|
 
 |
| REVIEW ARTICLE |
|
| Year : 2020 | Volume
: 14
| Issue : 1 | Page : 16-22 |
|
Airway-focused dentistry – Hype versus truth
Sukhbir Singh Chopra1, Sanjay Manohar Londhe2
1 CMDC (SC), Pune, Maharashtra, India
2 Dte Gen Dental Services, New Delhi, India
| Date of Submission | 17-Dec-2019 |
| Date of Acceptance | 20-Dec-2019 |
| Date of Web Publication | 31-Jan-2020 |
Correspondence Address:
Sukhbir Singh Chopra
CMDC (SC), Pune - 411 040, Maharashtra
India
 Source of Support: None, Conflict of Interest: None
DOI: 10.4103/JODD.JODD_3_19
Dental sleep medicine (DSM) is an emerging subspecialty in dentistry. Many dentists are adopting it in clinical practice to screen for and treat obstructive sleep apnea (OSA). The value of evidence-based medicine for OSA, oral appliance treatment, and good collaboration with sleep medicine physicians in sleep disorder care is important for all dentists who practice DSM. This article aims to assess the “hype” and “truth” in the arena of DSM from contemporary literature. DSM is a science with rapidly expanding body of information that is dynamically evolving and can challenge previously accepted concepts.
Keywords: Dental sleep medicine, obstructive sleep apnea, oral appliance therapy, sleep-disordered breathing, sleep-related breathing disorders
How to cite this article:
Chopra SS, Londhe SM. Airway-focused dentistry – Hype versus truth. J Dent Def Sect. 2020;14:16-22 |
| Introduction | |  |
For more than two decades, dental sleep medicine (DSM) and oral appliance therapy (OAT) management of sleep-related breathing disorders (SRBDs) such as snoring and obstructive sleep apnea (OSA) by dentists have been in vogue. A standardized approach to SRBDs optimally should be collaborative in nature between dentists and physicians.
DSM is taught less than optimally required in dental schools,[1] and many dental educators may have scant clinical expertise of DSM. They may be prejudiced in disseminating information based on mercenary mercantile commerce or outdated facts. Evidence-based DSM knowledge and protocols are unavoidable for optimal patient care in this evolving field, also contemporary information may challenge concepts previously accepted.[2]
OSA is generally treated with continuous positive airway pressure (CPAP), known as the OSA therapy gold standard.[3] CPAP and custom-made oral appliance (OA) are equally effective in the management of mild-to-moderate OSA patients.[4]
Many dentists find OSA to be solely anatomical due to a small upper airway (UA). Nevertheless, anatomy is just one of multitude of elements that affects severity and occurrence of OSA. The pathophysiology of OSA is complex and often incomplete. It is affected by age, body mass index (BMI), gender, pharyngeal muscle response, low threshold of excitement, decrease in sleep-related lung capacity, fluid redistribution, and UA surface tension.[5] Most patients with SRBD have several factors that lead to OSA.[6] The value of personalized medicine will, therefore, enable better patient phenotyping and the choice of best management approaches, whether CPAP or OAT with an exercise plan, pharmaceutical adjuncts, or weight loss.[7]
Aim
The aim of this article is to highlight commonly practiced concepts and clinical protocols that are not supported by contemporary evidence.
| All Patients Need to Be Screened for Obstructive Sleep Apnea | | |
Hype
Dentists are advised to test all patients for SRBD as an integral constituent of comprehensive medical and dental history to identify the signs of sleepiness, pain, snoring, or apneas and to determine risk factors such as obesity, retrognathy, or hypertension.[8]
Truth
Screening of the general population can lead to overdiagnosis and overtreatment of patients with mild OSA who would be requiring only education on factors that exacerbate their OSA. These patients could overburden the medical system particularly in health-care systems of the government providing treatment at no cost to the patients.
