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 Table of Contents  
REVIEW ARTICLES
Year : 2021  |  Volume : 5  |  Issue : 2  |  Page : 22-28

Paediatric obstructive sleep apnoea: Pathophysiology and the role of myofunctional therapy


Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong

Date of Submission10-Dec-2021
Date of Decision24-Feb-2022
Date of Acceptance08-May-2022
Date of Web Publication20-Jul-2022

Correspondence Address:
Yan Kiu Li
Li Ka Shing Faculty of Medicine, University of Hong Kong
Hong Kong
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/prcm.prcm_21_21

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  Abstract 

The pathophysiology of obstructive sleep apnoea (OSA) is well studied in the adult population, but not in the paediatric population, although it can be generally classified into anatomical, functional, and pathological factors, with the most common aetiology being adenotonsillar hypertrophy and a reduced neuromuscular tone of the upper airway (UA) muscles. It is vital to understand the pathophysiology behind paediatric OSA, so that treatment can be optimized. Although the first-line treatment remains to be adenotonsillectomy (AT), this is not always effective, as indicated by the complex pathophysiology of OSA, leading to residual OSA post-AT. Myofunctional therapy (MFT), a newer non-invasive method focusing on re-educating, strengthening, and stimulating UA muscles, improves neuromuscular tone and prevents airway collapse, as supported by multiple randomized controlled trials (RCTs). Outcomes after 2 months to 2 years of therapy have also been positive, with children experiencing improved sleep quality, reduced emotional distress and mood swings, and reduced daytime problems, whereas polysomnogram (PSG) results revealed a clinically significant reduced apnoea–hypopnoea index post-therapy. Major limitations include poor compliance for active MFT and the short duration of the studies with small sample sizes. Given the high prevalence rates of childhood OSA, it is essential that more high-quality studies and RCTs are performed to assess the effectiveness of this treatment method, with a specific emphasis on its long-term impacts, risks, and optimal treatment duration.

Keywords: Apnoea–hypopnoea index, children, myofunctional therapy, obstructive sleep apnoea, paediatric, pathophysiology, treatment


How to cite this article:
Li YK. Paediatric obstructive sleep apnoea: Pathophysiology and the role of myofunctional therapy. Pediatr Respirol Crit Care Med 2021;5:22-8

How to cite this URL:
Li YK. Paediatric obstructive sleep apnoea: Pathophysiology and the role of myofunctional therapy. Pediatr Respirol Crit Care Med [serial online] 2021 [cited 2022 Oct 3];5:22-8. Available from: https://www.prccm.org/text.asp?2021/5/2/22/351528




  Introduction Top


Obstructive sleep apnoea (OSA) is an increasingly prevalent form of sleep-disordered breathing (SDB), occurring in 1–5% of school-aged children.[1] A previous community-based local study involving 6447 children in Hong Kong revealed that OSA has a prevalence rate of 5.8% and 3.8% in boys and girls aged between 5 and 13, respectively,[2] which was identified upon sleep questionnaires and then further confirmed by polysomnography (PSG). This figure is towards the higher end of the global prevalence rates, indicating that it is a significant problem among the paediatric population. This may be due a higher prevalence of atopy in the Chinese population, especially allergic rhinitis, leading to the swelling of the soft tissue in the airway, compromising breathing. Another reason for this could be the use of different diagnostic cut-offs for the definition OSA based on PSG results, which differs among different laboratories, thus emphasizing the importance of standardization.[2] OSA is broadly defined as the recurrent episodes of prolonged partial or intermittent complete upper airway (UA) obstruction,[3] causing fragmented sleep with disrupted ventilation. Although OSA is highly prevalent in adults and children, its pathophysiology and treatment modalities differ vastly between the two populations. It is vital that the mechanisms behind childhood OSA are understood and the condition diagnosed and treated early to avoid morbidities and detrimental complications, such as delayed growth, neurobehavioural problems, and cardiovascular dysfunction.[3]

