Open access peer-reviewed chapter

Perspective Chapter: Role of the Oral Healthcare Team in the Management of Obstructive Sleep Apnea

Written By

Michael Greaves, Dwight McLeod and Ignacio Christian Marquez

Submitted: 24 October 2023 Reviewed: 01 November 2023 Published: 06 February 2024

DOI: 10.5772/intechopen.1003856

From the Edited Volume

Obstructive Sleep Apnea - New Insights in the 21st Century

Marco Carotenuto

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Abstract

Obstructive sleep apnea (OSA) represents a significant health issue with numerous social and health ramifications caused by disturbed sleep. Additionally, it is well-known that OSA has an influence on cardiovascular diseases. OSA has a multifactorial etiology, and therefore requires a multidisciplinary approach for both diagnosis and treatment. Traditionally, dentists have treated OSA at the request of physicians and do not routinely contribute to diagnosis and treatment; however, the awareness of OSA is increasing within the healthcare profession and the potential role of dental practitioners in its treatment is an emerging field. The dental profession is in a unique position to work with their medical colleagues in providing treatment which can dramatically improve quality of life.

Keywords

  • obstructive sleep apnea
  • dentist
  • oral healthcare team
  • mandibular advancement device
  • oral appliance therapy

1. Introduction

Oral healthcare professionals can play an important role in the screening, evaluation for clinical signs, and clinical management of obstructive sleep apnea (OSA). Dentists and other oral healthcare professionals are trained to evaluate for the clinical signs of obstructive sleep apnea, such as large tonsils, micro or retrognathia, bruxism, TMD, etc. Working with a patient’s team of medical professionals, the oral healthcare team can help provide treatment for mild to moderate OSA that includes the fabrication of oral appliances, management of dental considerations, and follow-up care to maximize treatment efficacy. In instances where patients cannot tolerate other treatment modalities, oral appliance therapy can also help in managing patients with severe OSA. Due to the high rates of patient adherence to oral appliance therapy and its efficacy, oral appliance therapy is similar in effectiveness to CPAP therapy in the treatment of mild to moderate OSA.

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2. Relevant anatomy

2.1 Oropharynx

The pharynx is located in the midline of the neck and connects the oral cavity to the gastrointestinal tract and the trachea. It is funnel-shaped with the upper portion being larger and is at the base of the skull, while the lower end is narrower and located at the level of the sixth cervical vertebra (C6). This is where the pharynx meets the larynx and the esophagus. It is formed of muscles and mucous membranes, which allows it to serve several functions related to both digestion and respiration, including food swallowing, air conduction, and voice production [1, 2, 3].

The pharynx is divided into three parts from superior to inferior: the nasopharynx, located behind the nasal conchae, the oropharynx, located posterior to the oral cavity, and the laryngopharynx, which is inferior to the epiglottis. The nasopharynx is part of the respiratory tract and conducts air from the nasal passages. Also, the lateral surface of the posterior wall of the nasopharynx includes two openings, which are called the auditory (or Eustachian/pharyngotympanic) tubes. These tubes are connected to the middle ears posteriorly. Their main function is to equalize pressure and to drain secretions of the middle ears. The oropharynx is a continuation of the oral cavity and serves to pass the bolus of food to the laryngopharynx.

The muscles of the soft palate contract to close the nasal cavity as the bolus passes from the oral cavity. This prevents the bolus from entering the nasal cavity. At the same time, the epiglottis (which is cartilage located at the superior portion of the larynx) is pushed anteriorly to close the opening to the airway and prevent food from entering. Finally, the laryngopharynx receives the bolus and moves it into the esophagus to continue digestion. Alternatively, air moves from either the nasal cavity to the nasopharynx or from the oral cavity to the oropharynx and enters the laryngopharynx to the trachea to continue its path on the respiratory tract (Figure 1) [2, 5, 6, 7].

Figure 1.

Anatomy of the upper airway [4].

2.2 Pathophysiology of obstructive sleep apnea

The pathophysiology of OSA contains many factors and differs between individuals. The major contributing components that impact the severity of the obstructive sleep apnea include anatomic obstruction of the upper airway, low respiratory arousal threshold, high loop gain (unstable respiratory control), and poor upper airway dilator muscle responsiveness [8].

The most prominent feature of the treatment of OSA is a widening of the lateral diameter of the airway, especially in the area behind the soft palate [9, 10], likely through soft tissue connections between the lateral airway wall muscles and the mandible [11]. This lateral widening of the airway can be brought about by the advancement of the mandible.

In dentistry, however, there are signs possibly related to OSA that can be observed: a hard palate that is narrow or exhibits a high arch, relationship between the maxillary and mandibular jaws, relative tongue size and other soft tissue characteristics (e.g., enlarged uvula and narrowing of the airway from the tonsillar area) [12, 13, 14].

Obstructive sleep apnea (OSA) is defined as repetitive and intermittent blockage of the upper airway during sleep [15]. The pharyngeal walls collapse, leading to this constrictor or blockage of the airway. A complete closure of blockage leads to apnea and a partial closure results in hypopnea. There can be significant consequences and changes in the nervous and circulatory systems from continued apnea events. Snoring is caused by a narrowing of the pharynx. The soft portions of the upper airway (the pharyngeal walls, uvula, and soft palate) vibrate, leading to the snoring sound (Figure 2).

Figure 2.

Blockage of the airway in obstructive sleep apnea [16].

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3. Common oral signs/symptoms

Dental professionals can identify many intraoral signs and symptoms associated with OSA during routine appointments in the dental office. Examples of the intraoral signs associated with OSA include redness of the soft palate and uvula area, narrow palate, enlarged tongue and bilateral mandibular tori. Symptoms may include dry mouth (xerostomia) and bruxism (grinding of the teeth). These signs and symptoms are not necessarily indicative of OSA, however, identification by dental professionals may serve the dental professional in identifying the need for further evaluation of OSA for the patient [17, 18]. There are several clinical indices, for example, the Mallampati index, that can be used to determine the risk level of the patient for OSA [19]. There are also several questionnaires/surveys, for example, the STOP-Bang, that can also be evaluated by dental professionals to help screen their patients for OSA [20, 21, 22]. OSA can negatively impact a patient’s oral and overall health, therefore dental professionals serve as an important resource within health care for identifying patients at risk for OSA and identifying non-adherent CPAP or OAT users.

A patient that exhibits a neck circumference greater than 40 centimeters, macroglossia, Mallampati score of Class 3 or 4, and a deep palatal vault have been shown to be predictive for a high risk for OSA [23]. When the dental professional identifies a patient exhibiting one or more of these findings, the dental professional should discuss the patient’s sleep history and screen the patient with a validated questionnaire and refer the patient for further evaluation/diagnosis if appropriate.

