Dr. Hansen is a graduate of the Marquette University School of Dentistry and University of Florida College of Dentistry. He is Interim Program Director of Oral and Maxillofacial Radiology at the University of Florida College of Dentistry where he is a Clinical Assistant Professor and has a joint appointment in the University of Florida College of Medicine Department of Radiology. He maintains a private practice in Oral and Maxillofacial Radiology with BeamReaders® and can be reached at: firstname.lastname@example.org
Obstructive Sleep Apnea (OSA) seems to be a hot topic in the world of dentistry. Much like temporomandibular joint dysfunction a decade ago, there is great interest in sleep disorders brought about by new diagnostic measures and treatment options. What was once the purview of the physician, OSA diagnosis and treatment is now intersecting with dentistry. With this new focus though comes misinformation with the disease and the role of the dentist, and in particular cone-beam CT, in its diagnosis. To clear up some of this confusion, let’s talk about OSA and what role imaging plays. In order to do so it’s important to have an understanding of obstructive sleep apnea, how it’s diagnosed, and what the treatment options are. So let’s begin there.
Obstructive Sleep Apnea
Obstructive sleep apnea is part of a larger spectrum of sleep diseases referred to as sleep disordered breathing or sleep-related breathing disorders. These disorders are broken into three distinct syndromes, each with its own diagnostic criteria.1
1. Obstructive sleep apnea-hypopnea syndrome (OSAHS or OSA), which we will focus on here.
2. Central sleep apnea-hypopnea syndrome (CSAHS or CSA), which is periodic cessation of breathing without airway obstruction; this is commonly seen in the setting of heart failure or stroke.
3. Sleep hypoventilation syndrome (SVHS), which comprises several disorders where control of breathing is impaired resulting in improper respiration.
CSA and SVHS may overlap with obstructive sleep apneas. In the aggregate though, these syndromes do not result in obstruction of the airway and we will not consider them in our discussion.
OSA is a chronic disease affecting around 2-4% of the adult population (3-14% men and 2-5% women) with the highest prevalence among middle-aged men of higher weight.2,3,6 It is characterized by cessation or reduction in breathing with a maintained or even increased respiratory effort.1 As the name implies this is due to obstruction, either partial or full, of the upper airway during sleep and can result in snoring, upper airway resistance syndrome, or obstructive sleep apnea. The repeated airway obstructions cause a progressive asphyxia. This creates an increased respiratory effort against the collapsed airway which continues until the individual is aroused from their sleep.2 The continuous arousal from deeper sleep and sleep fragmentation generates many of the symptoms these individuals complain of, mainly lack of concentration, daytime sleepiness, fatigue, and mood alteration. Over time these symptoms build upon themselves and, as the disease progresses, can cause impaired performance at work, reduction in quality of life, and even major work-related or road accidents.2 The risks do not end at sleepiness however, the Wisconsin sleep cohort study, established in 1988, found a significant increase in mortality over an 18 year period in subjects with OSA.4 With greater understanding of sleep apnea and its influence on health and quality of life, the rising prevalence is becoming a public health crisis.5
An apnea is defined as cessation of airflow for 10 seconds. In adults, a hypopnea is defined by a reduction in nasal pressure by at least 30% of baseline for a duration of at least 10 seconds and accompanied by oxygen desaturation ≥ 4%.7 In patients 18 or younger a hypopnea is defined as a reduction in nasal pressure of at least 50% compared with baseline, associated with an arousal, awakening, or oxygen desaturation of at least 3%, that lasts for a duration of at least two missed breaths.7 This loss of airflows result in increased respiratory effort to overcome the obstruction. It is this stage, the evaluation of obstructions, that we look to radiographic imaging.
An obstruction, or airway narrowing and/or abnormal anatomy, lays the groundwork for a sleep apnea. As we progress into deeper stages of sleep there is increased pharyngeal muscle relaxation and loss of the normal muscle tone which leads to an increase in upper airway resistance. It is also known that during sleep the upper airway reflex dilator response is impaired which further serves to increase airway collapsibility and resistance. When the airway collapses or becomes obstructed, we need a stronger respiratory effort to maintain the same airflow.
