Continuing Education (CE)

The continuing education article below is available to subscribers of Orthodontic Practice US. In order to earn continuing education credits, you must be a Free or Paid subscriber and complete a short quiz about the content of the article. Our Free CE is limited to only 2 free credit hours per year.

Purchase a subscription now.

Sleep, orthodontics, and myofunctional therapy

CE Publish Date: 09/21/2021
CEU (Continuing Education Unit): 2 Credits


Educational aims and objectives

This self-instructional course for dentists aims to show how orthodontics and myofunctional therapy combine to provide solutions for sleep-related breathing disorders.

Expected outcomes

Orthodontic Practice US subscribers can answer the CE questions by taking the quiz online at orthopracticeus.com to earn 2 hours of CE from reading this article. Correctly answering the questions will demonstrate the reader can:

  • Identify forms of sleep disorders and their prevalence.
  • Realize the connection between sleep disorders and growth and development of orofacial and dentofacial structures.
  • Identify OSA phenotypes.
  • Recognize the role that speech language pathologists and myofunctional practitioners have in treatment of sleep-breathing disorders.

Speech pathologist Sharon Moore discusses orofacial-nasal-pharyngeal function in the management of sleep-disordered breathing

This article outlines connections between medical and dental science, the whole-body health axis, the oral health-function axis, and sleep. The clinical relationship between the speech pathologist, who is dealing with processes and functions in the upper airway that govern alimentation and communication, is closely tied to the role of the orthodontist, who manages structural aspects of the stomatognathic system and dental-occlusal abnormalities in patients. These roles intersect with sleep and breathing.

The cost of poor sleep

“Sleep is not optional; it is a biological necessity.”1 The importance of sleep is recognized increasingly, largely through the explosion of research outlining the detrimental effects of poor sleep.2,3

In the past 100 years, sleep time has eroded by 20%, with 33% U.S. adults trying to survive on 6 hours or less a night.1 This is not enough. Similarly, in Australia, the 2016 Sleep Health Foundation (SHF) Australia survey showed 33% to 45% of Australian adults get inadequate sleep.4

When it comes to the cost of poor sleep, figures from the SHF in 2021 on the cost of untreated sleep problems revealed the fiscal burden to society of $14.4 billion and $36.6 billion in nonfinancial costs related to lack of well-being.5 Meanwhile, in the United States, health care utilization costs were $94.9 billion annually.6 The cost of untreated sleep problems is estimated at 1% to 3% GDP.7,8

Beyond the financial, physical, and mental costs of poor sleep, there are measurable changes at the level of DNA and microcellular structure irrespective of cause or severity.9 Yet sleep myths and misperceptions abound (Figure 1). Sleep health is serially missed, dismissed, and misdiagnosed by health professionals and the community alike.1,10 Subsequently, many sleep problems are left untreated. The good news is that we as health professionals are able to bust these myths, impart essential sleep health messages, and provide treatment options to our patients.

Figure 1

Defining good sleep

So, what is great sleep? Many believe getting plenty of sleep hours constitutes great sleep. However, good sleep means getting the right number of hours in addition to great sleep quality (Figure 2). Simply, you need both.11-14

Figure 2: The sleep formula — To get great sleep you need the correct number of hours, which varies by age, of quiet, uninterrupted sleep. The result of great sleep is waking refreshed and able to manage natural energy peaks and troughs throughout the day

What could go wrong?