There is insufficient evidence of using screening question sheets for adults without symptoms to properly identify who will benefit from additional OSA testing.[9] For moderate-to-severe OSA, mortality increases.[10] Nonetheless, mild OSA has not yet been shown to have adverse clinical outcomes and is associated with similar results to those without OSA.[10]
Contemporary data does not justify a general population screening.[11] It is the dentist's duty to refer to a physician for assessment and screening patients with a high probability of having OSA based on a validated checklist and a medical history.
| Patients May Be Treated for Snoring by Dentists Without Involving a Physician | | |
Hype
Many dentists have used an anti-snoring appliance to treat disruptive snoring patients. If the patient had no other comorbidities, such as obesity, excessive daytime sleepiness, or cardiovascular disease, it was assumed that no medical consultation was necessary.
Truth
The assumption that primary snoring was made by the patient is a de facto indication that the patient does not have OSA. Any type of sleep-disordered breathing (SDB) requires medical examination and adequate testing by a physician for a definitive diagnosis before a dentist begins therapy.
| Imaging for Obstructive Sleep Apnea Diagnosis and Determinant of Oral Appliance Therapy Success | | |
Cephalometry
Hype
Cephalometrics is an integral part of the armamentarium of each orthodontist. The involvement of OSA and OAT performance associated with factor cephalometric results. Among the results cited are retrognathy, narrower airway, shorter and thicker soft palate, or lower facial height.
Truth
Such results were contradictory and none predicted a high degree of the sensitivity and specificity of OSA.[12] Early studies concluded that there was no link between cephalometric variables and apnea of moderate sleep.[13] On imaging, only 52% of patients with OSA have a reduced posterior airway space.[14]
There is a strong relationship between craniofacial defects and OSA, but these are not diagnostic of OSA.[15] The UA width has also been postulated to correlate with OSA, but men have higher SDB predominance than women, whereas women have smaller airway than men.[16] Airway size does not, therefore, automatically indicate the presence or absence of SDB.
Airway closing also happens laterally, not anteroposteriorly, and hence, traditional lateral cephalometry will skip this dimension's narrowing. The normal airway is much less if a patient is prone (lying down, as in sleeping position) than if the patient is upright.[17] There is no connection between OSA severity and Sella-Hyoid (S-H) distance; hence, it is not advisable to use the S-H range as a screening test as a replacement for current diagnostic tests.[18]
There is no link between OAT performance and cephalometric findings.[19] At present, cephalometry neither cannot identify patients with high risk OSA nor can predict patients who are likely to benefit from OAT.
| Cone Beam Computed Tomography | | |
Hype
Patients with OSA have a smaller UA than that of controls without the disease. Compared to cephalometry, cone beam computed tomography (CBCT) can view the UA volumetrically. Three-dimensional evaluation of UA cross-section has been correlated with the outcomes on the Berlin Questionnaire, Epworth Sleepiness Scale, neck circumference, and BMI. The most relevant anatomical characteristic of the UA related to OSA pathogenesis is a minimal cross-sectional area.[20]
Truth
There is no significant difference in CBCT findings between moderate to severe OSA and mild to normal subjects.[21] If imaging is performed at the end of the expiration using dynamic computed tomography (CT), there is a discrepancy.[22] Dynamic CT is not available in most dental clinics. In a study that was monitored for BMI, gender, and age, the specific pharyngeal volume sub-regions did not correlate with apnea-hypopnea index (AHI). Screening with generic questionnaires and anthropomorphic measurements helps patients to avoid unnecessary radiation exposure with the same outcome as expected.[23] To date, as an indicator of effective OSA therapy with OAT, no study has shown a good model for improvements in UA size with or without an OAT in awake patients, likely because biomechanical findings cannot be directly associated with clinical outcome.[24] The use of CBCT is also complicated by the absence of uniform scanning protocols and different nomenclatures used in different studies.[25] There is insufficient evidence that CBCT-evaluated airway dimensional adjustments are appropriate for assessing care outcomes[26] and no prospective data are available on predicting OAT performance.
| Acoustic Reflection | | |
Hype
Acoustic reflection (AR) is a noninvasive technique that uses sound reflection to infer the transversal area of the UA. Research has established typical UA cross-sectional areas and has confirmed that AR-inferred airway area corresponds well with CT and magnetic resonance imaging determined UA region.[27]
Truth
Snorers had a smaller mean cross-section of the pharynx after breathing out compared to nonsnorers. Furthermore, after full breathing out, snorers with OSA and nonsnorers had a further reduction in the UA region, while snorers without OSA had no such reduction.[28] There is no link between success with OAT and the narrowest part of the UA as determined by AR.[29] A single case study was the only article that addressed directly using AR to predict the appropriate position of the mandible for optimal OA effect.[30] There is lack of literature for AR predicting OSA's presence or determining the mandibular position which would lead to OA's success.