For example, imagine running a marathon. At the start your muscles are fresh and oxygenated and you are likely nasal breathing. As the race progresses fatigue sets in and you likely switch to mouth breathing to overcome nasal restrictions. This is similar in a sense to OSA. We try to nasal breathe as it is more efficient but increased resistance causes us to mouth breathe. Obstructive sleep apnea is like trying to run a marathon while breathing only through a straw. As we fall asleep, we lose tone in the pharyngeal muscles. If the airway is small or abnormal to begin with, this may create the perfect condition to obstruct it. To overcome the obstruction, you need to breathe harder which is reflected in snoring, or the vibration of the pharyngeal tissues as the air moves past. A point where the airflow cannot be maintained and we have an apneic or hypopneic episode which causes an arousal. The arousal typically awakens us, muscle tone is restored, respiratory effort is balanced, and we gradually fall back into deeper sleep to start the cycle over again.
This is the major benefit of cone-beam CT imaging. it provides an anatomical evaluation of the airway at a lower radiation dose and cost than traditional multi-detector CT to detect possible obstructions. By allowing the dentist to evaluate the airway and correlate those findings with clinical examination and history, it puts them in the driver’s seat in identifying potential OSA sufferers and improving quality of life. With estimates that OSA is undiagnosed in 82% to 93% of adults, dentists can be at the forefront in screening for the disease.8
How is OSA Diagnosed
Notice that I said dentists can be at the forefront of screening, not diagnosis, as the role of dentistry in OSA has been somewhat controversial. That is because obstructive sleep apnea is a medical diagnosis, made by a physician, and in collaboration with a polysomnogram (sleep study). A recent joint statement by the American Academy of Sleep Medicine (AASM) and American Academy of Dental Sleep Medicine (AADSM) states “patients presenting with symptoms of OSA require a face-to-face evaluation conducted by a qualified physician trained in sleep medicine”.9 The diagnosis of OSA therefore requires consultation with a physician to include clinical examination and diagnostic testing. The clinical evaluation for OSA should incorporate a thorough sleep history and a physical examination that includes the respiratory, cardiovascular, and neurologic systems.10 Furthermore, polysomnography is the standard diagnostic test for the diagnosis of OSA in adult patients in whom there is a concern for OSA based on a comprehensive sleep evaluation.10
Diagnostic Criteria for OSA: The Canadian Thoracic Society enumerates this by stating that diagnosis must meet certain criteria as follows.1 The individual must fulfill criterion A or B, plus criterion C:
A. Excessive daytime sleepiness that is not better explained by other factors.
B. Two or more of the following that are not better explained by other factors:
- Choking or gasping during sleep;
- Recurrent awakenings from sleep;
- Unrefreshing sleep;
- Daytime fatigue; and
- Impaired concentration.
C. Sleep monitoring demonstrates five or more obstructive apneas/hypopneas per hour during sleep.
To state concisely, it is a polysomnogram properly interpreted by a physician trained in sleep medicine, and following a clinical examination, that provides the diagnosis for OSA.
A polysomnogram, or sleep study, is a diagnostic test designed to provide specific information about an individual through equipment and observation. This information can include O2 saturation levels, electrical activity in the brain, respiratory rates, heart rate, stage of sleep, eye movement, body movement, snoring, and unusual behaviors during sleep. This test is typically administered at a sleep clinic although home sleep apnea testing is gaining popularity. With testing at a sleep clinic being the gold standard, it is important that those utilizing home testing have the device evaluated for reliability and the results for validity. If there is any doubt then a proper polysomnogram is the preferred method.