What is preventing so many people from achieving consistent good sleep? Many factors influence our ability to sleep well, which can be divided into two categories: 1) diagnosable sleep disorders and 2) problems due to sleep health practices, including environment, behavior, and routines.11

Sleep problems due to unhealthy sleep practices may resolve relatively easily by modifying sleep habits and lifestyle. However, of the more than 90 sleep disorders, the most prevalent is insomnia, and the second most prevalent is sleep-disordered breathing (SDB). Obstructive sleep apnea (OSA) is the most serious form of SDB, requiring medical, dental, or allied health expertise (Figure 3). Interestingly, research by Krakow, et al., shows abnormal breathing is under-recognized in its role in insomnia with abnormal breathing leading to sleep fragmentation, suggesting SDB-OSA prevalence is likely higher than currently measured.15-18

Figure 3

Prevalence data for OSA across 16 countries, using American Academy of Sleep Medicine (AASM) 2012 diagnostic criteria and apnea-hypopnea index (AHI) threshold values, estimated that 936 million adults aged 30-69 years have mild-to-severe OSA, and 425 million adults aged 30-69 years have moderate-to-severe OSA. The number of affected individuals was highest in China, followed by the United States, Brazil, and India.19 Furthermore, OSA risk increases due to obesity and aging, and in some elderly groups, OSA prevalence was found to be as high as 90% in men and 78% in women.20 Studies suggest that up to 25% of adult males and 15% of adult females are habitual (every night or most nights) snorers, and the frequency of occasional snoring is even higher.21

SDB and orthodontics

Sleep medicine is embraced by many dental and orthodontic practices that are playing a critical role in assessing and treating patients suffering from SDB, in particular OSA.22,23 Orthodontists are well suited for treatment of SDB patients due to their expertise regarding the growth and development of orofacial and dentofacial structures, as well as orthopedic, orthodontic, and surgical correction of the jaws, and other supporting tissues.24,25

Upper airway collapsibility or impaired anatomy is the major driving force in the pathogenesis of OSA, including anatomical features like with microretrognathia or midface hypoplasia, which restricts the size of the bony compartment of the upper airway, leading to upper airway narrowing and closure during sleep independent of obesity for many individuals with OSA.26,27

Growth anomalies that limit oral space and hence tongue space, including those that limit transverse, anteroposterior, and/or vertical dimensions, contribute to oral crowding, rendering the upper airway susceptible to collapse, crowding, or obstruction.28 Malocclusion is an anatomical factor signaling possible SDB.29,30

Anatomical factors beyond the oral cavity in the upper airway may also play a part — the nose, turbinate nasal passages, paranasal sinuses, pharynx, and laryngopharynx.31 Narrowing can occur at one or multiple levels along the pharynx.32

The primary role of the orthodontist in SDB is oral appliance therapy (OAT) designed to bring the mandible and tongue forward to open the pharyngeal spaces, allowing for continuous breathing during sleep.33-35 There is a correlation between maxillomandibular size and nasopharyngeal width varying with the severity of OSA.36 There are a number of studies demonstrating the efficacy of expansion and bone growth guidance in children and adults.37-40

Environmental factors such as allergens and pollutants may be relevant considering their influence on soft-tissue health within the mouth and upper airway. Further, processes such as inflammatory, cerebral blood flow changes, hormonal changes, and postural alterations along with currently unknown variables may also contribute to OSA pathophysiology.41

Functional upper airway impairments — e.g., hypotonia — may contribute to pharyngeal collapsibility in SDB. Appreciation of the functional aspects of upper airway health alongside anatomical factors is important, with orthodontists well-positioned to note both anatomical and functional risk factors for OSA beyond the oral cavity.

Neither gold-standard medical treatment for OSA nor oral appliance therapy is always tolerated by patients or successful, underscoring the importance of alternative treatment modalities like myofunctional therapy that improve upper airway patency.42,43

OSA phenotypes

Consideration of the various OSA phenotypes, including the pathophysiology of OSA, assists treatment choices with patients, including suitability of mandibular advancement splint treatment (MAS, also known also as OAT), prediction, and efficacy. Eckert, et al., propose a personalized approach to target therapy or a combination of therapies based on four OSA phenotypes, which can play a crucial role in OSA pathogenesis for some patients.44

While some degree of “impaired” upper airway anatomy is a prerequisite for OSA, impairment in the non-anatomical traits is also an important contributor to OSA pathogenesis.45 The malleability of soft tissues of the upper airway render it vulnerable to closure and collapse during sleep along with other influencing factors (Figure 4).

