-chain (MyHC) isoforms. However, the monoclonal antibody specific for the mammalian IIB isoform does not detect MyHC IIB protein in man and MyHC IIX RNA is found in histochemically identified IIB fibres, suggesting that the IIB protein isoform may not be present in man; if this is not so, jaw-closing muscles, which express a diversity of isoforms, are likely candidates for their presence. ATPase histochemistry, immunohistochemistry polyacrylamide gel electrophoresis and in situ hybridization, which included a MyHC IIB-specific mRNA riboprobe, were used to compare the composition and RNA expression of MyHC isoforms in a human jaw-closing muscle, the masseter, an upper limb muscle, the triceps, an abdominal muscle, the external oblique, and a lower limb muscle, the gastrocnemius. The external oblique contained a mixture of histochemically defined type I, IIA and IIB fibres distributed in a mosaic pattern, while the triceps and gastrocnemius contained only type I and IIA fibres. Typical of limb muscle fibres, the MyHC I-specific mRNA probes hybridized with histochemically defined type I fibres, the IIA-specific probes with type IIA fibres and the IIX-specific probes with type IIB fibres. The MyHC IIB mRNA probe hybridized only with a few histochemically defined type I fibres in the sample from the external oblique; in addition to this IIB message, these fibres also expressed RNAs for MyHC I, IIA and IIX. MyHC IIB RNA was abundantly expressed in histochemical and immunohistochemical type IIA fibres of the masseter, together with transcripts for IIA and in some cases IIX. No MyHC IIB protein was detected in fibres and extracts of either the external oblique or masseter by immunohistochemistry, immunoblotting and electrophoresis. Thus, IIB RNA, but not protein, was found in the fibres of two different human skeletal muscles. It is believed this is the first report of the substantial expression of IIB mRNA in man as demonstrated in a subset of masseter fibres, but rarely in limb muscle, and in only a few fibres of the external oblique. These findings provide further evidence for the complexity of myosin gene expression, especially in jaw-closing muscles.

Correlation of the near-infrared spectroscopy signals with signal intensity in T 2-weighted magnetic resonance imaging of the human masseter muscle

The purpose of this study was to compare and contrast blood volume changes transcutaneously measured using near-infrared (NIR) spectroscopy against water signal intensity changes taken from a transverse T 2-weighted MR image of the masseter muscle in healthy human subjects before, during and after contraction. Eight healthy non-smoking males with no history of chronic muscle pain or vascular headaches participated (mean age: 23.9±0.6 years). The MRI data were gathered using a turbo spin echo sequence (TR: 2300 ms; TE: 90 ms; FOV: 188×300 mm; scanning time: 30 s; slice thickness: 10 mm) and the slice level was set at the mid-point between the origin and insertion of the masseter. Intramuscular haemoglobin (Hb) levels and water content of the right masseter muscle were continuously monitored for 2 min before, 30 s during and 15 min after a maximum voluntary clenching (MVC) task. Both the near-infrared and MRI data were baseline-corrected and normalized and mean levels were established and plotted. Plots of the data showed that both near-infrared-based total Hb and T 2-weighted MRI-based signal-intensity levels clearly decreased during contraction and a clear post-contraction rebound response was evident after the contraction. The near-infrared data were found to be highly correlated with MRI-based signal-intensity data (Pearson's r=0.909, P<0.0001). In conclusion, these data provide powerful evidence that near-infrared data (total Hb), transcutaneously taken from the masseter muscle in humans, will reflect the intramuscular water signal intensity changes seen using a T 2-weighted MRI imaging method.

Task-dependent control of human masseter muscles from ipsilateral and contralateral motor cortex.