Adenotonsillectomy (AT) is often employed to treat paediatric OSA, as a large proportion of children presenting with OSA suffer from adenotonsillar hypertrophy (ATH), which occurs in 42–70% of children,[4] thus obstructing airflow. However, studies have reported that the efficacy of AT ranges from 27% to 83%,[5],[6],[7] with lower efficacies observed if children are concurrently suffering from obesity, neuromuscular disorders, and/or craniofacial anomalies, resulting in residual OSA post-AT. Intranasal corticosteroids may be recommended in mild cases, especially if the child suffers from allergic rhinitis, or if AT is contraindicated.[8] Montelukast is another medication that may be used to alleviate symptoms of paediatric OSA, working as a leukotriene receptor antagonist to dilate airways and has proven to significantly reduce apnoea, hypopnoea, and respiratory arousals during sleep in meta-analysis studies and randomized controlled trials (RCTs).[9],[10] Continuous positive airway pressure (CPAP) has also proven to be an effective second-line treatment, but its uncomfortable and frequent side effects such as nasal dryness, mask pain, and skin irritations[11] have limited compliance to only 50% in children.[12] Furthermore, long-term usage may cause facial alterations.[13] Therefore, myofunctional therapy (MFT) has recently been introduced to treat paediatric OSA, as it is non-invasive, inexpensive, and easily applicable.

MFT was first used to treat orofacial myofunctional disorders in 1990,[14] such as tongue thrusting and impaired speech, mastication, and deglutition, but recent studies have shown its efficacy in treating residual paediatric OSA, with a meta-analysis study reporting a 62% reduction in the apnoea–hypopnoea index (AHI) afterwards,[15] which is the combined number of apnoea and hypopnoea episodes per hour during sleep. Through the combination of isotonic and isometric exercises, muscle strength, tone, and endurance can be increased.[16] Isotonic exercises refer to the pronunciation of an oral vowel sound intermittently, whereas isometric exercises involve pronouncing the sound continuously, with isotonic exercises also recruiting the pharyngeal muscles of the lateral wall.[17] It also increases the adherence to CPAP[18] by reducing the amount of pressure needed due to the strengthened UA muscles. Studies conducted in children with orthodontic problems have also demonstrated the role of MFT in re-establishing the normal orofacial anatomy.[19]

Given the high prevalence rates of paediatric OSA and its severe consequences on children’s quality of life, academic performance, brain development, and their physical and mental wellbeing, optimizing treatment is pivotal. As studies focusing on MFT and paediatric OSA remain limited, this literature review endeavours to present up-to-date information on this area, by first exploring the pathophysiology of childhood OSA, before moving onto the role of MFT in treating OSA and its implications for future patients.


  Pathophysiology of Paediatric Obstructive Sleep Apnoea Top


Structural and anatomic factors

As mentioned previously, the pathophysiology of paediatric and adult OSA is very different. In children, ATH is the most common predisposing factor for OSA.[3],[4],[20] However, an increase in the size of the soft palate, uvula, and lateral pharyngeal walls also reduces the anterior–posterior and lateral dimensions of the mouth, resulting in increased airway resistance. As younger children aged between 3 and 6 years have more prominent tonsils and adenoids,[21],[22] this may explain why OSA is more prevalent in children in this age group,[23] and why children with obesity have higher OSA prevalence rates.

Other structural factors increasing the risk of developing childhood OSA include craniofacial skeletal dysmorphologies in the mandible and maxilla.[21] Cephalometric studies have discovered that children with a narrow maxilla, mandibular retrognathia, excessive vertical lower facial development, and caudal placement of the hyoid bone are more prone to suffer from OSA, with this collection of findings termed ‘long face syndrome’.[21] These anomalies may lead to oral breathing, or ‘mouth breathing’, instead of nasal breathing, and the chronic exposure to this non-humidified and non-filtered air may elicit damage and inflammation to the UA muscles, as well as to the adenoids and tonsils, resulting in hypertrophy,[24] whereas vibratory stress, induced by prolonged oral breathing and snoring, may elicit pathological and inflammatory changes to the neuromuscular structures.[21] Additionally, continuous UA obstruction and oral breathing may induce even more craniofacial abnormalities, such as a high-arched palate and narrower maxilla,[21] leading to multiple sites of structural collapsibility.