Figure 4: SDB exists on a continuum. On the severe end of the continuum, OSA is a multi-factorial disorder, where anatomical and non-anatomical factors can contribute to pathophysiology or airway collapsibility, while mouth breathing is on the mild end of the continuum

Four proposed phenotypes

Anatomical 

  1. Pcrit: Pcrit is the critical closing air pressure below which the tissues collapse in the upper airway, unable to maintain an open airway during sleep, with measures linked to narrowing, crowding, or collapsibility in the upper airway.

Non-anatomical phenotypes

  1. Low arousal threshold (AT): AT is the breathing effort measured via eosphageal or epiglottic pressure swings that will lead to arousal. Impairment in OSA means waking with minor increases in breathing effort (low AT). Frequent arousals prevent deeper, more stable stages of slow wave sleep in conjunction with rapid changes in blood gases which destablize breathing patterns that may also interfere with recruitment of upper airway dilator muscles.
  2. High loop gain (LG): Breathing during sleep is regulated by partial pressure of carbon dioxide (PaCO2).LG refers to the magnitude of a ventilatory response to a ventilatory disturbance. High LG refers to high frequency of fluctuations between wake and sleep with unstable breathing and is thought to play a key role in OSA pathogenesis for at least 30% of patients.46,47
  3. Upper airway dilator response (UADR): UA dilator muscles that maintain upper airway patency are primarily genioglossus and levator veli palatini.48 Poor UADR is impacted by the many pressure-sensitive chemo- and mechano-receptors in the UA. These in turn are influenced by different sleep stages and neural drive to the dilator muscles. Negative pharyngeal pressures and blood gas exchanges may increase neural drive for dilator muscle activity influencing UADR. Further, snoring-induced changes in the distribution of muscle fiber types leave the UA more susceptible to fatigue.

The ideal candidate for MAS/OAT, based on current phenotyping concepts and the available evidence, is a patient with a mild-to-moderate collapsible upper airway with minimal or no impairment in the other non-anatomical phenotypes (i.e., the patient does not have high loop gain).

SDB, speech language pathology, and myofunctional therapy

While speech pathology and sleep may seem like unlikely bed partners, they fit together in two main ways. First, sleep problems interfere with a person’s memory, learning, thinking, behavior, emotional regulation, and communication skills.1 Given the nature and goals of speech pathology, treatments that address disorders of alimentation and/or communication, how can progress be possible when insufficient sleep is undermining the very learning faculties required to build skill, develop new patterns and behaviors, and ameliorate development?

Speech language pathologists and myofunctional practitioners look closely at the facial bones and muscle systems of the upper airway critical for eating, breathing, and speech — the same system that supports healthy breathing during sleep. Research showed that OSA can be improved by up to 62% in children and 50% in adults just by working with the muscles in the upper airway.49 Considering these statistics, mild-to-moderate OSA could be significantly improved, if not resolved, with myofunctional therapy intervention (Figure 5).

Figure 5

Eckert, et al., outline the complexity of underlying causes of airway collapse using four phenotypes. While anatomical features are highly relevant, the authors suggest ~30% may be a result of pharyngeal muscle collapsibility that may be responsive to oropharyngeal exercises.50

Another UADR strategy is stimulation of the hypoglossal nerve, which provides drive to the muscles of the tongue and reduces the AHI by up to 70% or more with accompanying improvements in OSA symptoms.31,51

Myofunctional therapy is a patient-specific tailored program of resistance-based isometric and isotonic exercises designed to improve upper airway patency.