OSA should be seen as a condition that needs to have the signs/symptoms identified in dental appointments and should be included in a routine oral exam [24]. The inter-professional collaboration between dental and medical professionals to promote quality care for patients with potential OSA should also be brought to the attention of dental/medical professionals in their education. This is in line with the new oral health definition [20], which brings a holistic view of different domains of overall health that impact oral health. Driving determinants, one domain of oral health, are factors that affect oral health: genetic and biological factors, social environment, physical environment, health behaviors, and access to care. This new definition and framework are used “to explain the multidimensions of oral health to our patients, other healthcare professionals, policy makers, and those others we seek to collaborate with and inform” [20]. Thus, understanding associations between oral health and OSA and interprofessional collaborations within healthcare is of importance. Increased training on OSA is required for oral health professionals. This additional knowledge is an important step that would improve patient communication, education, and treatment in the dental field along with increasing interprofessional collaboration between the oral health professionals and medical professionals.

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4. Impact of OSA on oral health and outcomes of oral healthcare

OSA is a widely prevalent problem in the general population [25]. Untreated OSA is associated with long-term health consequences including hypertension, heart disease, diabetes, depression, metabolic disorders, and stroke. The high risk group of OSA include patients with ischemic heart disease, heart failure, arrhythmias, cerebrovascular diseases, and type II diabetes [26]. Untreated OSA has been shown to be associated with cognitive dysfunction, impaired productivity in the workplace, and an increased risk of motor vehicle accidents, which could result in increased risk for injury or death. Impaired vigilance, daytime somnolence, performance deficits, morning headaches, mood disturbances, neurobehavioral impairments, and general malaise are reported in individuals with OSA [27]. These long-term health consequences can drastically reduce the quality of life and wellbeing, leading to premature death. Whether diagnosed or undiagnosed, OSA is a serious threat to the overall health and longevity in those individuals who are burdened by this widely prevalent sleep-related breathing disorder [28, 29, 30, 31, 32].

Obstructive sleep apnea is characterized by frequent episodes of airflow obstruction associated with a reduced caliber of the upper airway and is vulnerable to further narrowing and collapse. Both acute and continued effects of apnea and hypopnea include oxygen desaturation [33], reduction in intrathoracic pressure, excessive daytime sleepiness, impaired cognitive function and central nervous system arousals [27, 34]. Obesity is one of the major predisposing factors [35]. Three types of apneas have been recognized, obstructive, central and mixed with Obstructive sleep apnea being the most common [36]. Weight loss can lead to improvement in OSA. Treatments for OSA are based upon a thorough medical and physical examination and a sleep study or polysomnography. Medications are not effective in the management of sleep apnea but could help with reducing the effects of pathogenic mechanisms [22, 36, 37, 38]. Table 1 highlights some of the potential risk factors/pathogenic mechanisms for OSA as outlined by Jordan et al. Addressing individual pathogenic mechanisms may be alternative treatments even though it is understood that Constant Positive Airway Pressure (CPAP) is the acceptable treatment for Obstructive Sleep Apnea.

Risk factorsPathogenic mechanismPossible treatment
Nasal Congestion
Breathing
Small Upper Airway Lumen
Surface Forces
Surfactant
Genetic & Ethnic Origin
Craniofacial Structure
Obesity
Small Upper Airway Lumen
Small Upper Airway Lumen
Low Lung Volume
Respiratory Instability
Mandibular Advancement Device
Unknown
Oxygen or Drugs
SexSmall Upper Airway Lumen
Low Lung Volume
Respiratory Instability
Mandibular Advancement Device
Unknown
Oxygen or Drugs
AgeLow Lung Volume
Respiratory Instability
Poor Airway Muscle Function
Low Arousal Threshold
Unknown
Oxygen or Drugs
Hypoglossal Nerve Stimulation
Sedatives

Table 1.

Potential risk factors/pathogenic mechanism for obstructive sleep Apnea & Treatment.

This table is a modification of Figure 3. Risk factors, pathogenic mechanism, and possible treatments for obstructive sleep apnea as presented by Jordan et al. [37].

Figure 3.

STOP-bang sleep apnea questionnaire [39].

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5. Oral-related conditions associated with OSA

Mouth breathing is a common finding in patients diagnosed with OSA or those who show signs of OSA but are not diagnosed. Xerostomia is often associated with mouth breathers and can predispose to caries and periodontal disease through complete or partial reduction of protective salivary flow to portions of the dentition during sleep or during the day. OSA and periodontal disease share some of the same risk factors and it is not uncommon to see a greater periodontal disease prevalence in patients with OSA [40]. Common risk factors may include obesity, gender, male more than female, age, smoking and mouth breathing resulting in xerostomia, and alcoholism. Additionally, increased adrenocorticosteroids stemming from stress and fatigue of inadequate sleep can put a patient at risk for periodontal disease.

The association between xerostomia and OSA has been poorly investigated. Nocturnal xerostomia or sleep-related xerostomia causes discomfort or dryness in the mouth or throat making it difficult to swallow. In a clinical study investigating xerostomia and hyposalivation in patients with OSA, the authors reported the clinical implication that OSA patients showed a decreased pH value of oral fluid which may put patients at risk for the development of dental caries. They further demonstrated that dry mouth upon awakening is a common symptom with OSA and 22 (73.3%) of the 30 patients evaluated had dry mouth and the prevalence of sleep-related xerostomia is correlated with OSA severity. In the majority of patients, dry mouth was correlated with mouth breathing and not salivary hypofunction and only 20% of the patients exhibited objective signs of hyposalivation [41].

The quantity and quality of saliva serve as a protective mechanism for the hard and soft tissue of the periodontium while allowing optimal physiologic functions of phonation, mastication and homeostasis. When the quantity and quality of saliva are affected, the tendency for disease is increased because of loss of the beneficial elements in saliva and a likelihood for increase in bacterial plaque accumulation on soft and hard tissue structures leading to inflammation of soft tissues and the potential for the development of periodontal disease and dental caries. Duplancic and colleagues, evaluating salivary parameters and periodontal inflammation in OSA patients, showed that patients with hyposalivation and reduced salivation had higher concentrations of salivary electrolytes and lower salivary pH than subjects with normal salivation and that patients with severe OSA tended to have a higher clinical attachment levels and plaque volume. The authors noted that multiple interactions might impact salivary flow and electrolyte composition and that complex interrelationships might affect the integrity of oral health, especially considering OSA severity, inflammation, concomitant diseases and medication [40].

5.1 Temporomandibular joint disease

Individuals suffering from OSA complain of snoring, experienced apnoeas, waking up with a choking sensation, excessive sleepiness [42], fatigue or exhaustion, morning headache [43], and even temporomandibular joint pain [44]. A recent systematic review, linking an association between temporomandibular disorders (TMD) and their association with sleep disorders in adults, concluded that there is inclusive evidence between the relationship of TMD and sleep bruxism (SB) and insufficient evidence regarding the relationship with obstructive sleep apnea (OSA). There is consistent evidence that supports a link between TMD and sleep quality [45]. In a review of over 706 reports on tooth wear and the mentioned dental sleep disorders, the authors concluded that tooth wear is associated with the dental sleep disorders oro-facial pain, dry mouth, GERD, and sleep bruxism. As these dental sleep disorders are interlinked, it is difficult to determine the significant consequences of each individual disorder and leads more to indirect associations [46].