While the full study is interpreted, what we typically discuss is the apnea/hypopnea index or AHI. The AHI is the average number of apneic or hypopneic events during 1 hour of sleep. There are additional indexes we can look at that include respiratory effort-related arousal, commonly called the Respiratory Disturbance Index (RDI), but we will focus on AHI as that is what most are familiar with. The American Sleep Disorder Association classifies OSA as below:
Mild OSA = AHI 5-15
Moderate OSA = AHI 15-30
Severe OSA = AHI > 30
It is important to note that this is for adult patients only. There is no threshold for AHI in younger individuals, as any apneic or hypopneic events classifies them with obstructive sleep apnea.11 Another commonly reported value is the O2 saturation nadir, or the lowest recorded O2 saturation value. A typical O2 nadir may be around 95% while anything less than 92% may indicate sleep apnea. Levels around 86% indicate severe hypoxia which left untreated may lead to brain damage or even death.
How is OSA Treated
Treatment of OSA is somewhat of a misnomer. In my mind, treatment means a definitive endpoint and is something we are very familiar with in dentistry. A patient presents with a carious lesion in the distal of 13 which is treated with a class II restoration. That’s it, the disease in the tooth is eradicated. A necrotic molar gets a root canal or extraction and a missing premolar gets an implant or bridge. Simple treatment treated simply.
OSA requires a different mindset, one we aren’t used to as dentists. OSA, much like hypertension, requires management. This can come in many forms ranging from lifestyle modification to surgery, but requires the mentality that one solution does not fit all patients and that our service is not finalized at appliance insertion. Modification and adjustment of our management regimen, like titration, is important as OSA is a chronic disease. Our obligation does not end at the fabrication of an appliance.
Before we talk about treatment though, let’s back up a bit and talk about risk factors as an understanding of them can help you understand the various treatments. Clearly being a middle-aged male is a risk factor, so sex and age are risks. Studies have shown that men have an estimated 2 to 3 fold increase in OSA and have found a higher prevalence of the disease among middle-aged and older individuals.12 Other risks include:
- Hypertension and cardiovascular disease.
- Craniofacial morphology, something we as dentists are intimately familiar with. Specific areas of risk easily evaluated with CBCT:
- Elongated soft palate
- Posterior and inferior positioning of hyoid
- Cervical spine and TMJ abnormalities
- Familial and genetic influences play a role.
- Multiple studies have also shown that higher weight bodies have a higher prevalence of OSA.4,12
Understanding these risk factors, an initial treatment of OSA needs to consider the correlation of OSA with cardiovascular disease and higher body weights. Management will likely include CPAP, oral appliances, or even surgery too.
Continuous positive airway pressure (CPAP) treatment is the gold standard for OSA. The device relies on stabilizing the upper airway with a continuous column of air that prevents collapse of the airway and resultant obstruction. CPAP is well-studied with its efficacy proven at managing OSA and reducing comorbidities. Unfortunately, CPAP adherence is low with reports of nonadherence as high as 83%.14 The pattern of CPAP adherence is established early, typically within the first week, and is a good predictor of long-term use which makes it a critical time for success.14 Generally if an individual adapts quickly and maintains compliance, they will benefit from and use CPAP. Poorly adapted or non-compliant individuals, as shown, have very high nonadherence rates. A multitude of factors influence compliance with machine-induced claustrophobia and behavioral/psychological factors playing a key role. Advancements in design and manufacturing have helped alleviate some of these factors, but the problem remains that this is a mask with attached tubing that needs to be worn throughout the night.
Philips respironic CPAP machine
Oral appliances will be most familiar to dentists as this is our primary role in management. These can be split into two categories; oral pressure therapy devices and oral appliances.
Oral pressure therapy devices (OPTs) consist of a mouthpiece connected by tubing to a bedside station, similar to a CPAP without the mask. The device produces a gentle negative pressure in the oral cavity that pulls the tongue and soft palate forward to open up the airway and prevent collapse. OPTs have many positives including a high adherence rate and no severe adverse events.15 However, treatment success is low ranging from 25%-37% and individuals have complained of dry mouth, oral cavity discomfort, and dental discomfort.15
Winx brand oral pressure therapy device
Oral pressure therapy mechanism of action
Traditional oral appliances (OAs) are similar to OPTs in that they prevent collapse of the airway. Unlike CPAP and OPTs, there is no negative or positive pressure applied to the airway. Oral appliances work by repositioning the tongue, mandible, or lifting the soft palate to increase the volume dimension of the airway. Like CPAPs, these have a unique advantage in that some can be titrated to achieve a desired result. Where CPAP titration is based on determining the ideal air pressure for treatment, oral appliance titration is based on adjusting the degree of advancement the device provides. This provides some control to the clinician but is inferior when compared to that of CPAP. However, that is not to say they provide no efficacy. In a recent meta-analysis, the authors found robust evidence that oral appliances reduce apneas and hypopneas while improving quality of sleep.16 Additionally, adherence rates for OAs are consistently higher than those for CPAP.15 Oral appliances continue to be a valid treatment option in OSA.