Imaging may aid to identify the narrowest location of the UA, but it has not been shown to predict where the airway collapses, identify individuals who may or may not have OSA, or who will respond positively to OAT.
| Oral Appliance Therapy Is as Effective as Continuous Positive Airway Pressure | | |
Hype
Dentists assume OAT is as successful as CPAP at all times.
Truth
The collapsible airway is about 5 inches long in males and about 4 inches long in females.[31] Collapse may occur posterior to the tongue, soft palate, and/or hypopharynx. The collapse may be lateral, anterior/posterior, or concentric.[32] CPAP is the only treatment that effectively stents open the entire collapsible airway pneumatically and is not site-specific.
OAT has its most significant effect behind the tongue, less so behind the soft palate, with a declining effect closer to the epiglottis; the positive effect of OAT is marginal in those patients with supine positional sleep apnea with an important component of epiglottic blockage.[33] CPAP is not unique to the area, whereas OAT is specific to the site.
OAT's patient adherence rate is much higher than CPAP.[34] CPAP's daily use is <4.6 h a night,[35] whereas average OA use is 6.8 h a night.[36] A patient with mild to moderate OSA may not have OSA fully controlled by the OA, but uses the appliance throughout the night and is expected to achieve similar medical outcomes using either CPAP or OAT. In the first few months, both forms of therapy have a large dropout rate. More than 30% of patients avoid using OAT or CPAP relatively quickly.[37] Despite the control of subjective symptoms, there is probability that OAT will become less effective over time.
| Oral Appliance Therapy Has No Side Effects | | |
Hype
OAT is safe and noninvasive without any side effects.
Truth
OAT is based on an orthodontic device invented by Herbst in 1909[38] to permanently advance the mandible in children with retrognathia. Therefore, it may be inferred that the major side effects could be orthodontic in nature, i.e., significant labial tipping of the mandibular incisors.[39] Patatal tip of maxillary incisors occurs, no change in intermolar width is observed, and overjet and overbite are reduced. This may cause prematurity of incisors leading to open bite posteriorly. These orthodontic side effects of OAT are permanent and tend to increase with continued use of OA.[40]
While the OA is titrated to an effective position, temporomandibular joint signs and symptoms may increase temporarily, but over the long-term they will resolve.[41] The other commonly observed side effects include gingival and tooth discomfort, xerostomia, sub-optimal OA fit, breakage of mouthpiece, myalgia, and increased salivary flow. These are self-limiting and usually do not result in stoppage of OAT. Lack of efficacy and continuing symptoms are primary causes for patients discontinuing OAT.[41] Up to 45% of patients receive insufficient OAT care.[42] Sleep physicians may be consulted for alternative treatment choices.
| Increased Mandibular Advancement Improves Oral Appliance Therapy Efficiency | | |
Hype
In 25% of patients with 2 mm advancement, there is a 50% reduction in the oxygen desaturation index, 48% at 4 mm and 65% at 6 mm. The need for further advancement was primarily dependent on body size and the severity of nocturnal desaturation.[43] Many dentists extrapolated the results of these studies to patients who were naturally sleeping.
Truth
Most dentists advance the mandible arbitrarily more than 65% of the patient's protrusive range, disregarding the fact that >30% of patients are treated successfully at a lesser advancement.[44] Lesser mandibular advancement could lead to adequate treatment of OSA with fewer side effects.[45] Mandibular advancement as low as 1 mm is effective in treating certain OSA patients.[46]
| Orthodontic Therapy Can Cause or Prevent Obstructive Sleep Apnea | | |
Therapeutic extractions in orthodontics
Hype
Orthodontics adds to the burden of OSA, or has the ability to mitigate OSA. Many dentists perceive that four premolar extraction orthodontics aggravates OSA. Retraction of incisors contributing to crowding the tongue and decreasing UA space is also presumed. An OSA diagnosis after orthodontic therapy began to be correlated with changes in UA dimensions.
