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Orofacial Myology and Myofunctional Therapy for Sleep Related Breathing Disorders
Abstract
Orofacial myology or myofunctional therapy can help patients suffering from sleep breathing disorders. It aims to facilitate control of the extrinsic tongue muscles to correct, stabilize, and maintain breathing, speech, swallowing, and chewing; and to enhance the tone and mobility of orofacial structures. A speech therapist or language pathologist can design orophangeal exercises to develop improved tongue posture and enhanced nasal breathing.
... After identification of 22 potentially relevant studies, they were downloaded and the reviews of the reference lists yielded an additional 6 studies, for a total of 28 studies. [7][8][9][10][11][12][13][17][18][19][20][21][22][23][24][25][26][27][28][29][30][31][32][33][34][35][36] Nine were review articles, 8,20,22,27,30,[32][33][34]36 two reported no intervention, 24,31 two studied lip exercises and the effect on lip thickness, 21,37 one reported breathing exercises not involving oral cavity or oropharyngeal structures, 28 one was a letter to the editor, 11 and two studies were abstracts in which data were later reported in the authors' journal articles. 19,25 Eleven studies met criteria and were included in this review. ...
... After identification of 22 potentially relevant studies, they were downloaded and the reviews of the reference lists yielded an additional 6 studies, for a total of 28 studies. [7][8][9][10][11][12][13][17][18][19][20][21][22][23][24][25][26][27][28][29][30][31][32][33][34][35][36] Nine were review articles, 8,20,22,27,30,[32][33][34]36 two reported no intervention, 24,31 two studied lip exercises and the effect on lip thickness, 21,37 one reported breathing exercises not involving oral cavity or oropharyngeal structures, 28 one was a letter to the editor, 11 and two studies were abstracts in which data were later reported in the authors' journal articles. 19,25 Eleven studies met criteria and were included in this review. ...
Objective
To systematically review the literature for articles evaluating myofunctional therapy (MT) as treatment for obstructive sleep apnea (OSA) in children and adults and to perform a meta-analysis on the polysomnographic, snoring, and sleepiness data.
Data Sources
Web of Science, Scopus, MEDLINE, and The Cochrane Library.
Review Methods
The searches were performed through June 18, 2014. The Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) statement was followed.
Results
Nine adult studies (120 patients) reported polysomnography, snoring, and/or sleepiness outcomes. The pre- and post-MT apnea-hypopnea indices (AHI) decreased from a mean ± standard deviation (M ± SD) of 24.5 ± 14.3/h to 12.3 ± 11.8/h, mean difference (MD) -14.26 [95% confidence interval (CI) -20.98, -7.54], P < 0.0001. Lowest oxygen saturations improved from 83.9 ± 6.0% to 86.6 ± 7.3%, MD 4.19 (95% CI 1.85, 6.54), P =0.0005. Polysomnography snoring decreased from 14.05 ± 4.89% to 3.87 ± 4.12% of total sleep time, P < 0.001, and snoring decreased in all three studies reporting subjective outcomes. Epworth Sleepiness Scale decreased from 14.8 ± 3.5 to 8.2 ± 4.1. Two pediatric studies (25 patients) reported outcomes. In the first study of 14 children, the AHI decreased from 4.87 ± 3.0/h to 1.84 ± 3.2/h, P = 0.004. The second study evaluated children who were cured of OSA after adenotonsillectomy and palatal expansion, and found that 11 patients who continued MT remained cured (AHI 0.5 ± 0.4/h), whereas 13 controls had recurrent OSA (AHI 5.3 ± 1.5/h) after 4 y.
Conclusion
Current literature demonstrates that myofunctional therapy decreases AHI by approximately 50% in adults and 62% in children. Lowest oxygen saturations, snoring, and sleepiness outcomes improve in adults. Myofunctional therapy could serve as an adjunct to other OSA treatments.
... It is made up of more than just the genioglossus muscle and, as such, can take on many shapes and form. It can move in many ways so exercises designed to position the tongue can actually improve the airway and reduce many of the signs and symptoms of a sleep breathing disorder [9,10]. These exercises are termed myofunctional or oropharyngeal tongue exercises. ...
Oral appliances gained acceptance over the last decade and, at the same time, have been proven to be an effective way to manage sleep breathing disorders. Their role has become more acceptable since the first practice parameters paper was published in 1995. Over a 10-year period since then, they have gained an even larger and expanded role. This has occurred because of an increased number of articles with a higher level of evidence relative to efficacy, they are more widely recognized by the sleep medicine and physician community, and there are improved outcomes associated with their use. In the future, oral appliances will be more recognized and accepted. This will occur as two key areas emerge in the future: studies that validate the use of oral appliances, including long-term studies, and the role of oral appliances as part of combined therapy with positive airway pressure (PAP) devices.