Somnodent brand oral appliance
Airway cross-sectional measurement with and without mandibular advancement appliance
Surgical treatment is an additional option available to the patient that has been extensively studied. It is generally reserved for those with bulky or misshapen tissue, or those refractory to other treatments. These surgeries range from tongue suppression and resection, maxillomandibular advancement, pharyngeal modification, and nasal cavity surgery. While many of these procedures have been shown to be effective, concerns about morbidity and adverse effects are common.15
Lateral cephalometric demonstrating maxillomandibular advancement surgery combined with genial tubercle advancement to treat severe OSA
Sagittal view cone-beam CT demonstrating uvulopalatopharyngoplasty (UP3 or UPPP) to treat severe OSA. Note the tissue recontouring in the posterior nasopharynx and shortening of the soft palate.
Newer treatments for OSA include hypoglossal nerve stimulation to compensate for loss of genioglossus muscle tone during sleep, pharmaceuticals, and phenotyping to determine the specific pathophysiology of an individuals OSA.15 In reality, it is often a combination of treatments used to manage disease with lifestyle modification being first and foremost.
The Role of Imaging in Obstructive Sleep Apnea
To summarize our understanding of OSA, it is a disease whereupon the airway is narrowed or obstructed due to the tongue falling backwards and loss of tone in the pharyngeal musculature during sleep, which subsequently cause apneic and hypopneic events and a drop in blood oxygen levels. The disease is multifactorial and requires diagnosis by a trained physician aided by clinical examination and polysomnogram. There are multiple avenues of treatment with many patients requiring a combination of them to achieve control.
So where does radiographic imaging come in?
Well, it would stand to reason that an airway already reduced in dimension or obstructed would predispose an individual to sleep apnea; this belief forms the basis for radiographic imaging and it has now been established firmly that there is a strong correlation between airway narrowing in an awake patient and subsequent airway collapse during sleep.17
To be clear, CBCT does not diagnose OSA. Anyone that tells you otherwise is incorrect.
What CBCT does do is provide a detailed depiction of the airway and craniofacial anatomy that allows the clinician or radiologist to identify normal anatomy, variant anatomy, or pathological conditions that may cause obstruction of the airway. This invaluable information, combined with clinical screening, can help identify individuals that may suffer from sleep apnea. Indeed, with OSA afflicting a broad spectrum of people and dangerously underdiagnosed, dentists can serve on the front line of screening.2,3,6,8 Further supporting the dentists role in screening, CBCT made for dental treatment routinely includes portions or all of the upper airway and is made at a lower radiation dose and cost than traditional multi-detector CT used in medicine. Dentists and cone-beam CT are ideally situated for this task.
Before we talk about how, though let’s address the elephant in the room…How does a radiograph made of a patient standing up and awake have any reliability in predicting the anatomy of a patient supine and asleep?
Simple, it doesn’t.
Imaging is not a magic wand that you can wave over the patient and diagnose airway collapse, but it doesn’t matter and we don’t necessarily need the patient supine and asleep. As discussed above, studies have consistently shown there is a strong correlation between airway narrowing in an awake patient and subsequent development of apneas while asleep.17 The fact that a patient is awake and standing during a CBCT doesn’t matter. A narrow airway that will only get narrower when they fall asleep does.
Normal airway dimensional measurements
Narrow airway dimensional measurements with false color added to demonstrate restriction. Patient is at moderate risk for OSA.