Although the mechanism is not well understood, a study in the British Medical Journal 2005 showed regular didgeridoo playing is an effective treatment alternative well accepted by patients with moderate OSA.53 Other research highlighted the “favorable effects of playing certain wind instruments and singing in alleviating symptoms and risk of snoring and OSA.”54 Koka, et al., in 2021 concluded that orofacial myofunctional therapy offers good potential for the treatment of OSA as an alternative method for increasing muscle tone in a noninvasive manner.55

Further research outlined a role for myofunctional therapy as an alternative or adjunct to CPAP, oral appliance therapy, and adenotonsillectomy surgery to reduce snoring, modify tongue tone, and decrease the recurrence of SDB.56-61

Given the tongue is the primary airway dilator,  research is exploring the role of tongue function and mobility in SDB.62-66

Interrupting a circle of disease

This conversation is really about circles of health and disease. As we consider SDB within the context of our professional work, there are connections between oral and whole-body health, orthodontics, myofunctional science, and sleep. There are not only abundant physical and mental health impacts from untreated sleep problems, but also signs and symptoms of SDB and other major health problems associated with SDB that are evident in the mouth. Let’s consider the reason many patients seek dental-orthodontic expertise: headaches, bruxism and clenching, facial esthetics, TMJD, pain, and periodontal disease — all of which can be comorbid with SDB.67

Further, when the stomatognathic system is not functioning optimally, there are concomitant impacts on body functions — e.g., digestion and breathing. It goes both ways.

A healthy mouth contributes to digestive, nervous, cardiovascular, skeletal, lymphatic, respiratory, neuromuscular, integumentary, and endocrine system health highlighting circular relationships between oral, systemic, and whole-body health, as does resolution of SDB.68 Oral function plays a critical role in the oral health paradigm (Figure 6).

Figure 6

As we discuss the circle of life, so too can we discuss the circle of disease (Figure 7). Just as the mouth is a mirror of health, it is a mirror for common medical ailments like chronic sinus, reflux, anxiety, depression, diabetes, and atherosclerosis, which all have links to oral health and function and SDB.69 Considering that the consequences of untreated sleep problems impact cardiovascular, endothelial, metabolic, immune systems, and more, the circle of disease emerges with the mouth a mirror for disease.

Figure 7: The mouth is a litmus test for health and disease, including sleep health. We can break the circle of disease

Multidisciplinary teams are required to break the disease cycle and promote health by addressing root causes of oral-related health complaints, interrupting otherwise inevitable health problems.70 In doing so, assist identification of some of the many sufferers who go undiagnosed and untreated, until their disease becomes more serious.

OSA is shown to be linked to both anatomical and functional features within the stomatognathic system, highlighting treatment options and a natural synergy between the disciplines of orthodontics and speech language pathology.

There has never been a more important time for medical, dental, and orthodontic professionals to work together.

Summary

An increasing number of adults are not getting the sleep they need, and this takes a financial, occupational, physical, and emotional toll. Fortunately, orthodontists are well placed to assist. With expertise in orofacial and dentofacial structures, they have the knowledge required for diagnosing structural contributors to SDB, while their orthopedic, orthodontic skills, and surgical knowledge place them in a position to offer oral appliance or other therapy or recommend surgery. The importance of the orthodontist playing a role in management of sleep problems as a global health concern cannot be emphasized enough.

OSA is shown to be linked to both anatomical and functional features within the stomatognathic system, highlighting treatment options and a natural synergy between the disciplines of orthodontics and speech language pathology. Speech pathologists and myofunctional practitioners trained in re-educating the muscles of the upper airway can provide valuable support for these patients, as an adjunct to orthodontic or medical interventions, or as a stand-alone treatment for the many patients who cannot tolerate CPAP or OAT.

Ultimately, when all health professionals have sleep health on their radar as part of the overall care of their patients, taking a team approach to total patient care will achieve the best results. In doing so, we may interrupt the circle of disease and engage patients in the circle of health.

If you would like to learn more about sleep issues in kids and how to address them, please read Sleep-Wrecked Kids or visit http://www.wellspoken.com.au. Queries can be addressed to projects@wellspoken.com.au.