Functional factors

The UA size is mainly determined by static pharyngeal mechanics, neuromuscular tone, and luminal pressure,[25] with multiple studies reporting children with OSA having higher positive critical closing pressures of the pharynx (Pcrit), with airways collapsing easily in mild inspiratory negative pressures,[21],[26] and did not reach the Pcrit level in healthy subjects without OSA even after AT.[21] This indicates that other neuromuscular factors may play an integral role, with the passive Pcrit and mean airway closing pressure (Pclose) being −25 cm H2O and −7.4 cm H2O, respectively, in normal children, compared with −5 cm H2O and −2 cm H2O in children with OSA,[21],[27] indicating problems with neuromuscular compensation. These factors may also result in a low lung and tidal volume, reducing tracheal tug and bronchodilation forces, thus further increasing airway collapsibility.[21]

Indeed, the control and tone of the pharyngeal dilators, such as the genioglossus, hyoglossus, and styloglossus muscles, may be impaired and dysregulated in children with OSA. These muscles are usually activated by hypercapnia, hypoxaemia, and a drop in the luminal pressure, allowing children to maintain normal inspiratory airflow even at subatmospheric pressures.[23] However, this cannot be said for children with OSA, with the study by Marcus et al. showing a significant increase in maximal inspiratory flow (VImax) during hypercapnia in normal children (P < 0.001), as opposed to no statistically significant differences in children with OSA.[27] Moreover, when comparing the VImax of normal children and those with OSA during negative atmospheric pressures, there were significant differences (P < 0.01).[27] The study by Katz and White[25] also showed more significant decreases in the genioglossus muscle activity in children with OSA during sleep onset, when compared with normal children, especially during the rapid eye movement (REM) phase. The proposed mechanisms for these findings include muscle hypotonia, low responsiveness, and impaired afferent receptors in the UA, although this is still unconfirmed.[21]

Pathological factors

Intermittent hypoxia and re-oxygenation episodes induced by OSA stimulate tissue necrosis, oxidative stress, and macrophage infiltration,[28] resulting in localized inflammation and consequent systemic inflammation due to circulating cytokines released by proinflammatory immune cells. Indeed, studies have shown that proinflammatory markers, such as tumour necrosis factor alpha (TNF-α), interleukin (IL)-17, IL-23, and C-reactive protein (CRP),[23],[29] are significantly increased in children with OSA, a study by Huang et al.[29] revealing a significant increase in these cytokines among children with ATH. A positive correlation was also found between high-sensitivity CRP (HS-CRP), the apnoea index (r=0.498), and the percentage of awake time (r=0.528).[29] These elevated proinflammatory cytokines may also affect neurocognitive functions, as demonstrated by a decrease in executive functions and reaction times in children with increased TNF-α, IL-17, and IL-23,[29] suggesting that they have adverse effects on the neural structures, which may explain the unstable ventilatory drive and low arousal threshold in children with OSA, although more studies are warranted to confirm this.

It is vital to understand the pathophysiology of this disorder before examining potential treatments, to optimize the treatment strategy. The complex pathophysiology also explains why AT alone may not be able to treat OSA, especially if the child concurrently suffers from neuromuscular and other craniofacial anomalies.


  The Role of Myofunctional Therapy Top


MFT involves using specific orofacial and pharyngeal exercises to improve and enhance labial seal and lip tone and to promote nasal breathing, while also promoting favourable positioning and coordination of the tongue.[13] By practicing these exercises consistently every day, the tongue and UA muscles can be strengthened and appropriately stimulated, while also addressing and improving their stomatognathic functions, such as breathing, mastication, phonation, swallowing, and suction.[19] Soft palate elevation exercises involve practicing various humming sequences, blowing and suctioning exercises, and pronouncing various oral vowel sounds,[19] stimulating the palatoglossus, palatopharyngeal, and tensor and levator veli palatini muscles,[14] whereas tongue exercises involve moving and positioning the tongue in different planes, with isotonic exercises being performed intermittently and isometric exercises performed continuously.[19] Facial exercises address and strengthen the orbicularis oris, buccinators, and jaw muscles,[19] so that they can efficiently elevate the mandible to reduce mouth opening.