Radiographic evaluation of the airway requires systematic and thorough review of the anatomy combined with accurate measuring. If uncomfortable or unfamiliar this is a task best left to a trained radiologist. It is important to review all anatomy in the CBCT for abnormality; however, several key areas have been identified as strongly correlating with OSA:17
- Soft palate length
- Oropharyngeal airway length
- Tongue length
- Retropalatal cross-sectional measurement
- Retroglossal cross-sectional measurement
- Underdeveloped maxilla and/or mandible
- Inferiorly descended hyoid
Come on just give me the number.
The number, the oropharyngeal cross-sectional measurement encompassing the retropalatal and retroglossal measurements, the bane of the radiologists existence. Hyperbole aside, it is important to understand the cross-sectional measurement is just that…a measurement. It is a number generated by manual and augmented segmentation of the airway and susceptible to user variance, patient variance, and software variance. In and of itself it is meaningless, but as part of a systematic review and clinical screening, it can provide a vital understanding of the airway. The oropharyngeal cross-sectional measurement provides us with the smallest diameter of the airway, where it occurs, and whether it is predominantly mediolateral narrow, anteroposterior narrowing, or both.
Airway cross-sectional volume measurement demonstrating moderate to severe risk of OSA
The oropharyngeal cross section dates back to many of the early studies utilizing CT for airway assessment.18,19 These studies looked at anatomic abnormalities in patients with OSA to see if there were common findings and what role CT could play in screening. Across multiple studies, consistency started to arise between a cross-sectional measurement of ~50mm2 and severe obstructive sleep apnea. This baseline provides the scale that many radiologists use today:
Oropharyngeal airway cross-sectional measurement
Approximate risk of obstructive sleep apnea based off oropharyngeal cross-sectional measurement
Key areas of evaluation also include the soft palate length, the total oropharyngeal airway length, the position of the hyoid, and any craniofacial or cervical abnormalities. In younger individuals, it is common to see tonsillar hyperplasia. This strongly correlates with obstructive sleep apnea and adenotonsillectomy is a common first-line treatment of OSA in children.20
Long soft palate (yellow arrow) with narrow retropalatal space and large retroglossal space denoting a severe risk of OSA
Inferiorly descended hyoid and narrow oropharyngeal airway space denoting severe risk of OSA
Exaggerated cervical lordosis (yellow arrow) and narrow oropharyngeal airway denoting severe risk of OSA
Adenoidal hyperplasia (yellow arrow) and narrow oropharyngeal airway denoting severe risk of OSA
In summary, an airway evaluation is not just generating a number. It is systematic review of the entire anatomy to evaluate abnormalities and provide an understanding of clinical findings and patient concerns. Above, we just focused on the pharyngeal airway, in practice the nasal cavity, spinal architecture, TMJs, and skull base need evaluation. Our analysis extends from the tip of the nose to the epiglottis and is so much more than a single cross section. To return to our original question as to what role CBCT plays in obstructive sleep apnea evaluation, it turns out quite a bit. Generating a cross-sectional measurement can prove useful, but it is the 3-dimensional depiction of anatomy that proves of greatest benefit. If you’re on the fence about cone-beam CT and obstructive sleep apnea maybe this can help get you off it.
- Fleetham J, Ayas N, Bradley D, et al. Canadian Thoracic Society guidelines: diagnosis and treatment of sleep disordered breathing in adults. Can Respir J. 2006;13(7):387–392. doi:10.1155/2006/627096
- Spicuzza L, Caruso D, Di Maria G. Obstructive sleep apnoea syndrome and its management. Ther Adv Chronic Dis. 2015;6(5):273–285. doi:10.1177/2040622315590318
- org. (2020). Sleep breathing disorders – ERS. [online] Available at: https://www.erswhitebook.org/chapters/sleep-breathing-disorders/ [Accessed 3 Jan. 2020].
- Young T, Finn L, Peppard PE, et al. Sleep disordered breathing and mortality: eighteen-year follow-up of the Wisconsin sleep cohort. Sleep. 2008;31(8):1071–1078.