Corticotrigeminal projections to human masseter motoneuron pools were investigated with focal transcranial magnetic stimulation (TMS). Responses in left and right masseter muscles were quantified from the surface electromyogram (EMG) during different biting tasks. During bilateral biting, TMS elicited motor evoked potentials (MEPs) in both masseter muscles. On average, the MEP area in the masseter contralateral to the stimulus was 39% larger than in the ipsilateral muscle, despite comparable pre-stimulus EMG in both muscles. MEPs elicited while subjects attempted unilateral activation of one masseter muscle were compared with those obtained in the same muscle during a bilateral bite at an equivalent EMG level. MEPs in the masseter contralateral to the stimulated hemisphere were significantly smaller during unilateral compared with bilateral biting. There was no significant difference in the size of ipsilateral MEPs during ipsilateral and bilateral biting. We conclude that the corticotrigeminal projections to masseter are bilateral, with a stronger contralateral projection. The command for unilateral biting is associated with a reduced excitability of corticotrigeminal neurons in the contralateral, but not the ipsilateral motor cortex. We suggest that this may be accomplished by reduced activity of a population of corticotrigeminal neurons which branch to innervate both masseter motoneuron pools.

Pain mediation by prostaglandin E2 and leukotriene B4 in the human masseter muscle

The pathophysiology behind chronic pain from masticatory muscles is unclear. Our hypothesis was that this pain is of inflammatory origin and associated with release of inflammatory mediators. The aim of this study was therefore to investigate the presence of prostaglandin E2 (PGE2) and leukotriene B4 (LTB4) in the masseter muscle and plasma and their relation to myalgia. Nineteen patients with fibromyalgia, 19 with local myalgia of the masseter muscle, and 11 healthy individuals were examined with regard to local muscular pain intensity at rest and pressure pain threshold. Inclusion criteria were masseter muscle pain for at least 3 months and masseter muscle tenderness on digital palpation. Samples were obtained from the masseter muscle by microdialysis, and the dialysates and venous blood samples were analyzed with regard to PGE2 and LTB4 concentration. Intramuscular levels were found in all groups, with significantly higher levels of LTB4 in the patients with fibromyalgia, in whom PGE2 was positively correlated to muscular pain. In the healthy individuals PGE2 was negatively correlated to pressure pain threshold. In both patient groups but not in the healthy individuals LTB4 increased during the consecutive samplings. PGE2 and LTB4 were detectable in the plasma of all groups. In conclusion, both PGE2 and LTB4 were found in the human masseter muscle. LTB4 levels are increased on needle trauma in patients with myalgia. PGE2 levels are related to muscular pain in patients with fibromyalgia. Masseter muscle pain therefore seems to be partly of peripheral inflammatory origin in fibromyalgia.

Length changes in the human masseter muscle after jaw movement.

The human masseter is a multilayered, complex muscle contributing to jaw motion. Because variations in stretch may cause muscle fibers to function over different portions of their length-tension curves, the aim of this study was to determine how parts of the masseter lengthen or shorten during voluntary jaw movements made by living subjects. Magnetic resonance (MR) imaging and optically-based jaw-tracking were used to measure muscle-insertion positions for four parts of the muscle with six degrees of freedom (DOF), before and after maximum-opening, jaw protrusion and laterotrusion in four adult males. Muscle part lengths and intramuscular tendon lengths were calculated, and these data, with fiber-tendon ratios published previously, were used to estimate putative changes in fiber-length. During maximum jaw-opening, the largest increases in muscle length (34-83%) occurred in the medial part of the deep masseter, whereas the smallest changes occurred in the posterior-most, superficial masseter (2-19%). Smaller changes were found during movement to the ipsilateral side, than during protrusion and movement to the contralateral side. On maximum opening, putative fibers in the deep masseter lengthened up to 83%, whereas those of the superficial masseter stretched up to 72%. The masseter muscle does not stretch uniformly for major jaw movement. Jaw motion to the ipsilateral side causes little length change in any part, and the effect of tendon-stretch on estimated fiber lengths is not substantial. The stretch that occurs infers there are task-related changes in the active and passive tensions produced by different muscle regions.