Dentists have an important partnership with the medical community in the recognition and management of obstructive sleep apnea (OSA) in children. OSA negatively impacts the overall health and well-being of children, and an interdisciplinary approach to management may optimize care. Sleep medicine physicians, dentists, otolaryngologists, pediatricians, orofacial myologists and other health care providers have a role in the management of pediatric OSA.
The origins of Orofacial Myofunctional Therapy began in the early 1960's by orthodontists who recognized the importance of functional nasal breathing, proper swallowing, and more ideal oral rest postures. Re-patterning these functions through myofunctional therapy assisted with better orthodontic outcomes and improved stability. Experts in orofacial myology have concluded that improper oral rest postures and tongue thrusting may be the result of hypertrophy of the lymphatic tissues in the upper airway. Orthodontists are aware of the deleterious effects these habits have on the developing face and dentition. Sleep disordered breathing is a major health concern that affects people from infancy into adulthood. Physicians who treat sleep disorders are now referring patients for orofacial myofunctional therapy. Researchers have concluded that removal of tonsils and adenoids, along with expansion orthodontics, may not fully resolve the upper airway issues that continue to plague patients' health. Sleep researchers report that the presence of mouth breathing, along with hypotonia of the orofacial muscular complex, has been a persistent problem in the treatment of sleep disordered breathing. Orofacial myofunctional disorders (OMDs) coexist in a large population of people with sleep disordered breathing and sleep apnea. Advances in 3D Cone Beam Computed Tomography (CBCT) imaging offer the dental and medical communities the opportunity to identify, assess, and treat patients with abnormal growth patterns. These undesirable changes in oral structures can involve the upper airway, as well as functional breathing, chewing and swallowing. Leading researchers have advocated a multidisciplinary team approach. Sleep physicians, otolaryngologists, dentists, myofunctional therapists, and other healthcare professionals are working together to achieve these goals. The authors have compiled research articles that support incorporating the necessary education on sleep disordered breathing for healthcare professionals seeking education in orofacial myology.
Upper airway muscle function plays a major role in maintenance of the upper airway patency and contributes to the genesis of obstructive sleep apnea syndrome (OSAS). Preliminary results suggested that oropharyngeal exercises derived from speech therapy may be an effective treatment option for patients with moderate OSAS.
To determine the impact of oropharyngeal exercises in patients with moderate OSAS.
Thirty-one patients with moderate OSAS were randomized to 3 months of daily ( approximately 30 min) sham therapy (n = 15, control) or a set of oropharyngeal exercises (n = 16), consisting of exercises involving the tongue, soft palate, and lateral pharyngeal wall.
Anthropometric measurements, snoring frequency (range 0-4), intensity (1-3), Epworth daytime sleepiness (0-24) and Pittsburgh sleep quality (0-21) questionnaires, and full polysomnography were performed at baseline and at study conclusion. Body mass index and abdominal circumference of the entire group were 30.3 +/- 3.4 kg/m(2) and 101.4 +/- 9.0 cm, respectively, and did not change significantly over the study period. No significant change occurred in the control group in all variables. In contrast, patients randomized to oropharyngeal exercises had a significant decrease (P < 0.05) in neck circumference (39.6 +/- 3.6 vs. 38.5 +/- 4.0 cm), snoring frequency (4 [4-4] vs. 3 [1.5-3.5]), snoring intensity (3 [3-4] vs. 1 [1-2]), daytime sleepiness (14 +/- 5 vs. 8 +/- 6), sleep quality score (10.2 +/- 3.7 vs. 6.9 +/- 2.5), and OSAS severity (apnea-hypopnea index, 22.4 +/- 4.8 vs. 13.7 +/- 8.5 events/h). Changes in neck circumference correlated inversely with changes in apnea-hypopnea index (r = 0.59; P < 0.001).
Oropharyngeal exercises significantly reduce OSAS severity and symptoms and represent a promising treatment for moderate OSAS. Clinical trial registered with www.clinicaltrials.gov (NCT 00660777).
Pharyngeal dilator muscle activation (GGEMG) during wakefulness is greater in patients with obstructive sleep apnea (OSA) than in healthy control subjects, representing a neuromuscular compensatory mechanism for a more collapsible airway. As previous work from our laboratory has demonstrated a close relationship between GGEMG and epiglottic pressure, we examined the relationship between genioglossal activity and epiglottic pressure in patients with apnea and in control subjects across a wide range of epiglottic pressures during basal breathing, negative-pressure (iron-lung) ventilation, heliox breathing, and inspiratory resistive loading. GGEMG was greater in the patients with apnea under all conditions (p < 0.05 for all comparisons), including tonic, phasic, and peak phasic GGEMG. In addition, patients with apnea generated a greater peak epiglottic pressure on a breath-by-breath basis. Although the relationship between GGEMG and epiglottic negative pressure was tight across all conditions in both groups (all R values > = 0.69), there were no significant differences in the slope of this relationship between the two groups (all p values > 0.30) under any condition. Thus, the increased GGEMG seen in the patient with apnea during wakefulness appears to be a product of an increased tonic activation of the muscle, combined with increased negative-pressure generation during inspiration.