Truth
Extraction or nonextraction orthodontics reveals no statistical change in the volume of the UA.[47] Medical records of 5585 adult patients at the Health Partners of Minnesota reviewed by Larsen et al. in 2015 revealed that 50% patients had one premolar missing in each quadrant and it was indicative of an earlier orthodontic therapy. The patients were case controlled, matched for gender, age, and BMI. Polysomnography (PSG) was used for the confirmatory diagnosis of OSA. Two hundred and sixty-seven patients without missing premolars were diagnosed with OSA and 299 patients with missing premolars had a diagnosis of OSA. Hence, there was no significant difference in the prevalence of OSA between the two groups.[48]
| Rapid Palatal Expansion | | |
Hype
Commonly between 2 and 7 years when lymphoid tissues are largest childhood OSA tends to occur. Thus, childhood OSA is commonly treated with adenotonsillectomy. Many patients are cured with this therapy; however, a large subset of children suffer from residual OSA.[49] A small maxilla or mandible may be predisposing factor in children for SDB mediated by high nasal resistance and mouth breathing. This may alter tongue position and also oropharyngeal volume. Reduction of nasal resistance and subsequent rise of tongue toward the palate, improving muscle tone, and aiding nasal breathing is observed with rapid maxillary expansion (RME). Lower AHI and long-term SDB resolution has been exhibited in studies on children with craniofacial abnormalities and OSA treated with RME.[50]
Truth
Bimaxillary expansion had worsening of SDB was observed in significant number of children.[51] Kikuchi hypothesized, based on the functional matrix growth theory that orthodontic treatment of children with OSA would prevent SDB as they grew older.[52] However, there are no studies to support this.
Studies in both adults and children have found that surgical maxillary expansion helps to reduce AHI in those with transverse deficiencies.[53] However, there are no data that supports orthodontic therapy of patients with OSA without underlying craniofacial abnormality.[54]
| Obstructive Sleep Apnea, Sleep Bruxism, and Gastroesophageal Reflux Disease Causes and Effects | | |
Relationship between OSA, sleep bruxism (SB), and gastroesophageal reflux disease (GERD), found in 20%–35% of the general population has been hypothesized.[55]
| Obstructive Sleep Apnea and Gastroesophageal Reflux Disease | | |
Hype
The association between GERD and OSA is thought to be associated with producing negative intrathoracic pressure during obstructive apneas, which is expected to move stomach contents more easily into the esophagus. CPAP reduced reflux events in OSA and OSA-free controls.[56]
Truth
In a large demographic sample, there was only a small difference in the prevalence of GERD in those who had OSA and those without OSA. The severity of GERD is associated with OSA. However, the severity of OSA did not affect the prevalence of GERD.[55] There is also a physiological compensatory improvement that protects against reflux during respiratory events.[57]
There is no concomitant change in age-related rise of incidence of GERD, though incidence of OSA increases with age. The correlation with increased incidence of GERD in OSA patients may be associated with the common risk factors of family history, alcohol intake, obesity, female gender, hip circumference,[57] narcolepsy, and race.[58]
| Obstructive Sleep Apnea and Sleep Bruxism | | |
Hype
Occlusal discrepancies and stressful events were historically associated with SB. Practitioners of DSM have hypothesized a correlation between a breathing event and subsequent SB, as a physiologic reaction to a breathing event, which assists in reestablishment of an open airway.[58]
Truth
The relationship between SDB and SB has yet to be established.[59] The gold standard for SB diagnosis is PSG with electromyography leads over the major mastication muscles to identify rhythmic masticatory muscle activity. The presence of SB is often detected by clinicians using anamnestic patient report or tooth wear data. The involvement of tooth wear may also contribute to inaccuracies in the determination of SB.[60]
There is an age-related increase in the prevalence of OSA and decline of SB with age. SB is most common in children (14%–20%), stabilizes to approximately 8%–12% in teenagers and adults and thereafter decreases to 3%.[61] Hence, middle-aged, at-risk patients have the highest probability of an intersection of both disorders.