  Efficacy Top


As the UA neuromotor tone is vital in maintaining airway patency and preventing collapsibility, strengthening and stimulating these muscles may be beneficial in treating OSA. This section will review the efficacy of active MFT and passive MFT in treating paediatric OSA.

Traditional active myofunctional therapy

There were six studies assessing the role of active MFT in treating OSA or reducing the risk factors for OSA, such as oral breathing and low tongue strength and endurance, although the study by Huang et al.[19] in 2019 evaluated both active and passive MFT in treating OSA. Passive MFT involves using an oral device during sleep to reshape the mandible and strengthen the tongue muscles through rolling the tongue bead provided in the device.[19] Active MFT requires at least one parent and child practicing the exercises at least once per day, but preferably both in the morning and evening, with exercises such as tongue sweeping, where the tongue is moved around in an anteroposterior direction against the hard palate, along with other exercises such as pronouncing various vowel sounds and alternating bilateral chewing.[30] Passive MFT, on the contrary, involves using an oral device with a bead placed on the tip of the tongue during sleep, stimulating tongue activity during the light stages of sleep, while also placing the tongue in a forward position to open the airway.[30] This would theoretically increase compliance, as there would be no additional need to perform the oropharyngeal exercises during the day and would not require the aid of parents or caregivers. The treatment durations were also different in this study by Huang et al.[19] for the MFT and passive MFT groups, as none of the children in the MFT group attended the 1-year follow-up, but those who attended the 6-month follow-up had their PSG results recorded. Unfortunately, not all studies listed evaluated the AHI scores pre- and post-treatment, such as in the study by Lee et al.[31] in 2015, which only examined the AHI scores between the MFT and the control groups, whereas Cheng et al.[32] in 2017 focused more on assessing changes in tongue strength and reductions in oral breathing post-treatment and did not use PSG to evaluate the outcomes. The results and descriptions of the studies are summarized in [Table 1]. The mean ages of the participants are included for studies that provided information on age.
Table 1: Studies assessing the use of MFT in treating paediatric OSA

Click here to view


Passive myofunctional therapy

There were three studies assessing the role of passive MFT in treating paediatric OSA, as summarized in [Table 2]. Excluding the study by Huang et al., which is included in the active MFT table. The study by Chuang et al.[30] in 2017 also evaluated passive MFT in children with full-term births and premature births, with significant AHI improvements only noted during REM sleep in children with preterm births. Home sleep tests (HSTs) were also utilized to detect for OSA in the study by Levrini et al.,[35] if hospital PSG was not available or easily scheduled, which may have affected the precision of assessment. However, if HST was used to assess the pre-treatment values, then it would also be used post-treatment, so that the results would still be valid.
Table 2: Studies assessing the use of passive MFT in treating paediatric OSA