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6. Screening for OSA in the dental office

In this era where interprofessional education and interprofessional collaboration care are embedded in the curriculum and taught in most professional schools to a certain degree, obstructive sleep apnea (OSA) is often a common topic that brings professional teams together for the health benefit and wellbeing of the patient. Dental and dental hygiene students are learning more about how to incorporate assessment tooling to screen for OSA. There is evidence that the dental team spends more time with their patients than their medical counterparts. According to the ADA Health Policy Resources Center, in any given year 27 million Americans visit a dentist but do not see a physician. Another 108 million visit a physician but do not see a dentist, including more than 60 percent of children aged 1 through 4 years. Increased interprofessional collaboration between dentists and medical professionals will help to raise the awareness of providers and their patients to oral and overall health [47].

Dentists and dental hygienists are exceptionally educated to counsel patients on oral health and wellness topics. Dentists and dental hygienists’ in-depth knowledge of the anatomy of the head and neck, in particular the oral cavity and oropharyngeal area makes them well suited to assisting the medical team in identifying high risk patients [48] and referring them for definitive diagnosis and treatment. Berggren et al. reported that dental professionals, including dentists and hygienists, in general dentistry experience with OSA varies widely which leads to oral and overall health problems (such as OSA) not being recognized regularly. This lack of experience can be attributed to lack of knowledge about OSA and of validated indices/questionnaires that can be used to determine OSA risk or detect patients at risk of OSA [49].

It is important to train oral health professionals about OSA as an oral health determinant and which may promote interprofessional collaboration between dental and medical professionals. Practicing dental hygienist and dentists can play even a greater role in screening by the incorporation of screening questions as part of their routine medical history, identifying potential risk factors (retrognathia, high arched palate, enlarged tonsils or tongue, enlarged tori, high Mallampati score, poor sleep, supine sleep position, obesity, hypertension, morning headache or orofacial pain, bruxism) and collaborating with the medical team in making referrals [50]. The earlier undiagnosed cases are referred to the medical team from screening the dental office, the sooner cases can be diagnosed and treated which may reduce the morbidity and possible mortality of patients, especially those with severe OSA [51]. The dentist and dental team should be proactive in screening patients for OSA and making timely referrals for diagnosis and treatment.

The Table 2 outlines some surgical considerations to manage snoring and OSA or both. Surgical interventions are not always effective and predictable in the management of OSA and/snoring, but there are notable advantages to surgery which may widen airway spaces allowing better flow of oxygen and breathing [36, 60].

Tonsillectomy [52]Recommended for enlarged tonsils, reducing obstruction to breathing
Genioglossus Tongue Advancement [52]Creates a wider space at the posterior base of the tongue for improved breathing
Uvulopalatopharyngoplasty [53, 54]Effective in snoring reduction but not a predictive therapy for OSA
Laser-assisted Uvulopalatoplasty [55]More applicable for snoring reduction and not a predictive therapy for OSA
Maxillomandibular Advancement [56, 57]A more aggressive treatment consideration when other treatment procedures are not effective in controlling OSA
Radio frequency or Somnoplasty [58]A treatment consideration which shrinks internal tissue leaving external tissues intact and requires multiple treatment sessions. Effective against snoring and OSA
Hyoid Suspension [52, 56]Leads to a wider airway and is effective an effective treatment for OSA
Tracheostomy [52, 59]Old treatment method which is considered when OSA is severe, CPAP is ruled out and cardio-pulmonary failure has developed
Bilateral Mandibular TorectomyPrevents posterior displacement of tongue

Table 2.

Obstructive sleep apnea and its surgical management [36].

CPAP is the gold standard for treatment of OSA [61], and other treatment options can be considered for treating mild to moderate OSA cases such as oral appliances [51]. The dental team is suited to play a role in the treatment and management of OSA when oral appliances are recommended by the sleep physician. Referrals can be reciprocated back to the dental team from the medical team for those patients who are diagnosed but cannot tolerate continuous positive airway pressure (CPAP) therapy and could benefit from oral appliance, including tongue positioning and mandibular advancing devices. OSA is the most common sleep disorder [25] and with increasing awareness and diagnosis, healthcare providers can work with dentists [60], given their knowledge of the structures and function of the oral cavity, to provide a customized treatment plan that is cost effective, elicits compliance and improves sleep quality, culminating in a better quality of life.

Oral appliances, mainly the mandibular advancement devices which move the mandible forward and open the airway during sleep are used to treat mild to moderate OSA, can be beneficial for patients who do not tolerate CPAP, patients who are at high risk for surgery and patients who decline surgery as a treatment option. Treatment approach for oral appliances is simple, noninvasive, cost effective and reversible. Observed oral changes associated with oral appliances in the management of OSA include tooth mobility and repositioning, temporomandibular joint pain, tenderness of teeth, sore oral soft tissues and muscle pain (Figure 4).

Figure 4.

Intraoral signs of obstructive sleep apnea [62].

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7. Oral appliance therapy

7.1 Goals and mechanism of action of oral appliance therapy

Oral appliance therapy is an effective therapy for the treatment of obstructive sleep apnea. The goal of therapeutic interventions for OSA varies in literature but has a common factor in the decrease in the apnea-hypopnea index (AHI) [63]. The AHI is defined as the average number of apneas/hypopneas that occur per hour of sleep [64]. Mild OSA exhibits an AHI of 5–15, moderate OSA exhibits an AHI of 15–30, and severe OSA is classified as an AHI > 30 [64]. Generally, successful OSA treatment is recognized as an AHI <5, a 50% reduction in AHI, to a combination of a decrease in the AHI from baseline and final AHI [63]. Approximately two-thirds of patients treated with OAT will achieve a decrease in AHI greater than 50%, with at least one-third of these patients showing a complete response (AHI < 5) [10].

Oral appliances help treat OSA in three ways: maintaining the mandible in a more closed position, maintaining the mandible in a more anterior position (protrusion), and anterior movement of the tongue [63, 65, 66].

Protrusion of the mandible is the primary mechanism of action in oral appliances fabricated for the treatment of OSA [63]. The protrusion of the mandible leads to an increase in the space of the airway, created by a widening of the airway laterally in the velopharynx (posterior surface of the hard palate to the posterior wall of the pharynx) [63]. The advancement of the mandible and the protrusion of the tongue lead to an improvement, or decrease, in the collapsibility of the airway [66, 67], likely due to the airway enlargement [63]. This reduction in collapsibility of the airway decreases the number of episodes of complete or partial collapse of the airway, thereby improving the AHI of the patient [68]. Patients with mild OSA generally respond better to oral appliance therapy, as their airways are less collapsible and they tend to show a greater increase in the size of their pharynx with OAT [69]. It is not entirely clear why the protrusion of the mandible and tongue leads to stretching of the soft tissue connections between the mandible, tongue, lateral pharyngeal walls, and soft palate, which leads to an overall enlargement of the velopharynx as shown in Figure 5 [70].

