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 Table of Contents  
Year : 2020  |  Volume : 14  |  Issue : 1  |  Page : 16-22

Airway-focused dentistry – Hype versus truth

1 CMDC (SC), Pune, Maharashtra, India
2 Dte Gen Dental Services, New Delhi, India

Date of Submission17-Dec-2019
Date of Acceptance20-Dec-2019
Date of Web Publication31-Jan-2020

Correspondence Address:
Sukhbir Singh Chopra
CMDC (SC), Pune - 411 040, Maharashtra
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/JODD.JODD_3_19

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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

How to cite this URL:
Chopra SS, Londhe SM. Airway-focused dentistry – Hype versus truth. J Dent Def Sect. [serial online] 2020 [cited 2023 Mar 23];14:16-22. Available from: http://www.journaldds.org/text.asp?2020/14/1/16/276406

  Introduction Top

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 They may be prejudiced in disseminating information based on mercenary mercantile commerce or outdated facts.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]


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 Top


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]


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 Top


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.


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 Top



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.


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 Top


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]


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 Top


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]


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 Top


Dentists assume OAT is as successful as CPAP at all times.


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 Top


OAT is safe and noninvasive without any side effects.


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 Top


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.


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 Top

Therapeutic extractions in orthodontics


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.


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 Top


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]


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 Top

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 Top


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]


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 Top


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]


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 Top

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


Conflicts of interest

There are no conflicts of interest.

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