Introduction to Sleep-Disordered Breathing
Fostering success with collaborative patient care
Gregory K. Essick, DDS, PhD | Jonathan A. Parker, DDS | Jamison R. Spencer, DMD, MS | Andrew R. Blank, AAS, BS
National Sleep Foundation surveys show that 75% of Americans report at least one sleep symptom and approximately 60% of adults drive while drowsy each year.1 Obstructive sleep apnea (OSA) is one of the most prevalent sleep disorders, and it affects 26% of adults between the ages of 30 and 70.2 People with untreated OSA can experience a significantly reduced quality of life. It can lead to difficulty in daytime functioning due to daytime sleepiness, fatigue, irritability, and decreased cognitive function. In addition, research studies show that people with OSA have a higher risk of cardiovascular disease (hypertension, heart attack, stroke, atrial fibrillation, etc.), diabetes, asthma, cancer, and dementia.3,4 People with this condition are also more likely to have motor vehicle accidents, which affects all of us.5,6
Pathophysiology
Anatomical and neuromuscular factors underlie the pathophysiology of OSA. The thin-walled upper airway is surrounded by a soft-tissue mass that is bounded by the bony mandible anteriorly, and the spine posteriorly. Within the soft tissue mass are muscles that serve to keep the airway open. The most important of these pharyngeal dilator muscles is the genioglossus muscle, which protrudes the tongue. A mandible that is relatively too small (micro- and/or retro-gnathia), a soft-tissue mass that is relatively too large (eg, from a large tongue and/or cervical fat), or a dilator muscle response to airway resistance that is insufficient may compromise the patency of the airway.
In individuals with normal sleep respiration, the activity of the pharyngeal dilator muscles is in balance with the size of the bony enclosure and soft-tissue mass, maintaining an open upper airway.7 However, in individuals with OSA, activity of the dilator muscles is insufficient to keep the airway open continuously during sleep (Figure 1).8 Periodically there is collapse of the upper airway and obstruction to airflow behind the soft palate or tongue. The collapse tends to occur at the end of expiration when effort to keep the airway open is minimal, or during inspiration when intra-airway pressure is most negative. The brain senses the blockage of airflow and arouses from sleep, leading to deeper breaths and restoration of airflow. This process of collapse-obstruction-arousal constitutes a respiratory event. Respiratory events can occur hundreds of times during a night of sleep.
The arousals of respiratory events disrupt the normal sleep pattern. Many patients fail to reach Rapid Eye Movement (REM) “dream” sleep or the deeper restorative stages of non-REM sleep.9 Rather, patients remain in lighter stages of sleep, disrupted by arousals. This sleep fragmentation is associated with many of the symptoms reported by adult patients with sleep-disordered breathing (SDB), which differ strikingly from the effects in children.10,11
The arousals of respiratory events not only disrupt sleep architecture but also stimulate the sympathetic nervous system, thereby elevating blood pressure and leading to hypertension over time.12 Moreover, each blockage of airflow leads to a transient drop in the oxygen saturation of hemoglobin in the blood, further stimulating the sympathetic nervous system. The intermittent hypoxia and stimulation of the sympathetic nervous system activates inflammatory processes throughout the body and promotes tissue inflammation.
Diagnosis and Classification
A patient with symptoms of a sleep disorder needs to see a qualified physician for a comprehensive sleep evaluation. Routine examination in the dental office may also reveal possible anatomical risk factors, which may lead the dental professional to refer the patient to a qualified physician for sleep evaluation. Generally, a diagnostic sleep study will be ordered for patients who report symptoms of SDB such as disruptive snoring and excessive daytime sleepiness, or who have medical conditions suggestive of impaired sleep respiration such as essential hypertension. These overnight studies have traditionally been conducted in a sleep laboratory by a trained sleep technologist who monitors the patient from an observation room. Sensors measure and continously record eye movements, EEG brain activity, nasal pressure airflow, snoring, expired CO2, chest and abdominal movements reflecting respiratory effort, limb and jaw muscle, EMG activity, heart rate, and oxygen saturation of the blood.
More recently, the use of home sleep apnea testing (HSAT, also referred to as Out of Center Sleep Testing or OCST) has been advocated by some third-party payers for patients who have symptoms of SDB but are otherwise in good health. Home sleep apnea testing devices vary in complexity but collect only a few channels of data and rarely the brain activity required to definitively tell when the patient is asleep or in which stage of sleep.13 Regardless of the type of sleep study, it is standard of care that a board-certified sleep physician interpret the scored results of the study when ordered for diagnostic purposes.