Read more about myofunctional therapy in Nicole Cavalea’s article on how strengthening and retraining the muscles and educating patients on breathing techniques can aid in maintaining orthodontists’ results: https://orthopracticeus.com/ce-articles/treatment-and-delivery-methods-for-myofunctional-therapy/

Author Info

Sharon Moore is an author, speech path-ologist, and myofunctional practitioner with 40 years of clinical experience across a range of communication and swallowing disorders. Moore has a special interest in early identification of craniofacial growth anomalies in children, concomitant orofacial dysfunctions, and airway obstruction in sleep disorders.

References

  1. Walker, Matthew. Why We Sleep. Penguin Books; 2018.
  2. Ramar K, Malhotra RK, Carden KA, et al. Sleep is essential to health: An American Academy of Sleep Medicine position statement. J Clin Sleep Med. Online ahead of print.
  3. Worley SL. The extraordinary importance of sleep: The detrimental effects of inadequate sleep on health and public safety drive an explosion of sleep research. 2018;43(12):758-763.
  4. Adams R, Appleton S, Taylor A, McEvoy D, Antic N. Report to the Sleep Health Foundation 2016 sleep health survey of Australian adults. The University of Adelaide: The Adelaide Institute for Sleep Health Foundation website. https://www.sleephealthfoundation.org.au/pdfs/surveys/SleepHealthFoundation-Survey.pdf
  5. Rise and try to shine: The social and economic cost of sleep disorders in Australia. Sleep Health Foundation website. April 2021 https://www.sleephealthfoundation.org.au/files/Special_reports/Final_report_-_Cost_of_sleep_disorders_-_14042021.pdf.
  6. Huyett P, Bhattacharyya N. Incremental health care utilization and expenditures for sleep disorders in the United States. J Clin Sleep Med. Online ahead of print.
  7. Streatfeild J, Smith J, Mansfield D, Pezzullo L, Hillman D. The social and economic cost of sleep disorders. 2021.
  8. Mattei M. Zzzs to dollars: How much does sleep deprivation cost? Sleep Advisor Website. https://www.sleepadvisor.org/sleep-deprivation-cost/.
  9. Irwin MR, Wang M, Campomayor CO, Collado-Hidalgo A, Cole S. Sleep deprivation and activation of morning levels of cellular and genomic markers of inflammation. Arch Intern Med. 2006;166(16):1756–1762.
  10. Meaklim H, Jackson ML, Bartlett D, et al. Sleep Education for healthcare providers: Addressing deficient sleep in Australia and New Zealand. Sleep Health. 2020;6(5):636-650.
  11. Moore S. Sleep-Wrecked Kids. New York: Morgan James Publishing; 2019.
  12. Parliament of the Commonwealth of Australia: House of Representatives Standing Committee on Health, Aged Care and Sport. Inquiry into sleep health awareness in Australia, bedtime reading. https://www.aph.gov.au/Parliamentary_Business/Committees/House/Health_Aged_Care_and_Sport/SleepHealthAwareness/Report. April 2019.
  13. Buysse DJ. Sleep health: can we define it? Does it matter?. 2014;37(1):9-17.
  14. Krause AJ, Ben Simon E, Mander, BA, et al. The sleep-deprived human brain. Nat Rev Neurosci. 2017;18(7):404–418.
  15. Sateia MJ, Doghramji K, Hauri PJ, Morin CM. Evaluation of chronic insomnia. An American Academy of Sleep Medicine review. 2000;23(2):243-308.
  16. Meira E Cruz M, Kryger MH, Morin CM, et al. Comorbid insomnia and sleep apnea: mechanisms and implications of an underrecognized and misinterpreted sleep disorder. Sleep Med. 2021;84:283-288.