Figure 5.

Enlargement of the Velopharynx with mandibular advancement [70].

Maintaining the mandible in a more closed position allows for a reduction in the collapsibility of the airway [71]. Mouth breathing not only leads to an increase in airway collapsibility, it compromises the adherence of patients to OAT as compared to patients that breathe through their nose [72]. This leads to a decrease in overall efficacy of the treatment as the patients are not only wearing the appliances less but the appliances are less effective when they are worn.

7.2 Classifications of oral appliances

Oral appliances fabricated for the treatment of OSA are classified into two categories: mandibular advancement splits (MAS) or mandibular advancement devices (MAD) and tongue retaining devices (TRD) [63, 73]. MAS devices act by advancing the mandible forward, therefore reducing the collapsibility of the airway and increasing the size of the airway [73]. Tongue retaining devices work by suctioning the tongue in an anterior position [63, 73]. Since TRD’s have limited evidence showing their efficacy in the treatment of OSA [74], clinical guidelines relate to mandibular advancement devices (Figures 6 and 7) [63, 77].

Figure 6.

Titratable tongue retaining device [75].

Figure 7.

Mandibular advancement device [76].

There are a wide variety of MADs, ranging from custom-made to prefabricated [78]. Prefabricated MADs are made from thermoplastic material and are generally a lower cost alternative, as they are not custom fitted using bite registrations or plaster casts [78]. Custom-made appliances are fabricated using casts and a bite registration made by the oral healthcare team [78]. Evidence suggests that custom-made MADs are more efficacious in reducing OSA severity than the prefabricated MADs [79]. Due to the reduced efficacy of thermoplastic prefabricated MADs, these devices should not be used as a screening tool for the success of treatment OSA using OAT [79]. MADs vary from “monobloc,” where the upper and lower devices are attached, to “duobloc,” where the upper and lower devices are separated. The benefit of the newer duobloc designs is that they allow for titration of the advancement of the mandible and lead to less discomfort of the TMJ [78]. There are several types of duobloc designs summarized below in Figure 8 that allow for titration in a variety of ways [78].

Figure 8.

Example schematics of mandibular advancement devices [78].

7.3 Titration of oral appliances

The amount of protrusion of the mandible is a key factor in the efficacy of MAD therapy [80]. However, more protrusion does not necessarily mean a better result for the patient [80]. Since the optimal protrusion of the mandible depends on the individual patient, the device must be titrated to determine the greatest efficacy versus tolerability [80]. It has been suggested by literature that titration of the patient in the range of 50–75% of the patient’s MMP is the most efficacious, with evidence supporting no clinical difference between 50 and 75% MMP [81]. An increase in the protrusion can lead to heavier forces applied to the oral/maxillofacial system and lead to more side effects, including TMD and dental changes [81]. Therefore, a titration target of 50% of MMP is most beneficial in the decrease in airway collapsibility, increase in airway space, and limitation of potential side effects [81].

Evaluating the titration can be accomplished using a variety of methods. The patient should return to the dentist within 30 days to evaluate the calibration of the device The device can be titrated using a standardized stepwise protocol, advancing the protrusion if subjective criteria (such as daytime sleepiness or perceived reduction in apneic events) do not show signs of improvement and a reduction of the protrusion if there are side effects reported by the patient [82]. Evaluation of the device can also be completed using an at home monitoring device, such as a high-resolution pulse oximeter or home sleep apnea test (HSAT) [83]. The results of these objective tests can be sent to the patient’s physician, who can then discuss the titration of the device with the oral healthcare team. The HSAT must be evaluated by the patient’s physician [82]. Once the dentist has determined that the patient has achieved final calibration, the patient is referred back to the treating physician for evaluation of the success of the OAT [83].

7.4 Side effects/potential complications of oral appliance therapy

It is important that the dentist/oral healthcare team discuss fully with the patient the potential for complications and the importance of routine follow-ups to evaluate for both efficacy and possible side effects. During the initial stages of OAT, patients may report soreness or tenderness of the TMJ, teeth, and gums, along with either excessive salivation or dryness of the mouth [84]. These side effects are typically transient and can be related to the strain in the musculature of the due to protrusion or an increase in vertical dimension while the patient is wearing the appliance [84]. The first line treatment for soreness of the TMJ or muscles of mastication, joint sounds, excess salivation, and dry mouth associated with the appliance is watchful waiting [85]. During this time, the dentist will carefully observe and document the patient’s symptoms and discuss follow-up, depending on the persistence of the side effect [85]. Fortunately, long-term discomfort or impact that is detrimental to the TMJ do not seem to be long-term side effects [84]. Pain tends to decrease after 1–2 years, likely due to the adaptability of the temporomandibular complex [84].

A key part of the OAT would be the fabrication of a morning occlusal guide, also known as an AM aligner [85]. These guides function by engaging the patient’s biting force to help maintain the patient’s normal occlusal relationship in the morning following the use of the OAT at night [85]. These guides may also help in the stretching of the muscles of mastication [85]. This morning occlusal guide is fabricated by the oral healthcare team/dental laboratory and is made in the patient’s normal occlusion [85]. If the patient notices that he/she is unable to maintain the proper occlusion following wear of the oral appliance, the patient should immediately follow up with his/her oral healthcare provider to prevent permanent changes to the dentition or joint [85].

If the patient is experiencing soft-tissue irritation, gagging, or appliance breakage, modification of the appliance is necessary [85]. Passive jaw stretching exercises and palliative care with the use of intermittent application of ice, a soft diet, and use of anti-inflammatory medication are the first line therapy for tenderness in the muscles of mastication or persistent TMJ pain throughout the day [85]. Changes to the dentition, decreased overbite/overjet, and tooth mobility all require thorough evaluation by the dentist. In these cases, decreasing the titration of the appliance, changing the design of the appliance, or ceasing oral appliance therapy may be required [85]. To help avoid these changes, it is important for the patient to routinely use the morning occlusal guide.

Skeletal changes caused by the downward rotation of the mandible and an increase in the lower facial height are common with mandibular advancement OAT [84]. There is also a tendency for the development of a bilateral crossbite in the posterior dentition after long-term oral appliance therapy use [84]. Using a stepwise approach to the titration and calibration of the oral appliance helps lower the risk of mandibular advancement beyond the optimal position and therefore lessens the side effects experienced by the patient [84]. Due to the potential side effects and changes, it is important that the patient seek routine follow-up with the oral healthcare provider to prevent long-term changes that are detrimental to the patient’s health or function [85]. In some cases, it is prudent to cease OAT and consult with the patient’s physician (Table 3) [85].