Click here to view



  MFT and PSG Results Top


All studies evaluating MFT and AHI values pre- and post-treatment showed statistically significant results, ranging from P-values of 0.0001 to 0.0425,[19],[24],[30],[31],[32],[33],[34],[35],[36] whereas no statistically significant changes were observed in the control groups who did not undergo active MFT or passive MFT. However, the study by Lee et al.[31] only compared AHI differences between the MFT and control groups, although this also yielded a significant P-value of 0.015, which is supported by the study from Huang et al.,[19] yielding a P-value of 0.037 when comparing the AHI values between the MFT group post-treatment and the control group. Other important sleep breathing variables that were assessed with PSG include respiratory disturbance index (RDI), hypopnoea index (HI), mean oxygen saturation (SaO2), flow limitation, sleep latency, and arousal index (AI), such as in the study by Huang et al.,[19] noting statistically significant reductions in the RDI and AI and increased sleep latency, with P-values of 0.032, 0.048, and 0.036, respectively, among the 10 children who remained compliant and attended the 6-month follow-up PSG in the MFT group. Moreover, children with normal full-term births, as reported in the study by Chuang et al.,[30] had statistically significant decreases in the HI and AI (P = 0.029 and 0.021, respectively) after completing passive MFT for 6 months. The study by Guilleminault et al.[24] also assessed the lowest SaO2 (%) and flow limitation in children post-AT before and after MFT, with P-values of 0.01 and 0.0001, respectively, and all participants maintained normal PSG results, whereas the control group who did not undergo MFT had a recurrence of OSA, with AHI values increasing from 4.3 ± 1.6 to 5.3 ± 1.5, compared with the reduction to 0.5 ± 0.4 in the MFT group, and lowest SaO2 (%) of 91 ± 1.8, compared with 96 ± 1 in the MFT group.[24] However, the study by Levrini et al. did not reveal statistically significant improvements in the mean SaO2 (%) after 90 days of passive MFT, although this could have been influenced by the short duration of the study.


  MFT, Quality of Life (QOL), and Daytime Symptoms Top


Only one study, which was by Chuang et al.[36] in 2019, evaluated the impact of passive MFT on QOL and daytime symptoms before and after treatment, using the OSA-18 survey, revealing statistically significant improvements in symptoms such as mood swings (P = 0.000), aggression/hyperactivity (P = 0.008), difficulty awakening (P = 0.034), and QOL (P = 0.005).[36] The total score for sleep disturbance, physical symptoms, emotional distress, and daytime problems also improved before and after treatment, with P-values of 0.001, 0.003, 0.003, and 0.048, respectively, whereas there were no statistically significant outcomes in the control group.[36] Caregiver frustration was also decreased, with a P-value of 0.024.[36]

More studies should be performed to assess the effectiveness of MFT in improving the QOL and daytime symptoms experienced.


  MFT and Morphological and Functional Evaluations Top


Several studies assessed the role of MFT in improving airway morphology and function. The study by Villa et al.[33] in 2015 reported a statistically significant reduction in oral breathing (P = 0.002) and an increased labial seal (P < 0.001) and lip tone (P < 0.05) after treatment, which would coalesce to promote nasal breathing, the preferred respiratory route. This is supported by another study performed by Villa et al.[34] in 2017 assessing children with SDB, revealing significant decreases in oral breathing (P = 0.0002), increased lip tone (P = 0.003), reduced abnormal tongue resting position (P = 0.03), and increased tongue endurance (P < 0.01), strength (P < 0.000), and peak pressure (P < 0.000) in the MFT group after 2 months of treatment.

Similarly, the study by Cheng et al.[32] in 2017 showed statistically significant increases in the mean tongue strength (P = 0.018), from 6% to 76% after MFT, as well as improvements in stomatognathic functions such as breathing, deglutition, and mastication (P = 0.026), as assessed through Nordic Orofacial Tests.[30]


  MFT and Cephalometric Analysis Top


Several studies also examined the impact of MFT on cephalometric measurements, as shown in the study by Huang et al.[19] in 2019, identifying significant improvements in the passive MFT group, such as in the width of the airway at the level of the nasopharynx (P = 0.001) before and after treatment, with no significant changes observed in cephalometric analyses of the active MFT group. Similarly, the passive MFT studies by Chuang et al.[36] in 2019 reported statistically significant improvements in measurements such as the increased distance between the posterior nasal spine and adenoid tissues (P = 0.03) and increased width of the oropharynx (P = 0.007) in the passive MFT group after treatment. No side effects were reported, although long-term complications remain unknown, due to the limited follow-up studies performed. From the literature reviewed, the minimum length of duration to perform MFT is 2 months to see significant results, although most studies have demonstrated a duration of 6 months having more long-lasting results, and performing the exercises for around 30 min every day, with the youngest age group reported in the literature being 4–8 years old.