  17. Krakow B, Melendrez D, Ferreira E, et al. Prevalence of insomnia symptoms in-patients with sleep-disordered breathing. 2001;120(6):1923-1929.
  18. Mendes MS, dos Santos JM. Insomnia as an expression of obstructive sleep apnea syndrome – the effect of treatment with nocturnal ventilatory support. Rev Port Pneumol. 2015;21(4):203-208.
  19. Benjafield AV, Ayas NT, Eastwood PR, et al. Estimation of the global prevalence and burden of obstructive sleep apnoea: A literature-based analysis. Lancet Respir Med. 2019;7(8):687-698.
  20. Senaratna CV, Perret JL, Lodge CJ, et al. Prevalence of obstructive sleep apnea in the general population: A systematic review. Sleep Med Rev. 2017;34:70-81.
  21. Pandya C, Guilleminault C. In: Aminoff MJ, Daroff RB, eds. Encyclopedia of the Neurological Sciences (2nd edition). Academic Press: London, UK; 2018.
  22. Stark TR, Pozo-Alonso M, Daniels R, Camacho M. Pediatric considerations for dental sleep medicine. Sleep Med Clin. 2018;13(4):531-548.
  23. Addy N, Bennett K, Blanton AO. Policy statement on a Dentist’s role in treating sleep-related breathing disorders. Journal of Dental Sleep Medicine. 2018;05(01):25-26.
  24. Behrents RG, Shelgikar AV, Conley RS et al. Obstructive sleep apnea and orthodontics: An American Association of Orthodontists white paper. Am J Orthod Dentofacial Orthop. 2019;156(1):13- 28.
  25. Agarwal L, Gupta A. Role of Orthodontist in obstructive sleep apnea- An orthodontic review. J Orthod Endod. 2016;2:3.
  26. Okubo M, Suzuki M, Horiuchi A, et al. Morphologic analyses of mandible and upper airway soft tissue by MRI of patients with obstructive sleep apnea hypopnea syndrome. 2006;29(7):909-915.
  27. Simpson R, Oyekan AA, Ehsan Z, Ingram DG. Obstructive sleep apnea in patients with Down syndrome: current perspectives. Nat Sci Sleep. 2018;10:287-293.
  28. Ravesloot MJL, de Vries N. One hundred consecutive patients undergoing drug-induced sleep endoscopy: Results and evaluation. 2011;121(12):2710-2716.
  29. Miyao E, Noda A, Miyao M, Yasuma F, Inafuku S. The Role of malocclusion in non-obese patients with obstructive sleep apnea syndrome. Intern Med. 2008;47(18):1573-1578.
  30. Aroucha Lyra MC, Aguiar D, Paiva M, et al. Prevalence of sleep-disordered breathing and associations with malocclusion in children. J Clin Sleep Med. 2020;16(7):1007–1012.
  31. Koka V, De Vito A, Roisman G, et al. Orofacial myofunctional therapy in obstructive sleep apnea syndrome: A pathophysiological perspective. Medicina (Kaunas). 2021;57(4):323.
  32. Vroegop AV, Vanderveken OM, Boudewyns AN, et al. Druginduced sleep endoscopy in sleep-disordered breathing: Report on 1,249 cases. 2014;124(3):797-802.
  33. Lim J, Lasserson TJ, Fleetham J, Wright J. Oral appliances for obstructive sleep apnoea. Cochrane Database Syst Rev. 2006;2006(1).
  34. Ferguson KA, Cartwright R, Rogers R, Schmidt-Nowara W. Oral appliance for snoring and obstructive sleep apnea, a review. 2006;29(2): 244-262.
  35. Galeotti A, Festa P, Viarani V, et al. Correlation between cephalometric variables and obstructive sleep apnoea severity in children. Eur J Paediatr Dent. 2019;20(1):
    43-47.
  36. Wang SH, Keenan BT, Wiemken A, et al. Effect of weight loss on upper airway anatomy and the apnea–hypopnea index. the importance of tongue fat. Am J Respir Crit Care Med. 2020;201(6):718-727.