  • Transient morning jaw pain

  • Persistent temporomandibular joint pain

  • Tenderness in muscles of mastication

  • Joint sounds

  • Intraoral tissue-related side effects

  • Soft tissue and tongue irritation

  • Gingival irritation

  • Excessive salivation/drooling

  • Dry mouth

  • Occlusal changes

  • Altered occlusal contacts/bite changes

  • Incisor changes

  • Decreased overjet and overbite

  • Alterations in position of mandibular canines and molars

  • Interproximal gaps

  • Damage to teeth or restorations

  • Tooth mobility

  • Tooth fractures or damage to dental restorations

  • Appliance issues

  • Appliance breakage

  • Allergies to appliance material

  • Gagging

  • Anxiety

Table 3.

Oral appliance therapy related side effects [85].

7.5 Benefits of oral appliance therapy

Although there are potential complications with OAT, there are also numerous benefits that make OAT an appropriate first line therapy for patients with mild to moderate OSA or who are not able to tolerate PAP therapy in severe OSA. OAT and PAP have equivalent health outcomes [63]. This is due to the fact that PAP therapy is highly efficacious but has moderate usage/compliance, while OAT therapy is moderately efficacious with higher usage [63, 86]. Although PAP has a higher efficacy, it has a lower rate of compliance when compared to OAT and therefore has a similar effectiveness [86]. Furthermore, studies show patient preference toward OAT over PAP [86]. OAT has shown to be either equal or superior to PAP therapy when evaluating quality of life and subjective sleepiness scores [86]. Along with better patient compliance, OAT also shows an improvement over PAP in social factors such as perceptions of the partner, which would lead to further success of the OAT through better adherence [87]. Although PAP has been shown to be a highly efficacious treatment for OSA, OAT should also be considered for patients due to the improvements over PAP in adherence to OAT.

7.6 Combination therapy

Oral appliance therapy can be used in conjunction with other treatment modalities to improve adherence and patient outcomes. Using oral appliance therapy in conjunction with PAP can reduce the PAP pressure requirement [63, 88]. When used in combination, PAP and OAT together have been shown to decrease both AHI and oxygen desaturation of the patient [88]. Furthermore, patients undergoing combination PAP and OAT had lowered therapeutic pressures, which helps with patient compliance in patients who are PAP intolerant [88]. OAT has also been shown to be beneficial and an increase in efficacy when used in combination with uvulopalatopharyngoplasty (UPPP) vs. UPPP alone [89]. Along with the benefits of combining OAT with other treatments, combination therapy can allow for patients to use the treatments interchangeably depending on the patient’s preference [63]. For example, when a patient is traveling, the patient can use the oral appliance as a short term treatment [90]. Oral appliance therapy can be used to help improve outcomes when paired with other therapies or can provide a short term therapy for patients when compliance is difficult.

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8. Professional organizations

With the increase in the use of oral appliance therapy, there has been development in the number and specificity of organizations focused on the treatment of obstructive sleep apnea with oral appliance therapies. In the United States, the American Academy of Dental Sleep Medicine (AADSM) was founded in 1991 as the Sleep Disorders Dental Society and is the only non-profit national professional society dedicated solely to the practice of dental sleep medicine [91]. In 2004, the American Board of Dental Sleep Medicine was established. To support the training of qualified dentists, the AADSM has Mastery Programs that certify a dentist as a “Qualified Dentist” to practice dental sleep medicine. The AADSM has worked with the American Academy of Sleep Medicine (AASM) to establish guidelines for interdisciplinary treatment of OSA between physicians and dentists [92]. Furthermore, the American Dental Association has released an evidence brief [93] for the use of oral appliances for sleep-related breathing disorders and a policy statement in 2019 outlining the Role of Dentistry in Sleep Related Breathing Disorders [94]. In this policy statement, dentists are encouraged to screen for SRBDs and establishes that OAT is an appropriate treatment for patients with mild and moderate OSA or for severe OSA when CPAP is not tolerated by the patient [94]. In Europe, the European Academy of Dental Sleep Medicine promotes best practices to support the dental treatment of sleep related breathing disorders [95]. The growth of dental sleep medicine has been supported by the development of numerous organizations to help promote and guide the interdisciplinary treatment of OSA between dentists and physicians.

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9. Conclusion

OSA is a common sleep-related breathing disorder which predisposes to life-threatening disease and can affect the quality and well-being of life. Early screening is an effective approach which could lead to referral, diagnosis and treatment. The dental team can play a vital role in this process by incorporating an in-office screening program and making referrals to the medical team. Reciprocating referrals from the medical team for fabrication of oral appliances is another way the dental team can help to improve the quality of life and well-being of patients who are diagnosed with OSA.

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Acknowledgments

The authors acknowledge Ms. Maud Mundava for her assistance in conducting the literature search and compiling the references. The authors acknowledge Ms. Alyssa Timmer for her assistance in formatting the chapter. The authors would also like to acknowledge Ms. Danielle Williams for her assistance in obtaining permissions for the images and figures in this chapter. The authors would like to thank Dr. Hanan Omar for help in obtaining funding for this chapter and the ATSU Division of Research, Grants and Scholarly Innovations for their financial support in publishing this chapter.

Conflict of interest

The authors have no conflicts of interest to disclose.