There is no single explanation accounting for the SB mechanism and the association between SB and OSA, which has a complex relationship with many clinical commonalities such as an alteration in muscle tone, obesity, gender, race, and BMI.[62] Common features in adult patients associated with SB and SDB are related to sleep position, oropharyngeal muscle activity, sleep arousal, headache, and GERD. The common risk factors are obesity, age, gender, alcohol consumption, and smoking. All three diseases often coexist with intersecting lifetime prevalence and clinical characteristics that affect their clinical presentation; however, no causality can be inferred among these findings.[63]
| Conclusions | | |
Dentists must only screen those patients who are at high risk for OSA. Validated sleep questionnaires and review of medical data may be utilized. For the final diagnosis, patients must be referred to a physician. Dentists should maintain regular communication with the physician of the patient and other health-care providers about the progress of the patient's diagnosis and any prescribed follow-up treatment.
There is scant contemporary evidence to prove that the imaging used in dentistry is effective in diagnosing OSA patients or predicting OA's therapeutic outcome.
OAT should not be the only option for treatment. Multiple treatment options may be incorporated as half of the OA receiving patients will be treated inadequately and 37% may discontinue therapy within the 1st year. The titration of the OA should be reduced to the minimum necessary to effectively monitor the SDB, thus maintaining improved health outcomes with possible occlusal changes.
Orthodontic therapy for OSA patients with craniofacial abnormalities such as transverse deficiency may have a positive effect on sleep parameters. However, without such an abnormality, this cannot be extrapolated to patients.
Future research aimed primarily at prospective studies based on the disputed areas that change previous criteria and further enhance the diagnosis and treatment of OSA patients. It is predicted that dentists will play a much greater role in screening and the treatment of SRBDs in the coming years.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
| 1. | Ivanoff CS, Pancratz F. Incidence of sleep disorders reported by patients at UTHSC college of dentistry: A two-year follow-up and proposed educational program. J Dent Educ 2015;79:548-56.  |
| 2. | Levine M, Bennett KM, Michelle K, Cantwell MK, Postol K, Schwartz DB. Dental sleep medicine standards for screening, treating, and managing adults with sleep-related breathing disorders. J Dent Sleep Med 2018;5:61-8. |
| 3. | Sharples LD, Clutterbuck-James AL, Glover MJ, Bennett MS,Chadwick R, Pittman MA, et al. Meta-analysis of randomised controlled trials of oral mandibular advancement devices and continuous positive airway pressure for obstructive sleep apnoea-hypopnoea. Sleep Med Rev 2015;27:108-24. |
| 4. | Dal-Fabbro C, Garbuio S, D'Almeida V, Cintra FD, Tufik S, Bittencourt L. Mandibular advancement device and CPAP upon cardiovascular parameters in OSA. Sleep Breath 2014;18:749-59. |
| 5. | Sutherland K, Cistulli PA. Recent advances in obstructive sleep apnea pathophysiology and treatment. Sleep Biol Rhythms 2015;13:26-40. |
| 6. | Malhotra A, Orr JE, Owens RL. On the cutting edge of obstructive sleep apnoea: Where next? Lancet Respir Med 2015;3:397-403. |
| 7. | Iftikhar IH, Bittencourt L, Youngstedt SD, Ayas N, Cistulli P, Schwab R, et al. Comparative efficacy of CPAP, MADs, exercise-training, and dietary weight loss for sleep apnea: A network meta-analysis. Sleep Med 2017;30:7-14. |
| 8. | |
