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Position Statement: The Sleep-disordered Breathing Patient

The Sleep-disordered Breathing Patient

Position Statement of the American College of Prosthodontists
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Sleep-disordered breathing (SDB) includes, but is not limited to, mouth breathing, snoring, upper airway resistance syndrome (UARS), and obstructive sleep apnea (OSA). OSA is defined as 5 or more episodes of complete (apnea) or partial (hypopnea) upper airway obstruction per hour of sleep. It is estimated to involve 24% of middle-aged men and 9% of middle-aged women. Two to three percent of children have OSA; increasing to 30 to -40% in obese children.1 Patients suffer from daytime drowsiness, cognitive impairment, and increased risk of heart attacks, strokes, uncontrolled hypertension, and diabetes. Untreated OSA can significantly impair a patient’s quality of life and increase morbidity due to medical complications or transport- or work-related accidents.

Diagnosis

Oral examination

Most airway obstructions occur behind the maxilla and mandible at the level of the soft palate, tongue, and lateral fat pads. The size and shape of the upper airway are among factors to consider in the likelihood of upper airway collapse. A smaller airway (obesity or small maxilla and/or mandible) is more susceptible to collapsing than a larger airway. Imaging studies of the upper airway have demonstrated a larger volume of soft tissue structures (tongue size and fat in the posterior area) in patients affected by OSA. Many OSA patients tend to present with a compromised upper airway resulting from skeletal and/or soft tissue abnormalities.2 An evaluation of the size of the tongue, the presence and size of the tonsils, the opening of the oral and nasal airways, and the size of the neck can raise concerns on the patency of the airway.3

The presence of tooth wear and TMJ symptoms is important, because these may play a role in OSA. The terminology “night bruxism” should be replaced by sleep bruxism (SB), because it occurs during sleep periods, which are not necessarily at night. There is some evidence of a possible association between SB and OSA.4-6 While the strength of this association is uncertain, a sub-group of bruxers do appear to have clinical commonalties7 in which the activation of the masseter muscle is thought to stabilize the mandible, enabling the genioglossus to dilate the upper airway more efficiently.8-10 SB can occur before a breathing event, after a breathing event, or unrelated to a breathing event.11,12 A significant number of bruxism patients may have OSA, with bruxism increasing muscle tone and possibly dilating the airway.13,14

Associated comorbidities

Obesity or increased body mass index (BMI) are associated with OSA. The presence of hypertension, cardiovascular disease, stroke, diabetes, and thyroid disease have been identified as aggravating factors or the results of OSA.15

OSA in children

OSA in children is often due to enlarged tonsils and adenoids peaking at 5 to 6 years of age.16 Craniofacial morphological characteristics often present in children with airway problems are a narrow maxilla, anterior open-bite, mouth breathing, and dolichocephalic profile.17

Daytime sleepiness and snoring

Snoring occurs in a high percentage of patients with OSA. Witnessed apneas and excessive daytime sleepiness are also important symptoms, but only witnessed apneic events are pathognomonic for OSA. The Epworth Sleepiness Scale (ESS) is a simple questionnaire commonly used in the assessment of daytime sleepiness and screening for potential OSA. When patients with SB and/or temporomandibular disorder (TMD) complain about insomnia, snoring, cessation of breathing during sleep, sleepiness of unidentified causes, uncontrolled hypertension, or hypertension requiring multiple medications, it is prudent to screen for the presence of OSA.7

Diagnosis and Treatment

The diagnosis must be made by a sleep physician who will prescribe a polysomnography (PSG) test and prescribe the best modality of treatment depending on the severity of OSA. A PSG study performed in a sleep laboratory is the gold standard for the diagnosis of OSA. The role of the prosthodontist is to screen patients using the ESS, STOPBANG, and Berlin assessment tools, and an oral examination and refer the patient to a sleep physician for diagnostic and treatment prescription when OSA is suspected.
The final management of OSA may require input from ear-nose-throat (ENT) specialists, pneumologists, oral and maxillofacial surgeons (OMFS), prosthodontists or dentists trained in dental sleep medicine, and other professionals as required.

Conclusion

It is the position of the American College of Prosthodontists that due to the complexity and extensive amount of time and financial expenses involved in a prosthodontic rehabilitation as well as the serious health risks of untreated OSA, prosthodontists should consider screening for OSA through questionnaires for their patients. The simple question, “Do you snore?” in the medical questionnaire is an excellent marker that can be complemented by OSA questionnaires and specific oral examination.