References

  1. 1. Sakamoto Y. Gross anatomical observations of attachments of the middle pharyngeal constrictor. Clinical Anatomy. 2014;27(4):603-609
  2. 2. Heyd C, Yellon R. Anatomy, Head and Neck, Pharynx Muscles. Treasure Island (FL): StatPearls Publishing; 2022
  3. 3. Ball M, Hossain M, Padalia D. Anatomy, Airway. Treasure Island (FL): StatPearls Publishing; 2022
  4. 4. Blausen.com Staff. Medical gallery of Blausen medical 2014. WikiJournal of Medicine. 2014;1(2). DOI: 10.15347/wjm/2014.010. ISSN 2002-4436
  5. 5. Kagaya H, Yokoyama M, Saitoh E, et al. Isolated pharyngeal swallow exists during normal human feeding. The Tohoku Journal of Experimental Medicine. 2015;236(1):39-43
  6. 6. Shaw SM, Martino R. The normal swallow: Muscular and neurophysiological conrol. Otolaryngologic Clinics of North America. 2013;46(6):937-956
  7. 7. Casale J, Shumway KR, Hatcher JD. Physiology, Eustachian Tube Function. Treasure Island (FL): StatPearls Publishing; 2023
  8. 8. Eckert DJ, Atul M. Pathophysiology of adult obstructive sleep apnea. Proceedings of the American Thoracic Society. 2008;5(2):144-153
  9. 9. Chan AS, Lee RW, Srinivasan VK, et al. Nasopharyngoscopic evaluation of oral appliance therapy for obstructive sleep Apnoea. The European Respiratory Journal. 2010;35:836-842
  10. 10. Chan AS, Sutherland K, Schwab RJ, Zeng B, Petocz P, Lee RW, et al. The effect of mandibular advancement on upper airway structure in obstructive sleep apnoea. Thorax. 2010;65(8):726-732. DOI: 10.1136/thx.2009.131094
  11. 11. Brown EC, Cheng S, McKenzie DK, Butler JE, Gandevia SC, Bilston LE. Tongue and lateral upper airway movement with mandibular advancement. Sleep [Internet]. 2013;36(3):397-404. DOI: 10.5665/sleep.2458
  12. 12. Adult Obstructive Sleep Apnea Task Force of the American Academy of Sleep Medicine. Clinical guidelines for the evaluation, management, and long-time care of obstructive sleep apnea in adults. Journal of Clinical Sleep Medicine. 2009;5:263-276
  13. 13. Patil PS, Schneider H, Schwartz AR, et al. Adult obstructive sleep apnea pathophysiology and diagnosis. Chest. 2007;132:325-337
  14. 14. Pahkala R, Puustinen R, Tuomilehto H, et al. Risk factors for sleep-disordered breathing: The role of craniofacial structure. Acta Odontologica Scandinavica. 2011;69:137-143
  15. 15. Rodríguez-Lozano FJ, Sáez-Yuguero Mdel R, Linares Tovar E, et al. Sleep apnea and mandibular advancement device. Revision of the literature. Medicina Oral, Patología Oral y Cirugía Bucal. 2008;13(9):E549-E554
  16. 16. Mayo Foundation for Medical Education and Research. Obstructive Sleep Apnea [Internet]. Mayo Foundation for Medical Education and Research; Available from: https://www.mayoclinic.org/diseases-conditions/obstructive-sleep-apnea/symptoms-causes/syc-20352090
  17. 17. Ruangsri S, Jorns TP, Puasiri S, et al. Which oropharyngeal factors are significant risk factors for obstructive sleep apnea? An age-matched study and dentist perspectives. Nature and Science of Sleep. 2016;8:215-219 [Online]
  18. 18. Vuorjoki-Ranta TR, Lobbezoo F, Vehkalahti M, et al. Treatment of obstructive sleep apnoea patients in community dental care: Knowledge and attitudes among general dental practitioners and specialist dentists. Journal of Oral Rehabilitation. 2016;43(12):937-942
  19. 19. Chung F, Subramanyam R, Liao P, et al. High STOP-bang score indicates a high probability of obstructive sleep apnoea. British Journal of Anaesthesia. 2012;108(5):768-775
  20. 20. Chung F, Yegneswaran B, Liao P, et al. STOP questionnaire: A tool to screen patients for obstructive sleep apnea. Anesthesiology: The Journal of the American Society of Anesthesiologists. 2008;108(5):812-821
  21. 21. Mallampati S, Gatt S, Gugino L, et al. A clinical sign to predict difficult tracheal intubation: A prospective study. Canadian Anaesthetists' Society Journal. 1985;32(4):429-434
  22. 22. Jauhar S, Orchardson R, Jauhar I, et al. The role of the dentist in sleep disorders. Dental Update. 2010;37(10):674-679
  23. 23. Glick M, Williams DM, Kleinman DV, et al. A new definition for oral health developed by the FDI world dental federation opens the door to a universal definition of oral health. The Journal of the American Dental Association. 2016;147(12):915-917
  24. 24. Kale SS, Kakodkar P, Shetiya SH. Assessment of oral findings of dental patients who screen high and no risk for obstructive sleep apnea (OSA) reporting to a dental college—a cross sectional study. Sleep Science. 2018;11(2):112-117
  25. 25. Franklin KA, Lindberg E. Obstructive sleep apnea is a common disorder in the population-a review on the epidemiology of sleep apnea. Journal of Thoracic Disease. 2015;7(8):1311
  26. 26. Garvey JF, Pengo MF, Drakatos P, Kent BD. Epidemiological aspects of obstructive sleep apnea. Journal of Thoracic Disease. 2015;7(5):920-929
  27. 27. Morsy NE, Farrag NS, Zaki NFW, Badawy AY, Abdelhafez SA, El-Gilany A-H, et al. Obstructive sleep apnea: Personal, societal, public health, and legal implications. Reviews on Environmental Health (Berlin/Boston). 2019;34(2):153-169
  28. 28. Stepnowsky C, Sarmiento KF, Bujanover S, Villa KF, Li VW, Flores NM. Comorbidities, health-related quality of life, and work productivity among people with obstructive sleep apnea with excessive sleepiness: Findings from the 2016 US National Health and wellness survey. Journal of Clinical Sleep Medicine. 2019;15(2):235-243
  29. 29. Iacono Isidoro S, Salvaggio A, Lo Bue A, Romano S, Marrone O, Insalaco G. Quality of life in patients at first time visit for sleep disorders of breathing at a sleep centre. Health and Quality of Life Outcomes. 2013;11:207
  30. 30. D'Ambrosio C, Bowman T, Mohsenin V. Quality of life in patients with obstructive sleep apnea: Effect of nasal continuous positive airway pressure—A prospective study. Chest. 1999;115(1):123-129
  31. 31. Lacasse Y, Godbout C, Sériès F. Health-related quality of life in obstructive sleep apnoea. The European Respiratory Journal. 2002;19(3):499-503
  32. 32. Diamanti C, Manali E, Ginieri-Coccossis M, et al. Depression, physical activity, energy consumption, and quality of life in OSA patients before and after CPAP treatment. Sleep & Breathing. 2013;17(4):1159-1168
  33. 33. Punjabi NM. The epidemiology of adult obstructive sleep apnea. Proceedings of the American Thoracic Society. 2008;5(2):136-143
  34. 34. Young T, Peppard PE, Gottlieb DJ. Epidemiology of obstructive sleep apnea: A population health perspective. American Journal of Respiratory and Critical Care Medicine. 2002;165(9):1217-1239