- American Academy of Sleep Medicine – Association for Sleep Clinicians and Researchers. (2020). Rising prevalence of sleep apnea in U.S. threatens public health – American Academy of Sleep Medicine – Association for Sleep Clinicians and Researchers. [online] Available at: https://aasm.org/rising-prevalence-of-sleep-apnea-in-u-s-threatens-public-health/ [Accessed 3 Jan. 2020].
- Kapur, V., Auckley, D., Chowdhuri, S., Kuhlmann, D., Mehra, R., Ramar, K. and Harrod, C. (2020). Clinical Practice Guideline for Diagnostic Testing for Adult Obstructive Sleep Apnea: An American Academy of Sleep Medicine Clinical Practice Guideline.
- Rajagopalan N. Obstructive sleep apnea: Not just a sleep disorder. Journal of Postgraduate Medicine. 2011;57(2):168. doi:10.4103/0022-3859.81866.
- Chiang HK, Long A, Carrico CK, Robinson R. The prevalence of general dentists who screen for obstructive sleep apnea. J Dent Sleep Med. 2018;5(3):55-60.
- American Academy of Sleep Medicine; American Academy of Dental Sleep Medicine. Policy Statement on the Diagnosis and Treatment of OSA. American Academy of Dental Sleep Medicine website. [Accessed 3 Jan. 2020]. http://aadsm.org/osapolicystatement.aspx. Published December 7, 2012.
- Kapur VK, Auckley DH, Chowdhuri S, Kuhlmann DC, Mehra R, Ramar K, Harrod CG. Clinical practice guideline for diagnostic testing for adult obstructive sleep apnea: an American Academy of Sleep Medicine clinical practice guideline. J Clin Sleep Med. 2017;13(3):479–504.
- Berry RB, Albertario CL, Harding SM, et al for the American Academy of Sleep Medicine. The AASM Manual for the Scoring of Sleep and Associated Events: Rules, Terminology and Technical Specifications, Version 2.5, www.aasmnet.org, American Academy of Sleep Medicine, Darien, IL 2018.
- Yaggi H. K., & Strohl K. P. Adult obstructive sleep apnea/hypopnea syndrome: Definitions, risk factors, and pathogenesis. Clinics in Chest Medicine, 2010;31(2), 179–186.
- Peppard PE, Young T, Palta M, Dempsey J, Skatrud J. Longitudinal Study of Moderate Weight Change and Sleep-Disordered Breathing. 2000;284(23):3015–3021.
- Weaver TE, Grunstein RR. Adherence to continuous positive airway pressure therapy: the challenge to effective treatment. Proc Am Thorac Soc. 2008;5(2):173–178. doi:10.1513/pats.200708-119MG
- Calik MW. Treatments for Obstructive Sleep Apnea. J Clin Outcomes Manag. 2016;23(4):181–192.
- Zhu, H. Long, F. Jian, J. Lin, J. Zhu, M. Gao, et al. The effectiveness of oral appliances for obstructive sleep apnea syndrome: a meta-analysis. J Dent. 2015;43 (12): 1394-1402
- Whyte A, Gibson D. Imaging of adult obstructive sleep apnoea. Eur J Radiol. 2018;102:176–187. doi: 10.1016/j.ejrad.2018.03.010.
- Li HY, Chen NH, Wang CR, Shu YH, Wang PC. Use of 3-dimensional computed tomography scan to evaluate upper airway patency for patients undergoing sleep-disordered breathing surgery. Otolaryngol Head Neck Surg 2003:129:336–342.
- Galvin JR, Rooholamini SA, Stanford W. Obstructive sleep apnea: diagnosis with ultrafast CT. Radiology. 1989;171:775–778.
- Lind MG, Lundell BP. Tonsillar hyperplasia in children. A cause of obstructive sleep apneas, CO2 retention, and retarded growth. Arch Otolaryngol. 1982 Oct;108(10):650–654. doi: 10.1001/archotol.1982.00790580044015.
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