  37. Sánchez-Súcar AM, Sánchez-Súcar FB, Almerich-Silla JM, et al. Effect of rapid maxillary expansion on sleep apnea-hypopnea syndrome in growing patients. A meta-analysis. J Clin Exp Dent. 2019;11(8):e759–e767.
  38. Kim JE, Hwang KJ, Kim SW, Liu SYC, Kim SJ. Correlation between craniofacial changes and respiratory improvement after nasomaxillary skeletal expansion in pediatric obstructive sleep apnea patients. Sleep Breath. Online ahead of print.
  39. Machado AJ Jr, Crespo AN. Cephalometric study of alterations induced by maxillary slow expansion in adults. Braz J Otorhinolaryngol. 2006;72(2):166-172.
  40. Handelman CS, Wang L, BeGole EA, Haas AJ. Nonsurgical rapid maxillary expansion in adults: Report on 47 cases using the haas expander. Angle Orthod. 2000;70(2):129–144.
  41. Dempsey JA, Veasey SC, Morgan BJ, O’Donnell CP. Pathophysiology of sleep apnea. Physiol Rev. 2010;90(1):47-112.
  42. Rotenberg BW, Murariu D, Pang KP. Trends in CPAP adherence over twenty years of data collection: a flattened curve. J Otolaryngol Head Neck Surg. 2016;45:43.
  43. Saglam-Aydinatay B, Taner T. Oral appliance therapy in obstructive sleep apnea: Long-term adherence and patients experiences. Med Oral Patol Oral Cir Bucal. 2018;23(1):e72-e77.
  44. Carberry JC, Amatoury J, Eckert DJ. Personalized management approach for OSA. 2018;153(3):744-755.
  45. Lai V, Carberry JC, Eckert DJ. Sleep apnea phenotyping: Implications for dental sleep medicine. J Dent Sleep Med. 2019;6(2).
  46. Wellman A, Jordan AS, Malhotra A, et al. Ventilatory control and airway anatomy in obstructive sleep apnea. Am J Respir Crit Care Med. 2004;170(11):1225-1232.
  47. Eckert DJ, White DP, Jordan AS, Malhotra A, Wellman A. Defining phenotypic causes of obstructive sleep apnea. Identification of novel therapeutic targets. Am J Resp Crit Care Med. 2013;188(8):996-1004.
  48. Saboisky JP, Butler JE, Fogel RB, et al. Tonic and phasic respiratory drives to human genioglossus motoneurons during breathing. J Neurophysiol. 2006;95(4):2213-2221.
  49. Camacho M, Certal V, Abdullatif J, et al. Myofunctional therapy to treat obstructive sleep apnea: A systematic review and meta-analysis. 2015;38(5):669-675.
  50. Owens RL, Edwards BA, Eckert DJ, et al. An integrative model of physiological traits can be used to predict obstructive sleep apnea and response to non positive airway pressure therapy. 2015;38(6):961-970.
  51. Strollo PJ Jr, Soose RJ, Maurer JT, et al. Upper-airway stimulation for obstructive sleep apnea. N Engl J Med. 2014;370(2):139-149.
  52. Eastwood PR, Barnes M, Walsh JH, et al. Treating obstructive sleep apnea with hypoglossal nerve stimulation. 2011;34(11):1479-1486.
  53. Puhan MA, Suarez A, Cascio CL, Zahn A, Heitz M, Braendli O. Didgeridoo playing as alternative treatment for obstructive sleep apnoea syndrome: randomised controlled trial. 2006;332(7536):266-270.
  54. Baba RY. Role of playing wind instruments and singing in snoring and obstructive sleep apnea. J Clin Sleep Med. 2020;16(9):1429–1430.
  55. Diaferia G, Badke L, Santos-Silva R, Bommarito S, Tufikand S, Bittencourt L. Effect of speech therapy as adjunct treatment to continuous positive airway pressure on the quality of life of patients with obstructive sleep apnea. Sleep Med. 2013;14(7):628-635.
  56. Lee SY, Guilleminault C, Chiu HY, Sullivan SS. Mouth breathing, “nasal disuse,” and pediatric sleep-disordered breathing. Sleep Breath. 2015;19(4):1257-1264.