  35. 35. Mokdad AH, Serdula MK, Dietz WH, Bowman BA, Marks JS, Koplan JP. The spread of the obesity epidemic in the United States, 1991-1998. JAMA. 1999;282:1519-1522
  36. 36. Sunitha C, Kumar SA. Obstructive sleep apnea and its management. Indian Journal of Dental Research. 2010;21(1):119-124
  37. 37. Jordan AS, McSharry DG, Malhotra A. Adult obstructive sleep apnoea. Lancet. 2014;383(9918):736-747
  38. 38. Hudgel DW, Thanakitcharu S. Pharmacologic treatment of sleep-disordered breathing. American Journal of Respiratory and Critical Care Medicine. 1998;158:691-699
  39. 39. Chung F, Yegneswaran B, Liao P, Chung SA, Vairavanathan S, Islam S, et al. STOP questionnaire. Anesthesiology [Internet]. 2008;108(5):812-821. DOI: 10.1097/aln.0b013e31816d83e4
  40. 40. Tranfić Duplančić M, Pecotić R, Lušić Kalcina L, Pavlinac Dodig I, Valić M, Roguljić M, et al. Salivary parameters and periodontal inflammation in obstructive sleep apnoea patients. Scientific Reports. 2022;12(1):19387
  41. 41. Makeeva IM, Budina TV, Turkina AY, Poluektov MG, Kondratiev SA, Arakelyan MG, et al. Xerostomia and hyposalivation in patients with obstructive sleep apnoea. Clinical Otolaryngology. 2021;46(4):782-787
  42. 42. Malhotra A, White DP. Obstructive sleep apnoea. Lancet. 2002;360:237-245
  43. 43. Chervin RD. Sleepiness, fatigue, tiredness, and lack of energy in obstructive sleep apnea. Chest. 2000;118:372-379
  44. 44. Sanders AE, Essick GK, Fillingim R, et al. Sleep apnea symptoms and risk for temporomandibular disorder: OPPERA cohort. Journal of Dental Research. 2013;92:70S-77S
  45. 45. Al-Jewair T, Shibeika D, Ohrbach R. Temporomandibular disorders and their association with sleep disorders in adults: A systematic review. Journal of Oral & Facial Pain and Headache. 2021;35(1):41-53. DOI: 10.11607/ofph.2780
  46. 46. Wetselaar P, Manfredini D, Ahlberg J, Johansson A, Aarab G, Papagianni CE, et al. Associations between tooth wear and dental sleep disorders: A narrative overview. Journal of Oral Rehabilitation. 2019;46(8):765-775
  47. 47. Marko Vujicic PD, Hilton Israelson DDS, James Antoon DMD, Roger Kiesling DDS, DDS TP, DDS MZ. A profession in transition. The Journal of the American Dental Association (JADA). 2014;145(2):118-121
  48. 48. Demko BG. Screening for obstructive sleep apnea in the dental office setting. Journal of the Massachusetts Dental Society. 2008;57(1):18-20
  49. 49. Berggren K, Broström A, Firestone A, Wright B, Josefsson E, Lindmark U. Oral health problems linked to obstructive sleep apnea are not always recognized within dental care-as described by dental professionals. Cllinical and Experimental Dental Research. 2022;8(1):84-95
  50. 50. Lyons-Coleman M, Bates C, Barber S. Obstructive sleep apnoea and the role of the dental team. British Dental Journal. 2020;228(9):681-685. DOI: 10.1038/s41415-020-1523-9
  51. 51. Parmenter D, Millar BJ. How can general dental practitioners help in the management of sleep apnoea? British Dental Journal. 2023;234(7):505-509. DOI: 10.1038/s41415-023-5684-1
  52. 52. Mehra P, Wolford LM. Surgical management of obstructive sleep apnea. Proc (Bayl Univ Med Cent). 2000;13:338-342
  53. 53. Ikematsu T. Study of snoring, 4th report: Therapy. Journal of Otolaryngology of Japan. 1964;64:434-435
  54. 54. Fujita S, Conway W, Zorick F, Roth T. Surgical correction of anatomic abnormalities in obstructive sleep apnea syndrome: Uvulopalatopharyngoplasty. Otolaryngology–Head and Neck Surgery. 1981;89:923-934
  55. 55. Ferguson KA, Heighway K, Ruby RR. A randomized trial of laser-assisted uvulopalatoplasty in the treatment of mild obstructive sleep apnea. American Journal of Respiratory and Critical Care Medicine. 2003;167:15-191
  56. 56. Rw R, Powell NB, Guilleminault C. Obstructive sleep apnea syndrome: A surgical protocol for dynamic airway reconstruction. Journal of Oral and Maxillofacial Surgery. 1993;51:742-747
  57. 57. Reiche-Fischel O, Wolford LM. Posterior airway space changes after double jaw surgery with counter-clockwise rotation. Journal of Oral and Maxillofacial Surgery. 1996;54:96-99
  58. 58. Cartwright R, Venkatesan TK, Caldarelli D, Diaz F. Treatments for snoring: A comparison of somnoplasty and an oral appliance. Laryngoscope. 1999;110:1680-1683
  59. 59. Tiner BD. Surgical management of obstructive sleep apnea. Journal of Oral and Maxillofacial Surgery. 1996;54:1109-1114
  60. 60. Tanna N, Smith BD, Zapanta P, et al. Surgical management of obstructive sleep apnea. Plastic and Reconstructive Surgery. 2016;137:1263-1272
  61. 61. Motamedi KK, McClary AC, Amedee RG. Obstructive sleep apnea: A growing problem. The Ochsner Journal. 2009;9:149-153
  62. 62. Simmons M. What your Dentist Looks for In Diagnosing Sleep Apnea [Internet]. Dear Doctor, Inc.; 2010. Available from: https://www.deardoctor.com/articles/sleep-disorders-and-dentistry/page2.php
  63. 63. Sutherland K, Cistulli PA. Oral appliance therapy for obstructive sleep apnoea: State of the art. Journal of Clinical Medicine. 2019;8(12):2121. DOI: 10.3390/jcm8122121
  64. 64. American Academy of Sleep Medicine. Obstructive Sleep Apnea. Illinois: American Academy of Sleep Medicine; 2008
  65. 65. Isono S, Tanaka A, Tagaito Y, Ishikawa T, Nishino T. Influences of head positions and bite opening on collapsibility of the passive pharynx. Journal of Applied Physiology. 2004;97(1):339-346, Policy Statement 2019
  66. 66. Ng AT, Gotsopoulos H, Qian J, Cistulli PA. Effect of oral appliance therapy on upper airway collapsibility in obstructive sleep apnea. American Journal of Respiratory and Critical Care Medicine. 2003;168(2):238-241. DOI: 10.1164/rccm.200211-1275OC. Epub 2003 Apr 30
  67. 67. Issa FG, Sullivan CE. Upper airway closing pressures in obstructive sleep apnea. Journal of Applied Physiology: Respiratory, Environmental and Exercise Physiology. 1984;57(2):520-527. DOI: 10.1152/jappl.1984.57.2.520
  68. 68. Goyal M, Johnson J. Obstructive sleep apnea diagnosis and management. Missouri Medicine. 2017;114(2):120-124
  69. 69. Marklund M. Update on oral appliance therapy for OSA. Current Sleep Medicine Reports. 2017;3(3):143-151. DOI: 10.1007/s40675-017-0080-5. Epub 2017 Jul 10
  70. 70. Sutherland K, Takaya H, Qian J, Petocz P, Ng AT, Cistulli PA. Oral appliance treatment response and polysomnographic phenotypes of obstructive sleep apnea. Journal of Clinical Sleep Medicine. 2015;11(8):861-868. DOI: 10.5664/jcsm.4934
  71. 71. Labarca G, Sands SA, Cohn V, Demko G, Vena D, Messineo L, et al. Mouth closing to improve the efficacy of mandibular advancement devices in sleep apnea. Annals of the American Thoracic Society. 2022;19(7):1185-1192. DOI: 10.1513/AnnalsATS.202109-1050OC
