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Obstructive sleep-disordered breathing is a syndrome of upper airway dysfunction during sleep. It has a wide spectrum and is characterized by snoring, pauses in breathing or abnormal breathing, upper airway resistance, and partial obstruction to complete airway obstruction. Unfortunately, sleep-disordered breathing is commonly undiagnosed in many individuals with the condition. It is estimated that 23% of women and 50% of men aged 40 to 85 years are affected by moderate to severe sleep-disordered breathing. Among other effects, sleep-disordered breathing can have neurologic, metabolic, and cardiovascular consequences. Some individuals affected by sleep-disordered breathing develop obstructive sleep apnea (OSA). OSA is a sleep disorder that is characterized by marked reduced airflow (ie, hypopnea) or absent airflow (ie, apnea) accompanied by oxygen desaturation. Continuous positive airway pressure (CPAP) therapy is the standard of care in treatment for OSA; however, mandibular advancement devices can also be used to manage the disorder.1
The Relationship Between Development and Breathing
The functional matrix theory proposes that growth in the craniofacial and dentofacial complex occurs in response to functional needs and possibly in response to growth of the nasal cartilage.2 The nasal cavity is responsible for almost two thirds of airway resistance.3 The narrowest portion of the nasal airway is the internal nasal valve. Small changes in nasal valve size result in large changes in airflow resistance, which in turn affects nasal function. Normal nasal breathing promotes harmonious growth and exerts influence on the development of craniofacial structures by stimulating the associated structures of the head and neck region during mastication, swallowing, and breathing.
The soft tissue stretch theory postulates that mouth breathing leads to altered head posture and an altered pattern of muscle recruitment, which in turn, presents as an adverse contributory factor in craniofacial and dental development.4 Fitzpatrick and colleagues described how continuous mouth breathing can lead to a significant increase in upper airway resistance.5 Mouth breathing reduces the retropalatal and retroglossal areas. Furthermore, it lengthens the pharyngeal airway as a result of further posterior retraction of the tongue. Low tongue posture has been considered to be a factor in mouth breathing, and nasal obstruction can aggravate mouth breathing. However, the treatment of severe nasal obstruction can reduce mouth breathing during sleep.6 Nighttime mouth breathing was found to be higher in patients with OSA.7
There is emerging evidence to suggest a link between sleep-disordered breathing, sleep bruxism, and temporomandibular disorders. Tay and colleagues found that children suffering from upper airway resistance adapt to an "awake-disordered breathing" during growth.8 Interestingly, they found that Southeast Asians are more prone to develop sleep-disordered breathing because of their "restricted craniofacial bony enclosure" (ie, smaller maxilla, smaller and retro-positioned mandible, shorter and steeper anterior cranial base). Head posture was also found to be sensitive to fluctuations in airway resistance. Patients with upper airway resistance were found to have a high risk of sleep bruxism (90.7%), forward head posture (90%), and nasal congestion (91.9%). The study further suggests that a posterior displaced condyle may be a physiologic adaptation during growth in response to daytime dysfunctional breathing. In addition, some research suggests that chronic inflammation may be an underlying mechanism for the association between sleep disturbances and persistent temporomandibular disease.
Sleep bruxism is a masticatory muscle activity during sleep that has been shown to commonly co-occur with mild-to-moderate OSA.9 In adults, the prevalence of OSA is estimated to range from 9% to 38% and the prevalence of sleep bruxism is estimated to be 13%. Depending on the literature, the prevalence rates of sleep bruxism in children have been shown to range from 5.9% to 49.6%.10 CPAP therapy and adenotonsillectomy have been shown to reduce bruxism events. Following adenotonsillectomy, known risk factors for the recurrence of symptoms of sleep-disordered breathing include nasal obstruction, mouth breathing, short lingual frenum, relative macroglossia, and limited range of tongue mobility.11 One may argue that the correct diagnostic term for relative macroglossia is relative narrow skeletal/dental arches.
Surgical Treatment Options
There are several surgical treatment options that can be pursued in the management of sleep-disordered breathing and OSA. These options are associated with both benefits and risks; therefore, patient selection should be carefully considered to ensure the most appropriate intervention.
Maxillomandibular Advancement
The most common surgical treatment for OSA is maxillomandibular advancement. A meta-analysis of 22 studies that included 627 subjects with OSA determined that maxillomandibular advancement has surgical success and cure rates of approximately 86% and 43%, respectively.12 Maxillomandibular advancement surgery is typically reserved for patients with severe OSA and severe craniofacial abnormalities. Although this surgery is highly effective, it comes with surgical risk, high cost, and limited medical insurance reimbursement. Maxillomandibular advancement surgery is rarely covered for patients that have no apneic events, which makes it less of an option for patients who suffer from sleep-disordered breathing without OSA.