Patients with obstructive sleep apnea (OSA) develop repetitive pharyngeal airway closure during sleep. Sophisticated physiologic and imaging studies have significantly advanced our understanding of the anatomic risk factors for OSA and illuminated the biomechanical mechanisms by which therapeutic interventions for this disorder such as continuous positive airway pressure, weight loss, oral appliances, and surgery increase upper airway caliber. Pharyngeal airway patency is maintained by a balance of forces between the activity of the upper airway muscles that dilate and stiffen the airway and negative intraluminal pressure. However, this balance can be disturbed by abnormalities in upper airway anatomy and neural control. Patients with OSA have been shown to have a narrowed, more collapsible pharyngeal airway. Sleep-related reduction in upper airway dilating muscle activity can lead to greater negative intraluminal pharyngeal pressure that further narrows and completely closes the airway.
During wakefulness, obstructive sleep apnoea patients appear to compensate for an anatomically narrow upper airway by increasing upper airway dilator muscle activity, e.g. genioglossus, at least partly via a negative-pressure reflex that may be diminished in sleep. Previous studies have assessed the negative-pressure reflex using multi-unit, rectified, moving-time-average EMG recordings during brief pulses of negative upper-airway pressure. However, moving-time averaging probably obscures the true time-related reflex morphology, potentially masking transient excitatory and inhibitory components. This study aimed to re-examine the genioglossus negative-pressure reflex in detail, without moving-time averaging. Bipolar fine-wire electrodes were inserted per orally into the genioglossus muscle in 17 healthy subjects. Two upper airway pressure catheters were inserted per nasally. Genioglossus EMG reflex responses were generated via negative-pressure stimuli (approximately -10 cmH2O at the choanae, 250 ms duration) delivered during wakefulness and sleep. Ensemble-averaged, rectified, genioglossus EMG recordings demonstrated reflex activation (onset latency 26+/-1 ms; peak amplitude 231+/-29% of baseline) followed by a previously unreported suppression (peak latency 71+/-4 ms; 67+/-8% of baseline). Single-motor-unit activity, clearly identifiable in approximately 10% of trials in six subjects, showed a concomitant increase in the interspike interval from baseline (26+/-9 ms, P=0.01). Genioglossus negative-pressure reflex morphology and amplitude of the initial peak were maintained in non-rapid eye movement (NREM) sleep but suppression amplitude was more pronounced during NREM and declined further during REM sleep compared to wakefulness. These data indicate there are both excitatory and inhibitory components to the genioglossus negative-pressure reflex which are differentially affected by state.
Both nasal obstruction and nasal anesthesia result in disordered breathing during sleep in humans, and bypassing the nasal route during tidal breathing in experimental animals produces decreased electromyographic activity of upper airway (UA) dilating muscles. To investigate UA responses to breathing route in normal awake humans, we studied eight healthy males (ages 21-38 yr) during successive trials of voluntary nose breathing (N), voluntary mouth breathing (M), and mouth breathing with nose occluded (MO). We measured genioglossus electromyographic activity (EMGgg) with perorally inserted bipolar electrodes, alae nasi (EMGan) and diaphragm EMG activity (EMGdi) with surface electrodes, and minute ventilation (VE) with a pneumotachograph. Mean phasic inspiratory EMG activity of both UA muscles was significantly greater during N than during M or MO, even when a 2.5-cmH2O.l-1.s inspiratory resistance was added to MO (P less than 0.01). In contrast, neither EMGdi nor VE was consistently affected by breathing route. EMGgg during N was significantly decreased after selective topical nasal anesthesia (P less than 0.002); a decrease in EMGan did not achieve statistical significance. These data suggest that peak UA dilating muscle activity may be modulated by superficial receptors in the nasal mucosa sensitive to airflow.
Obstructive sleep apnea is a fairly common disorder with significant adverse health consequences. However, the pathogenetic mechanisms remain incompletely understood. Upper airway (UA) patency is determined by several neuromuscular and nonneuromuscular factors including (1) UA dilating muscle activity, (2) the collapsing transmural pressure generated during inspiration, (3) changes in caudal traction, (4) vasomotor tone, and (5) mucosal adhesive forces. This review addresses the effect of sleep on UA function and how these factors conspire to cause UA obstruction.