  72. 72. Bachour A, Maasilta P. Mouth breathing compromises adherence to nasal continuous positive airway pressure therapy. Chest. 2004;126:1248-1254
  73. 73. Medical Advisory Secretariat. Oral appliances for obstructive sleep apnea: An evidence-based analysis. Ontario Health Technology Assessment Series. 2009;9(5):1-51. Epub 2009 Sep 1
  74. 74. Chang ET, Fernandez-Salvador C, Giambo J, Nesbitt B, Liu SY, Capasso R, et al. Tongue retaining devices for obstructive sleep apnea: A systematic review and meta-analysis. American Journal of Otolaryngology. 2017;38(3):272-278. DOI: 10.1016/j.amjoto.2017.01.006. Epub 2017 Jan 18
  75. 75. Alshhrani WM, Hamoda MM, Okuno K, et al. The efficacy of a titrated tongue-stabilizing device on obstructive sleep apnea: A quasi-experimental study. Journal of Clinical Sleep Medicine. 2021;17(8):1607-1618
  76. 76. Mandibular repositioning device [Internet]. Healthwise, Incorporated. 2022. Available from: https://www.cigna.com/knowledge-center/hw/mandibular-repositioning-device-zm6313 [Accessed: September 1, 2023]
  77. 77. Ramar K, Dort LC, Katz SG, Lettieri CJ, Harrod CG, Thomas SM, et al. Clinical practice guideline for the treatment of obstructive sleep apnea and snoring with oral appliance therapy: An update for 2015 an American Academy of sleep medicine and American Academy of dental sleep medicine clinical practice guideline. Journal of Clinical Sleep Medicine. 2015;11(7):773-827
  78. 78. Dieltjens M, Vanderveken O. Oral appliances in obstructive sleep apnea. Healthcare (Basel). 2019;7(4):141. DOI: 10.3390/healthcare7040141
  79. 79. Vanderveken OM, Devolder A, Marklund M, Boudewyns AN, Braem MJ, Okkerse W, et al. Comparison of a custom-made and a thermoplastic oral appliance for the treatment of mild sleep apnea. American Journal of Respiratory and Critical Care Medicine. 2008;178(2):197-202. DOI: 10.1164/rccm.200701-114OC. Epub 2007 Aug 2
  80. 80. 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(4):1065-1072. DOI: 10.1378/chest.117.4.1065
  81. 81. Ma Y, Yu M, Gao X. The effect of gradually increased mandibular advancement on the efficacy of an oral appliance in the treatment of obstructive sleep apnea. Journal of Clinical Sleep Medicine. 2020;16(8):1369-1376
  82. 82. de Ruiter MHT, Aarab G, de Vries N, Lobbezoo F, de Lange J. A stepwise titration protocol for oral appliance therapy in positional obstructive sleep apnea patients: Proof of concept. Sleep & Breathing. 2020;24(3):1229-1236. DOI: 10.1007/s11325-020-02045-w. Epub 2020 Mar 11
  83. 83. Levine M, Bennett K, Cantwell M, Postol K, Schwartz D. Dental sleep medicine standards for screening, treating, and managing adults with sleep-related breathing disorders. Journal of Dental Sleep Medicine. 2018;5(3):61-68
  84. 84. Martins OFM, Chaves Junior CM, Rossi RRP, Cunali PA, Dal-Fabbro C, Bittencourt L. Side effects of mandibular advancement splints for the treatment of snoring and obstructive sleep apnea: A systematic review. Dental Press Journal of Orthodontics. 2018;23(4):45-54. DOI: 10.1590/2177-6709.23.4.045-054.oar
  85. 85. Sheats RD, Schell TG, Blanton AO, et al. Management of side effects of oral appliance therapy for sleep-disordered breathing. Journal of Dental Sleep Medicine. 2017;4(4):111-125
  86. 86. Phillips CL, Grunstein RR, Darendeliler MA, Mihailidou AS, Srinivasan VK, Yee BJ, et al. Health outcomes of continuous positive airway pressure versus oral appliance treatment for obstructive sleep apnea: A randomized controlled trial. American Journal of Respiratory and Critical Care Medicine. 2013;187(8):879-887. DOI: 10.1164/rccm.201212-2223OC
  87. 87. Gjerde K, Lehmann S, Bjorvatn B, Berge M, Thuen F, Berge T, et al. Partner perceptions are associated with objective sensor-measured adherence to oral appliance therapy in obstructive sleep apnea. Journal of Sleep Research. 2022;31:e13462
  88. 88. Liu HW, Chen YJ, Lai YC, Huang CY, Huang YL, Lin MT, et al. Combining MAD and CPAP as an effective strategy for treating patients with severe sleep apnea intolerant to high-pressure PAP and unresponsive to MAD. PLoS One. 2017;12(10):e0187032. DOI: 10.1371/journal.pone.0187032. Erratum in: PLoS One. 2018;13(4):e0196319
  89. 89. Yang D, Zhou HF, Xie Y. Efficacy of uvulopalatopharyngoplasty combined with oral appliance in treatment of obstructive sleep apnea-hypopnea syndrome. Irish Journal of Medical Science. 2015;184(2):329-334. DOI: 10.1007/s11845-014-1112-5. Epub 2014 Apr 16
  90. 90. Almeida FR, Mulgrew A, Ayas N, Tsuda H, Lowe AA, Fox N, et al. Mandibular advancement splint as short-term alternative treatment in patients with obstructive sleep apnea already effectively treated with continuous positive airway pressure. Journal of Clinical Sleep Medicine. 2013;9(4):319-324. DOI: 10.5664/jcsm.2576
  91. 91. About - American academy of dental sleep medicine [Internet]. Aadsm.org. Available from: https://www.aadsm.org/about.php [Accessed: September 1, 2023]
  92. 92. American Academy of Sleep Medicine – Association for Sleep Clinicians and Researchers [Internet]. AASM and AADSM Issue New Joint Clinical Practice Guideline for Oral Appliance Therapy. American Academy of Sleep Medicine – Association for Sleep Clinicians and Researchers; 2017. Available from: https://aasm.org/aasm-and-aadsm-issue-new-joint-clinical-practice-guideline-for-oral-appliance-therapy/ [Accessed: July 6, 2019]
  93. 93. American Dental Association. Evidence Brief: Oral Appliances for Sleep-Related Breathing Disorders [Internet]. American Dental Association. Available from: https://www.ada.org/-/media/project/ada-organization/ada/ada-org/files/resources/research/ada_sci_oralappl_srbd_brief_final_15.pdf; [Accessed: September 1, 2023]
  94. 94. American Dental Association. Policy Statement on the Role of Dentistry in the Treatment of Sleep Related Breathing Disorders [Internet]. Darien, IL: American Dental Association; 2017. Available from: https://www.ada.org/-/media/project/ada-organization/ada/ada-org/files/resources/research/oral-health-topics/ada_2019_policy_role_of_dentistry_sleep_related_breathing_disorders.pdf; [Accessed: September 1, 2023]
  95. 95. About [Internet]. EADSM. European Academy of Dental Sleep Medicine’. Bad Reichenhall, Germany; 2014. Available from: https://eadsm.academy/about/ [Accessed: September 2, 2023]

Written By

Michael Greaves, Dwight McLeod and Ignacio Christian Marquez

Submitted: 24 October 2023 Reviewed: 01 November 2023 Published: 06 February 2024