Prosthodontists play an important role in preserving patients’ general health by restoring and maintaining physiological oral function and esthetic appearance. Sleep bruxism and oro-facial pain are conditions for which the dentist has diagnostic and management skills. With their additional training and expertise in oral anatomy, occlusion, and temporomandibular joint function, prosthodontists should recognize the signs and symptoms of OSA, refer to the sleep physician for diagnosis, and collaborate with the health team surrounding the patient in providing care that will improve the patient’s oral and general health.
 

References

  1. Bhattacharee R, Kim J, Kheirandish-Gozal L: Obesity and obstructive sleep apnea syndrome in children: a tale of inflammatory cascades. Pediatr Pulmonol 2001; 46:313-323.

  2. Lavigne GJ, Cistulli PA, Smith MT: Anatomic predisposing factors in OSA. In Lavigne GJ, Cistulli PA, Smith MT (eds): Sleep Medicine for Dentists: A Practical Overview. Hanover Park, IL, Quintessence, 2009, p. 43

  3. Chi L: Identification of craniofacial risk factors for obstructive sleep apnea using three-dimensional MRI. Eur Respir J 2011; 38:348-358

  4. Okeson JP, Phillips BA, Berry DT, Cook YR, Cabelka JF. Nocturnal bruxing events in subjects with sleep-disordered breathing and control subjects. J Craniomandib Disord 1991; 5:258-64.

  5. Tachibana M, Kato T, Kato-Nishimura K, et al: Associations of sleep bruxism with age, sleep apnea, and daytime problematic behaviors in children. Oral Dis 2016; 22:557–565

  6. Saito M, Yamaguchi T, Mikami S, et al: Weak association between sleep bruxism and obstructive sleep apnea. A sleep laboratory study. Sleep Breath 2016; 20:703-709.

  7. Balasubramaniam R, Klasser G, Cistulli P, et al: The link between sleep bruxism, sleep disordered breathing and temporomandibular disorders: An evidence-based review. J Dent Sleep Med 2014; 1:27-37.

  8. Yoshida K: A polysomnographic study on masticatory and tongue muscle activity during obstructive and central sleep apnea. J Oral Rehabil 1998; 25:603-609.

  9. Hollowell DE, Suratt PM: Activation of masseter muscles with inspiratory resistance loading. J Appl Physio 1989; 67:270-275.

  10. Hollowell DE, Surrat PM: Mandible position and activation of submental and masseter muscles during sleep. J Appl Physiol 1991; 71:2267-2273.

  11. Carra MC, Huynh N, Lavigne G: Sleep bruxism: A comprehensive overview for the dental clinician interested in sleep medicine. Dent Clin North Am 2012; 56:387-413.

  12. Holley AB, Lettieri CJ, Shah AA. Efficacy of an adjustable oral appliance and comparison with continuous positive airway pressure for the treatment of obstructive sleep apnea syndrome. Chest. 2011;140(6):1511-1516.

  13. Schames SE, Schames JM, Schames M, et al: Sleep bruxism, an autonomic self-regulatory response by triggering the trigeminal cardiac reflex. J Calif Dent Assoc 2012; 40:670-676.

  14. Saito M, Yagamaguchi T, Mikami S, et al: Temporal association between sleep apnea-hyponea and sleep bruxism events. J Sleep Res 2013 Nov 4. Doi: 10.1111/jsr.12099. [Epub ahead of print].

  15. Lavigne GJ, Cistulli PA, Smith MT: Clinical approach to diagnosis of obstructive sleep apnea. In Lavigne GJ, Cistulli PA, Smith MT (eds): Sleep Medicine for Dentists: A Practical Overview. Hanover Park, IL, Quintessence, 2009, p. 56.

  16. Gozal D, Pope DW Jr: Snoring during early childhood and academic performance at ages thirteen to fourteen years. Pediatrics 2001; 107:1394-1399.

  17. Flores-Mir C, Korayem M, Heo G, et al: Craniofacial morphological characteristics in children with obstructive sleep apnea syndrome: a systemic review and meta-analysis. J Am Dent Assoc 2013; 144:269-277.

    Authors

    Jean C. Wu, DDS
    Nancy M.G. Dubois, DMD, Cert Prostho, MDSc, FRCD (C)
    James G. Linkous, DMD, MS, FACP

    Date

    Original source document dated Feb. 4, 2005
    Revised and approved ACP Board of Directors: June 13, 2015
    Revised and approved ACP Board of Directors: June 3, 2016
    Revised and approved ACP Board of Directors August 13, 2020

     

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