  57. Camacho M, Guilleminault C, Wei JM, et al. Oropharyngeal and tongue exercises (myofunctional therapy) for snoring: A systematic review and meta-analysis. Eur Arch Otorhinolaryngol. 2018;275(4):849-855.
  58. Villa MP, Evangelisti M, Martella S, Barreto M, Del Pozzo M. Can myofunctional therapy increase tongue tone and reduce symptoms in children with sleep-disordered breathing? Sleep Breath. 2017;21(4):1025-1032.
  59. Guilleminault C, Huang YS, Monteyrol PJ, Sato R, Quo S, Lin CH. Critical role of myofascial reeducation in pediatric sleep-disordered breathing. Sleep Med. 2013;14(6):518-525.
  60. Wang W, Di C, Mona S, Wang L, Hans M. Tongue function: An underrecognized component in the treatment of obstructive sleep apnea with mandibular repositioning appliance. Can Respir J. 2018(30):1-7.
  61. Villa MP, Brasili L, Ferretti A, et al. Oropharyngeal exercises to reduce symptoms of OSA after AT. Sleep Breath. 2015;19(1):281-289.
  62. Zaghi S, Valcu-Pinkerton S, Jabara M, et al. Lingual frenuloplasty with myofunctional therapy: Exploring safety and efficacy in 348 cases. Laryngoscope Investig Otolaryngol. 2019;4(5):489-496.
  63. Guilleminault C, Huseni S, Lo L. A frequent phenotype for paediatric sleep apnoea: short lingual frenulum. ERJ Open Res. 2016;2(3):00043-2016.
  64. Yoon AJ, Zaghi S, Ha S, Law CS, Guilleminault C, Liu SY. Ankyloglossia as a risk factor for maxillary hypoplasia and soft palate elongation: A functional – morphological study. Orthod Craniofac Res. 2017;20(4):237-244.
  65. Yuen HM, Au CT, Chu WCW, Li AM, Chan KC. Reduced Tongue Mobility: An Unrecognised Risk Factor of Childhood Obstructive Sleep Apnoea. 2021 Aug 25:zsab217. doi: 10.1093/sleep/zsab217. Epub ahead of print. PMID: 34432065.
  66. Schar MS, Omari TI, Woods CM, et al. Altered swallowing biomechanics in people with moderate-severe obstructive sleep apnea. J Clin Sleep Med. 2021;17(9):1793–1803.
  67. NT Huynh, E Emami, JI Helman, RD Chervin. Interactions between sleep disorders and oral diseases. Oral Dis. 2014;20(3):236–245
  68. Baiju RM, Peter ELBE, Varghese NO, Sivaram R. Oral Health and Quality of Life: Current Concepts. J Clin Diagn Res. 2017;11(6):ZE21-ZE26.
  69. Maples S, Kightlinger Decouteau D. Blabber Mouth. Blabber Mouth Press; 2015
  70. Olshansky SJ. From lifespan to healthspan. 2018;320(13):1323–1324.

 

Stay Relevant with Orthodontic Practice US

Join our email list for CE courses and webinars, articles and mores

Read our following terms and conditions before subscribing.

Terms and Conditions checkbox is required.
Something went wrong. Please check your entries and try again.

Subscribe Today

Orthodontic Practice US is a leading dental journal and your publication for Orthodontic continuing education, Orthodontic case studies, and more. Subscribe to Orthodontic Practice US today!

Online Dental CE

Earn 16 dental continuing education credits as an Orthodontic Practice US subscriber per year.

Other Dental Publications
Dental Sleep Practice
Endodontic Practice
Implant Practice
Orthodontic Practice

MedMark Media is the leading interactive marketing and advertising company specializing in marketing and advertising, custom media, and public relations for the U.S. dental industry.

AGD PACE MedMark White (1)

Copyright © 2021 Orthodontic Practice US - Dental Journal and Online Dental CE | MedMark LLC
15720 North Greenway Hayden Loop, Suite #9 Scottsdale, AZ 85260 | All rights Reserved | Privacy Policy | Terms & Conditions

Scroll to Top