Pharyngeal dilator muscles are clearly important in the pathogenesis of obstructive sleep apnoea syndrome. Substantial data support the role of a local negative pressure reflex in modifying genioglossal activation across inspiration during wakefulness. Using a model of passive negative pressure ventilation, we have previously reported a tight relationship between varying intrapharyngeal negative pressures and genioglossal muscle activation (GGEMG) during wakefulness. In this study, we used this model to examine the slope of the relationship between epiglottic pressure (Pepi) and GGEMG, during stable NREM sleep and the transition from wakefulness to sleep. We found that there was a constant relationship between negative epiglottic pressure and GGEMG during both basal breathing (BB) and negative pressure ventilation (NPV) during wakefulness (slope GGEMG/Pepi 1.86+/-0.3 vs. 1.79+/-0.3 arbitrary units (a.u.) cmH2O(-1)). However, while this relationship remained stable during NREM sleep during BB, it was markedly reduced during NPV during sleep (2.27+/-0.4 vs. 0.58+/-0.1 a.u. cmH2O(-1)). This was associated with a markedly higher pharyngeal airflow resistance during sleep during NPV. At the transition from wakefulness to sleep there was also a greater reduction in peak GGEMG seen during NPV than during BB. These data suggest that while the negative pressure reflex is able to maintain GGEMG during passive NPV during wakefulness, this reflex is unable to do so during sleep. The loss of this protective mechanism during sleep suggests that an airway dependent upon such mechanisms (as in the patient with sleep apnoea) will be prone to collapse during sleep.
Obstructive sleep apnea is an anatomic illness caused by evolutionary changes in the human upper respiratory tract. These changes include shortening of the maxillary, ethmoid, palatal and mandibular bones, acute oral cavity-skull base angulation, pharyngeal collapse with anterior migration of the foramen magnum, posterior migration of the tongue into the pharynx, descent of the larynx and shortening of the soft palate with loss of the epiglottic-soft palate lock-up. While it is commonly believed that some of these changes had positive selection pressures for bipedalism, binocular vision and locomotion, development of voice, speech and language ultimately became a substantial contributing factor. Here it is shown that these changes are the anatomic basis of obstructive sleep apnea.
The purpose of this study was to test whether the tongue position affects the electromyographic (EMG) activities of masticatory muscles. We recorded the EMG activities of the masseter and anterior temporalis muscles in 10 skeletal Class I adults. Tongue position was monitored by two pressure transducers embedded in the midpalatal region and the lingual flange of a custom-made acrylic monoblock. We instructed subjects to assume three different tongue positions: rest, superior, and anterior. Friedman's test and Sheffe's F-test were used to statistically examine differences in muscle activities induced by changes in tongue position. Significant differences were found in masseter muscle activity between the rest and anterior positions and in anterior temporalis muscle activity between the rest and both the anterior and the superior tongue positions. We concluded that masticatory muscle activity is affected by tongue position.
One postulated mechanism for obstructive sleep apnoea (OSA) is insufficient drive to the upper-airway musculature during sleep, with increased (compensatory) drive during wakefulness. This generates more electromyographic activity in upper airway muscles including genioglossus. To understand drives to upper airway muscles, we recorded single motor unit activity from genioglossus in male groups of control (n = 7, 7 +/- 2 events h(-1)) and severe OSA (n = 9, 54 +/- 4 events h(-1)) subjects. One hundred and seventy-eight genioglossus units were recorded using monopolar electrodes. Subjects were awake, supine and breathing through a nasal mask. The distribution of the six types of motor unit activity in genioglossus (Inspiratory Phasic, Inspiratory Tonic, Expiratory Phasic, Expiratory Tonic, Tonic and Tonic Other) was identical in both groups. Single unit action potentials in OSA were larger in area (by 34%, P < 0.05) and longer in duration (by 23%, P < 0.05). Inspiratory units were recruited earlier in OSA than control subjects. In control subjects, Inspiratory Tonic units peaked earlier than Inspiratory Phasic units, while in OSA subjects, Inspiratory Tonic and Phasic units peaked simultaneously. Onset frequencies did not differ between groups, but the peak discharge frequency for Inspiratory Phasic units was higher in OSA (22 +/- 1 Hz) than control subjects (19 +/- 1 Hz, P = 0.003), but conversely, the peak discharge frequency of Inspiratory Tonic units was higher in control subjects (28 +/- 1 Hz versus 25 +/- 1 Hz, P < 0.05). Increased motor unit action potential area indicates that neurogenic changes have occurred in OSA. In addition, the differences in the timing and firing frequency of the inspiratory classes of genioglossus motor units indicate that the output of the hypoglossal nucleus may have changed.
Pharyngeal muscle tone decreases in sleep and this predisposes some individuals to obstructive sleep apnea. This review summarizes the control of the genioglossus muscle by sleep-state dependent neuromodulators at the hypoglossal motor nucleus, the source of motor output to the genioglossus muscle of the tongue. Knowledge of such mechanisms is relevant to identifying and developing new strategies to augment pharyngeal muscle activity in sleep, potentially as treatments for obstructive sleep apnea.
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