Surgically Assisted Rapid Palatal Expansion
When there is a severe transverse discrepancy, it may be best to perform surgically assisted rapid palatal expansion before skeletal advancements. Based on systematic reviews, changes in the airway volume from surgically assisted rapid palatal expansion alone do not correlate to improved respiratory function. According to the review of Buck and colleagues, the inclusion of pterygomaxillary disjunction as part of the surgery did not appear to increase the magnitude of volume change in the nasal cavity.13 Traditional surgically assisted rapid palatal expansion used dental expanders bonded to the dentition and had a relapse rate as high as 64%.14
Distraction Osteogenesis Maxillary Expansion
There have been modifications to the traditional surgically assisted rapid palatal expansion protocol to reduce the surgical risk and improve the stability. Distraction osteogenesis maxillary expansion uses a mini-implant palatal expander, Le Fort 1 fracture, and an anterior nasal spine incision.15 By placing mini-implants along the midpalatal suture, it reduces the need for the pterygoid plate fracture, which has the most surgical risk.
Indications for distraction osteogenesis maxillary expansion include patients with OSA who present with absolute skeletal transverse hypoplasia and an associated crossbite. It is also indicated for patients with mild OSA or upper airway resistance syndrome (UARS) with complaints of persistent nasal obstruction and associated narrow, high arched palates who have undergone previous nasal surgeries or do not present with significant septal deviation, inferior turbinate hypertrophy, or nasal valve collapse.16 Distraction osteogenesis maxillary expansion has been shown to increase the nasal floor, reduce the airflow velocity, improve nasal obstructive symptoms, and reduce the severity of OSA.15,17
Microimplant-Assisted Rapid Palatal Expansion
The current non-surgical approach to maxillary expansion is referred to as microimplant-assisted rapid palatal expansion. Microimplant-assisted rapid palatal expansion involves either a tooth and bone-borne or solely bone-borne device that includes a rigid element connected to mini implants inserted into the palate. This configuration delivers the expansion force directly to the basal bone of the maxilla, enhancing skeletal expansion.18 With the assistance of mini implants along the midpalatal suture, skeletal palatal expansion and nasal cavity expansion are achieved. As the tongue posture changes, the oral cavity space increases, releasing pressure from the soft palate and stretching the pharyngeal walls. Improvement in nasal flow and decreased nasal resistance decrease pharyngeal collapsibility and improve nasal breathing.
Storto and colleagues found that microimplant-assisted rapid palatal expansion resulted in improvement in inspiratory and expiratory pressure. Furthermore, the increase in airway volume had a positive effect on airflow and muscular strength during maximum inspiratory pressure.19 Palatal expansion may increase the nasal airway as well as improve tongue function and posture. As the upper arch widens, the tongue may posture more comfortably on the palate. This new tongue posture can increase the pharyngeal airway space and alter the muscular dynamics, improving overall airflow and respiratory function. Enhanced respiratory muscle strength may lead to an increase in oral expiratory peak flow.
Benefits of Maxillary Skeletal Expansion
Williams and colleagues found persistent nasal obstruction in patients with narrow, high-arched hard palates despite prior nasal surgical intervention. They suggested that these nonresponders may benefit from additional skeletal remodeling procedures, such as nonsurgical maxillary expansion.20
Maxillary skeletal expansion, both surgical and nonsurgical, has many benefits. Maxillary skeletal expansion can restore nasal structure and improve nasal function,21,22 and because the negative pressure in the airway space is reduced, improve head and tongue posture.23-25 In some cases, the mandible is displaced forward, which increases the lower airway space.26 Maxillary expansion improves sleep metrics, reduces apnea-hypopnea index and respiratory disturbance index scores, and improves overall sleep quality.27,28
One of the major challenges of smile design involves developing the proper buccal corridor. This may require the clinician to be more aggressive with preparation design. Narrow palates tend to be associated with a greater number of respiratory events. They characterize a phenotype of sleep-disordered breathing patients with increased nasal resistance and posterior tongue displacement. For these patients, maxillary expansion can help optimize respiration and improve the buccal corridor, enabling restorative treatment that is more minimally invasive.
Conclusion
The mode of breathing can impact soft tissue, skeletal and dental anatomy, and dental function. Therefore, it is important to understand a patient's mode of breathing before determining the appropriate dental treatment plan. One must evaluate all of the medical comorbidities and consider the risk of skeletal and dental malocclusion.
Patients who present with negative spaces in the buccal corridor are maxillary deficient. In some cases, the maxillary deficiency is accompanied by compromised airway. Maxillary expansion may increase nasal volume, improve nasal function, and influence nasal ventilation. Nonsurgical skeletal expansion can not only improve the airway but also improve facial esthetics.
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References
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