| 9. | Jonas DE, Amick HR, Feltner C, Weber RP, Arvanitis M, Stine A, et al. Screening for obstructive sleep apnea in adults: Evidence report and systematic review for the us preventive services task force. JAMA 2017;317:415-33. |
| 10. | Pan L, Xie X, Liu D, Ren D, Guo Y. Obstructive sleep apnoea and risks of all-cause mortality: Preliminary evidence from prospective cohort studies. Sleep Breath 2016;20:345-53. |
| 11. | |
| 12. | Doff MH, Hoekema A, Pruim GJ, van der Hoeven JH, de Bont LG, Stegenga B. Effects of a mandibular advancement device on the upper airway morphology: A cephalometric analysis. J Oral Rehabil 2009;36:330-7. |
| 13. | Zucconi M, Ferini-Strambi L, Palazzi S, Orena C, Zonta S, Smirne S. Habitual snoring with and without obstructive sleep apnoea: The importance of cephalometric variables. Thorax 1992;47:157-61. |
| 14. | Milano F, Billi MC, Marra F, Sorrenti G, Gracco A, Bonetti GA. Factors associated with the efficacy of mandibular advancing device treatment in adult OSA patients. Int Orthod 2013;11:278-89. |
| 15. | Caron CJ, Pluijmers BI, Joosten KF, Mathijssen IM, van der Schroeff MP, Dunaway DJ, et al. Obstructive sleep apnoea in craniofacial microsomia: A systematic review. Int J Oral Maxillofac Surg 2015;44:592-8. |
| 16. | Mohsenin V. Effects of gender on upper airway collapsibility and severity of obstructive sleep apnea. Sleep Med 2003;4:523-9. |
| 17. | Anegawa E, Tsuyama H, Kusukawa J. Lateral cephalometric analysis of the pharyngeal airway space affected by head posture. Int J Oral Maxillofac Surg 2008;37:805-9. |
| 18. | Gulati A, Chate RA, Howes TQ. Can a single cephalometric measurement predict obstructive sleep apnea severity? J Clin Sleep Med 2010;6:64-8. |
| 19. | Cunha TCA, Guimarães TM, Schultz TCB, Almeida FR, Cunha TM, Simamoto PC Junior, et al. Predictors of success for mandibular repositioning appliance in obstructive sleep apnea syndrome. Braz Oral Res 2017;31:e37. |
| 20. | Chen H, Aarab G, de Ruiter MH, de Lange J, Lobbezoo F, van der Stelt PF. Three-dimensional imaging of the upper airway anatomy in obstructive sleep apnea: A systematic review. Sleep Med 2016;21:19-27. |
| 21. | Enciso R, Shigeta Y, Nguyen M, Clark GT. Comparison of cone-beam computed tomography incidental findings between patients with moderate/severe obstructive sleep apnea and mild obstructive sleep apnea/healthy patients. Oral Surg Oral Med Oral Pathol Oral Radiol 2012;114:373-81. |
| 22. | Yucel A, Unlu M, Haktanir A, Acar M, Fidan F. Evaluation of the upper airway cross-sectional area changes in different degrees of severity of obstructive sleep apnea syndrome: Cephalometric and dynamic CT study. AJNR Am J Neuroradiol 2005;26:2624-9. |
| 23. | Rodrigues MM, Pereira Filho VA, Gabrielli MF, Oliveira TF, Batatinha JA, Passeri LA. Volumetric evaluation of pharyngeal segments in obstructive sleep apnea patients. Braz J Otorhinolaryngol 2017. pii: S1808-8694(17)30001-0. |
| 24. | Van Holsbeke C, De Backer J, Vos W, Verdonck P, Van Ransbeeck P, Claessens T, et al. Anatomical and functional changes in the upper airways of sleep apnea patients due to mandibular repositioning: A large scale study. J Biomech 2011;44:442-9. |
| 25. | Stuck BA, Maurer JT. Airway evaluation in obstructive sleep apnea. Sleep Med Rev 2008;12:411-36. |
| 26. | Alsufyani NA, Al-Saleh MA, Major PW. CBCT assessment of upper airway changes and treatment outcomes of obstructive sleep apnoea: A systematic review. Sleep Breath 2013;17:911-23. |
| 27. | Marshall I, Maran NJ, Martin S, Jan MA, Rimmington JE, Best JJ, et al. Acoustic reflectometry for airway measurements in man: Implementation and validation. Physiol Meas 1993;14:157-69. |
