Oropharyngeal exercises significantly reduce OSAS severity and symptoms and represent a promising treatment for moderate OSAS.

Current literature demonstrates that myofunctional therapy decreases apnea-hypopnea index 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 obstructive sleep apnea treatments.

This systematic review demonstrated that myofunctional therapy has reduced snoring in adults based on both subjective questionnaires and objective sleep studies.

Our results suggest that in patients with OSAS, myofunctional therapy may be considered as an adjuvant treatment and an intervention strategy to support adherence to CPAP.

Oropharyngeal exercises appear to effectively modify tongue tone, reduce SDB symptoms and oral breathing, and increase oxygen saturation, and may thus play a role in the treatment of SDB.

Despite experimental and orthodontic data supporting the connection between orofacial muscle activity and oropharyngeal development as well as the demonstration of abnormal muscle contraction of upper airway muscles during sleep in patients with SDB, myofunctional therapy rarely is considered in the treatment of pediatric SDB. Absence of myofascial treatment is associated with a recurrence of SDB.

The present study aimed to assess the presence of potential injury to neuronal areas measured as reduced grey matter volume in a group of pediatric OSA patients relative to a large set of comparable control subjects.

Participants with short sleep had reduced leptin and elevated ghrelin. These differences in leptin and ghrelin are likely to increase appetite, possibly explaining the increased BMI observed with short sleep duration. In Western societies, where chronic sleep restriction is common and food is widely available, changes in appetite regulatory hormones with sleep curtailment may contribute to obesity.

Insufficient or poor-quality sleep affects the immune system, weight management, glucose metabolism, cardiovascular and cerebrovascular health, cognition, work productivity, psychological well-being, and public safety.

Assessment of mouth breathing during sleep should be systematically performed post-adenotonsillectomy and the persistence of mouth breathing should be treated with myofunctional therapy.

Considering all this, it is therefore essential to address any problems such as chronic mouth breathing that contributes to poor skeletal and airway development in children. Under these circumstances, patients may not have enough room to accommodate the tongue or other structures, such as the palatine and lingual tonsils, that may become obstructive elements during sleep. Limited airway space from poor skeletal development may also prevent patients from maintaining adequate airway patency as they progress through the natural stages of sleep and their muscles relax. The combination of these elements may ultimately result in airflow limitation during sleep that leads to frequent arousals and drops in the blood-oxygen saturation levels, which defines what is known as obstructive sleep apnea.

The interaction between oral-facial structural growth and muscle activity starts early in development and continues through childhood. Chronic oral breathing is an important clinical marker of orofacial muscle dysfunction, which may be associated with palatal growth restriction, nasal obstruction, and/ or a primary disorder of muscular or connective tissue dysfunction. It is easily documented objectively during sleep. Treatment of pediatric obstructive-sleep-apnea (OSA) and sleep-disordered-breathing (SBD) means restoration of continuous nasal breathing during wakefulness and sleep; if nasal breathing is not restored, despite short-term improvements after adenotonsillectomy (T&A), continued use of the oral breathing route may be associated with abnormal impacts on airway growth and possibly blunted neuromuscular responsiveness of airway tissues. Elimination of oral breathing, i.e., restoration of nasal breathing during wake and sleep, may be the only valid end point when treating OSA. Preventive measures in at-risk groups, such as premature infants, and usage of myofunctional therapy as part of the treatment of OSA are proposed to be important approaches to treat appropriately SDB and its multiple co-morbidities.

Lingual frenuloplasty with myofunctional therapy is safe and potentially effective for the treatment of mouth breathing, snoring, clenching, and myofascial tension in appropriately selected patient candidates. Further studies with objective measures are merited.

Restricted tongue mobility was associated with narrowing of the maxillary arch and elongation of the soft palate in this study. These findings suggest that variations in tongue mobility may affect maxillofacial development.

A short lingual frenulum left untreated at birth is associated with obstructive sleep apnoea syndrome at a later age.

Short lingual frenulum may lead to abnormal orofacial growth early in life, a risk factor for development of SDB. Careful surveillance for abnormal breathing during sleep should occur in the presence of short lingual frenulum.

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