The sleep study data are inspected and scored for respiratory events. An apnea (A) is scored when airflow ceases for 10 or more seconds in adults. A hypopnea (H) is scored when airflow decreases for 10 or more seconds, along with other criteria. The criteria established by the American Academy of Sleep Medicine—generally accepted as the authority on sleep medicine in the United States—can differ from the criteria required by some third-party payers for treatment, explaining why some patients may receive a diagnosis of OSA yet may not meet criteria for insurance coverage of treatment.14 A respiratory effort related arousal (RERA) is scored when the patient arouses from sleep due to the increased respiratory effort to maintain normal airflow and blood oxygen levels.15
The severity of SDB is defined as the frequency of apneas plus hypopneas per hour. An apnea-hypopnea index (AHI) of ≥5 events/hour is considered mild OSA; ≥15 events/hour, moderate OSA; and ≥30 events/hour, severe OSA.16 Although an AHI of <5 events/hour is considered normal, epidemiological studies have shown that these individuals are at increased risk of diseases such as cardiovascular disease and periodontal disease.17,18 Moreover, patients with a normal AHI but with RERAs often report the same debilitating daytime symptoms of OSA, such as excessive daytime sleepiness and cognitive impairment.
References
1. National Sleep Foundation 2005 Sleep in America Poll. https://sleepfoundation.org/sites/default/files/2005_summary_of_findings.pdf. Published March 29, 2005. Accessed October 3, 2015.
2. Peppard PE, Young T, Barnet JH, et al. Increased prevalence of sleep-disordered breathing in adults. Am J Epidemiol. 2013;177(9):1006-1014.
3. Huang QR, Qin Z, Zhang S, Chow CM. Clinical patterns of obstructive sleep apnea and its comorbid conditions: a data mining approach. J Clin Sleep Med. 2008; 4(6):543-550.
4. Abrams B. Hierarchy of comorbidity indicators for obstructive sleep apnea. Chest. 2010;137(6):1491-1492.
5. Hiestand D, Phillips B. Obstructive sleep apnea syndrome: assessing and managing risk in the motor vehicle operator. Curr Opin Pulm Med. 2011;17(6):412-418.
6. Tregear S, Reston J, Schoelles K, Phillips B. Obstructive sleep apnea and risk of motor vehicle crash: systematic review and meta-analysis. J Clin Sleep Med. 2009;5(6):573-581.
7. Tsuiki S, Isono S, Ishikawa T, et al. Anatomical balance of the upper airway and obstructive sleep apnea. Anesthesiology. 2008;108(6):1009-1015.
8. Remmers JE, deGroot WJ, Sauerland EK, Anch AM. Pathogenesis of upper airway occlusion during sleep. J Appl Physiol Respir Environ Exerc Physiol. 1978; 44(6):931-938.
9. Fietze I, Quispe-Bravo S, Hansch T, et al. Arousals and sleep stages in patients with obstructive sleep apnoea syndrome: Changes under nCPAP treatment. J Sleep Res. 1997;6(2):128-133.
10. Guilleminault C, Partinen M, Quera-Salva MA, et al. Determinants of daytime sleepiness in obstructive sleep apnea. Chest. 1988;94(1):32-37.
11. Capdevila OS, Kheirandish-Gozal L, Dayyat E, Gozal D. Pediatric obstructive sleep apnea: complications, management, and long-term outcomes. Proc Am Thorac Soc. 2008;5(2):274-282.
12. Arnardottir ES, Mackiewicz M, Gislason T, et al. Molecular signatures of obstructive sleep apnea in adults: a review and perspective. Sleep. 2009;32(4):447-470.
13. Collop NA, Anderson WM, Boehlecke B, et al. Clinical guidelines for the use of unattended portable monitors in the diagnosis of obstructive sleep apnea in adult patients. Portable Monitoring Task Force of the American Academy of Sleep Medicine. J Clin Sleep Med. 2007;3(7):737-747.
14. Berry RB, Budhiraja R, Gottlieb DJ, et al. Rules for scoring respiratory events in sleep: update of the 2007 AASM Manual for the Scoring of Sleep and Associated Events. Deliberations of the Sleep Apnea Definitions Task Force of the American Academy of Sleep Medicine. J Clin Sleep Med. 2012;8(5):597-619.
15. Guilleminault C, Stoohs R, Clerk A, et al. A cause of excessive daytime sleepiness. The upper airway resistance syndrome. Chest. 1993;104(3):781-787.
16. Epstein LJ, Kristo D, Strollo PJ, Jr., et al. Clinical guideline for the evaluation, management and long-term care of obstructive sleep apnea in adults. J Clin Sleep Med. 2009;5(3):263-276.
17. Asker M, Asker S, Kucuk U, Kucuk HO. An overlooked cause of resistant hypertension: upper airway resistance syndrome—preliminary results. Clinics (Sao Paulo). 2014;69(11):731-734.
18. Sanders AE, Essick GK, Beck JD, et al. Periodontitis and Sleep Disordered Breathing in the Hispanic Community Health Study/Study of Latinos. Sleep. 2014.
About the Authors
Gregory K. Essick, DDS, PhD
Professor
Department of Prosthodontics and Center for Pain Research and Innovation School of Dentistry
University of North Carolina
Chapel Hill, North Carolina
Jonathan A. Parker, DDS
Owner
Clinical Director
Snoring and Sleep Apnea Dental Treatment Center Edina, Minnesota
Jamison R. Spencer, DMD, MS
Director
The Center for Sleep Apnea and TMJ
Boise, Idaho
Andrew R. Blank, AAS, BS
Dental Student
East Carolina University School of Dental Medicine
Greenville, North Carolina