| 28. | Bradley TD, Brown IG, Grossman RF, Zamel N, Martinez D, Phillipson EA, et al. Pharyngeal size in snorers, nonsnorers, and patients with obstructive sleep apnea. N Engl J Med 1986;315:1327-31. |
| 29. | Friedman M, Shnowske K, Hamilton C, Samuelson CG, Hirsch M, Pott TR, et al. Mandibular advancement for obstructive sleep apnea: Relating outcomes to anatomy. JAMA Otolaryngol Head Neck Surg 2014;140:46-51. |
| 30. | Agarwal SS, Jayan B, Kumar S. Therapeutic efficacy of a hybrid mandibular advancement device in the management of obstructive sleep apnea assessed with acoustic reflection technique. Indian J Dent Res 2015;26:86-9. [ PUBMED] [Full text] |
| 31. | Segal Y, Malhotra A, Pillar G. Upper airway length may be associated with the severity of obstructive sleep apnea syndrome. Sleep Breath 2008;12:311-6. |
| 32. | Lee CH, Hong SL, Rhee CS, Kim SW, Kim JW. Analysis of upper airway obstruction by sleep videofluoroscopy in obstructive sleep apnea: A large population-based study. Laryngoscope 2012;122:237-41. |
| 33. | Marques M, Genta PR, Sands SA, Azarbazin A, de Melo C, Taranto-Montemurro L, et al. Effect of sleeping position on upper airway patency in obstructive sleep apnea is determined by the pharyngeal structure causing collapse. Sleep 2017;40:1-8. |
| 34. | Sutherland K, Phillips C, Cistulli PA. Efficacy versus effectiveness in the treatment of obstructive sleep apnea: CPAP and oral appliances.J Dent Sleep Med 2015;2:175-81. |
| 35. | 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. |
| 36. | de Almeida FR, Lowe AA, Tsuiki S, Otsuka R, Wong M, Fastlicht S, et al. Long-term compliance and side effects of oral appliances used for the treatment of snoring and obstructive sleep apnea syndrome. J Clin Sleep Med 2005;1:143-52. |
| 37. | Bachour P, Bachour A, Kauppi P, Maasilta P, Mäkitie A, Palotie T. Oral appliance in sleep apnea treatment: Respiratory and clinical effects and long-term adherence. Sleep Breath 2016;20:805-12. |
| 38. | Pancherz H. History, background and development of the Herbst appliance. Semin Orthod 2003;9:3-11. |
| 39. | Almeida FR, Lowe AA, Otsuka R, Fastlicht S, Farbood M, Tsuiki S. Long-term sequellae of oral appliance therapy in obstructive sleep apnea patients: Part 2. Study-model analysis. Am J Orthod Dentofacial Orthop 2006;129:205-13. |
| 40. | Minagi HO, Okuno K, Nohara K, Sakai T. Predictors of side effects with long-term oral appliance therapy for obstructive sleep apnea. J Clin Sleep Med 2018;14:119-25. |
| 41. | Doff MH, Veldhuis SK, Hoekema A, Slater JJ, Wijkstra PJ, de Bont LG, et al. Long-term oral appliance therapy in obstructive sleep apnea syndrome: A controlled study on temporomandibular side effects. Clin Oral Investig 2012;16:689-97. |
| 42. | Paoli JR, Dekeister C, Lacassagne L, Tiberge M, Montemayor T, Boutault F. Efficacy of oral appliance for obstructive sleep apnea syndrome: Result of a series of 70 patients. J Cranio Maxilo Surg 2006;34 Suppl S1:58. |
| 43. | Kato J, Isono S, Tanaka A, Watanabe T, Araki D, Tanzawa H, et al. Dose-dependent effects of mandibular advancement on pharyngeal mechanics and nocturnal oxygenation in patients with sleep-disordered breathing. Chest 2000;117:1065-72. |
| 44. | Walker-Engström ML, Ringqvist I, Vestling O, Wilhelmsson B, Tegelberg A. A prospective randomized study comparing two different degrees of mandibular advancement with a dental appliance in treatment of severe obstructive sleep apnea. Sleep Breath 2003;7:119-30. |
| 45. | Anitua E, Durán-Cantolla J, Almeida GZ, Alkhraisat MH. Minimizing the mandibular advancement in an oral appliance for the treatment of obstructive sleep apnea. Sleep Med 2017;34:226-31. |