  Limitations Top


Unfortunately, the major limitation of MFT is the lack of compliance to therapy, due to the requirement to perform these exercises daily, along with regular meetings with myofunctional therapists.[30] Therefore, parental involvement is crucial to ensure proper completion of this training, which is a major problem in the current society, with both parents often working full-time jobs with long working hours. Furthermore, the use of MFT as a stand-alone therapy, along with its long-term effects, optimal overall treatment duration and exercise duration for each session, and whether its effects remain after cessation of therapy or whether it requires consistent practice in the long run, warrants further investigation, as this remains unknown. Younger children may also find it difficult to practice these exercises and may even perform it incorrectly, which is why parental and therapist guidance and involvement are essential.

However, the major limitation of these studies is the small sample size, large age ranges among the children assessed, absence of long-term follow-up, and the short duration of the studies, with passive MFT studies ranging from 90 days to 1 year and regular MFT studies ranging from 2 months to 2 years. There are also possible biases elicited in these studies, such as performance bias, due to the lack of blinding in the participants. However, attrition bias may be the most significant, due to the vast number of loss of follow-ups, resulting in incomplete outcome data. Heterogeneity on the duration and type of exercises performed was also presented across the studies, with some studies requiring a minimum of 20 min daily[19] and others requiring up to 45 min.[32]

Future implications

Adopting passive MFT may be helpful in increasing compliance, as it requires little involvement from parents, and children often rapidly adapt to it.[19],[30] However, potentially unfavourable impacts of passive MFT on the mandibular development remain unknown, although clinical and imaging evaluations did not detect any alterations when the device was used for 6 months.[19]

Poor compliance can also be resolved by providing adequate education and support to patients and caregivers, such as through visual coaching, smartphone health apps, and support programmes. For instance, patients participating in a 12-week MFT support programme consisting of in-person education seminars and interactions, and frequent phone calls and messages offering support, coaching, and guidance from therapists, saw significant increases in self-efficacy and decreases in AHI and daytime sleepiness (P = 0.02, 0.039, and 0.028, respectively) when compared with the control group who did not receive support and accountability and had an 82.06 ± 23.70% MFT adherence rate, compared with 72.52 ± 30.09% in the control group.[37] This is supported by an RCT conducted by O’Connor-Reina et al.,[38] in which the MFT adherence rate was 90% in patients interacting with a smartphone app for 90 sessions, compared with 50% in the control group, with the app enabling constant communication with health professionals and feedback on patient performance. As MFT is non-invasive, inexpensive, and does not carry major risks, what most patients require is simply education, motivation, and support.


  Conclusion Top


The pathophysiology of OSA in children remains complex, with multiple anatomical, functional, and pathological factors interacting with each other. It is pivotal that treatment options are optimized, due to its high prevalence rates in Hong Kong. Due to the multifactorial nature of this disorder, AT alone may not be able to resolve the issue, requiring other forms of treatment or conjunct therapy. Due to MFT and passive MFT’s proven beneficial effects on the UA muscular framework, as reported in the literature reviewed, it should be used as a treatment modality for OSA in children. However, more high-quality studies are required to clarify the adequate protocols, long-term effects, and risks of active MFT and passive MFT, and whether or not it can be used as a stand-alone therapy, as this is a relatively new treatment option, which warrants further research and understanding among physicians and patients.

Directions for future research

  • An increase in randomized multi-institutional studies, with double blinding and allocation concealment, investigating the effectiveness of MFT in treating paediatric OSA as a stand-alone therapy should be performed. It is also necessary to evaluate the optimal overall treatment duration and exercise session duration for MFT and risks it could elicit in the long run or if the exercises are not performed correctly.


  • MFT educational and support groups/programmes should be further evaluated upon, as well as other interventional studies to improve adherence to MFT, focusing on patient-centred outcomes.


  • Funding sources

    This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.

    Financial support and sponsorship

    Nil.

    Conflicts of interest

    There are no conflicts of interest.



     
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    Abstract
    Introduction
    Pathophysiology ...
    The Role of Myof...
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    MFT and PSG Results
    MFT, Quality of ...
    MFT and Morpholo...
    MFT and Cephalom...
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