| 46. | Remmers J, Charkhandeh S, Grosse J, Topor Z, Brant R, Santosham P, et al. Remotely controlled mandibular protrusion during sleep predicts therapeutic success with oral appliances in patients with obstructive sleep apnea. Sleep 2013;36:1517-25. |
| 47. | Valiathan M, El H, Hans MG, Palomo MJ. Effects of extraction versus non-extraction treatment on oropharyngeal airway volume. Angle Orthod 2010;80:1068-74. |
| 48. | Larsen AJ, Rindal DB, Hatch JP, Kane S, Asche SE, Carvalho C, et al. Evidence supports no relationship between obstructive sleep apnea and premolar extraction: An electronic health records review. J Clin Sleep Med 2015;11:1443-8. |
| 49. | Huang YS, Guilleminault C, Lee LA, Lin CH, Hwang FM. Treatment outcomes of adenotonsillectomy for children with obstructive sleep apnea: A prospective longitudinal study. Sleep 2014;37:71-6. |
| 50. | Pirelli P, Saponara M, Guilleminault C. Rapid maxillary expansion (RME) for pediatric obstructive sleep apnea: A 12-year follow-up. Sleep Med 2015;16:933-5. |
| 51. | Shine NP, Lannigan FJ, Coates HL, Wilson A. Adenotonsillectomy for obstructive sleep apnea in obese children: Effects on respiratory parameters and clinical outcome. Arch Otolaryngol Head Neck Surg 2006;132:1123-7. |
| 52. | Kikuchi M. Orthodontic treatment in children to prevent sleep-disordered breathing in adulthood. Sleep Breath 2005;9:146-58. |
| 53. | Vinha PP, Eckeli AL, Faria AC, Xavier SP, de Mello-Filho FV. Effects of surgically assisted rapid maxillary expansion on obstructive sleep apnea and daytime sleepiness. Sleep Breath 2016;20:501-8. |
| 54. | Huynh NT, Desplats E, Almeida FR. Orthodontics treatments for managing obstructive sleep apnea syndrome in children: A systematic review and meta-analysis. Sleep Med Rev 2016;25:84-94. |
| 55. | Basoglu OK, Vardar R, Tasbakan MS, Ucar ZZ, Ayik S, Kose T, et al. Obstructive sleep apnea syndrome and gastroesophageal reflux disease: The importance of obesity and gender. Sleep Breath 2015;19:585-92. |
| 56. | Ing AJ, Ngu MC, Breslin AB. Obstructive sleep apnea and gastroesophageal reflux. Am J Med 2000;108 Suppl 4a:120S-5S. |
| 57. | Kuribayashi S, Massey BT, Hafeezullah M, Perera L, Hussaini SQ, Tatro L, et al. Upper esophageal sphincter and gastroesophageal junction pressure changes act to prevent gastroesophageal and esophagopharyngeal reflux during apneic episodes in patients with obstructive sleep apnea. Chest 2010;137:769-76. |
| 58. | Khoury S, Rouleau GA, Rompré PH, Mayer P, Montplaisir JY, Lavigne GJ. A significant increase in breathing amplitude precedes sleep bruxism. Chest 2008;134:332-7. |
| 59. | Carra MC, Huynh N, Lavigne G. Sleep bruxism: A comprehensive overview for the dental clinician interested in sleep medicine. Dent Clin North Am 2012;56:387-413. |
| 60. | Abe S, Yamaguchi T, Rompré PH, De Grandmont P, Chen YJ, Lavigne GJ. Tooth wear in young subjects: A discriminator between sleep bruxers and controls? Int J Prosthodont 2009;22:342-50. |
| 61. | Shetty S, Pitti V, Babu S, Kumar GP, Deepthi BC. Bruxism: A literature review. Indian Prosthodont Soc 2010;10:131-48. Available from: https://10.1007/s191-011-0041-5/. [Last accessed on 2020 Jan 12]. |
| 62. | Hesselbacher S, Subramanian S, Rao S, Casturi L, Surani S. Self-reported sleep bruxism and nocturnal gastroesophageal reflux disease in patients with obstructive sleep apnea: Relationship to gender and ethnicity. Open Respir Med J 2014;8:34-40. |
| 63. | Balasubramanian R, Klasser GD, Cistulli PA, Lavigne GJ. The link between sleep bruxism, sleep disordered breathing and temporomandibular disorders: An evidence-based review. J Dent Sleep Med 2014;1:27-37. |
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