Approach to obstructive sleep apnea

Case description

A 77-year-old man presented to the family medicine clinic with recurring diurnal fatigue, dizziness, nocturia, and frequent awakenings for the past 3 weeks. His medical history included OSA syndrome treated with the use of a continuous positive airway pressure (CPAP) machine. His symptoms had resolved, according to self-assessment, and he had not used his CPAP for the past year. One week before symptom onset, he underwent dental surgery consisting of multiple dental extractions and placement of dual jaw-implant–supported dentures.

He did not describe irritative urinary symptoms. Reviews of cardiovascular, respiratory, and neurology systems had negative findings. Physical examination findings were normal. Orthostatic hypotension was ruled out. Blood count and dysthyroidism panel results were negative. Prostate palpation findings were normal.

Sources of information

Literature searches of the PubMed and MEDLINE databases were performed with no date limitations on March 30, 2025. The medical subject headings sleep apnea syndromes and clinical/practice guidelines were searched independently as were free-word searches for sleep apnea and similar terms. We also searched for descriptions of the uses of dentures with implant oral restoration.

Main message

While sleep apnea and hypopnea can be categorized as central and obstructive to describe the underlying cause, this review focuses on the latter.

Pathophysiology. The pathophysiology of OSA is biomechanical, with the negative pressure during inspiration causing a partial or complete collapse of the upper airway soft tissues, which results in partial or complete obstruction of airflow despite respiratory effort. During inspiration, the genioglossus muscle and associated upper airway dilator muscles contract to prevent posterior collapse of the tongue.^4,11 Narrowing of the upper airway axial surface due to fat deposition or hypertrophic tonsils and upper airway neuromuscular pathology can lead to OSA. Individual phenotypes or morphologic traits (Box 1),⁴ including a narrow upper airway and low respiratory arousal threshold, can also contribute to OSA.¹²

Signs and symptoms. The signs and symptoms of OSA are diverse and demonstrate the overall impact of sleep on physiology. The various manifestations are both patient- and severity-dependent. While some patients may be asymptomatic, most develop a variety of symptoms, including nocturnal awakenings, nocturia, unrefreshing sleep, daytime sleepiness and fatigue, impaired concentration, and chronic morning headaches.^3,6,13,14 While nonspecific to OSA, loud snoring is a common concern among patients’ partners and others who sleep nearby.¹⁵ Episodes of apnea are sometimes followed by abrupt awakenings with gasping.¹⁵

Analyses and reviews describe hypertension,⁵ type 2 diabetes,¹⁶ atrial fibrillation,⁵ heart failure,⁴ cardiovascular disease,⁴ anxiety disorders,⁵ depression,¹⁷ and others^4,5 as potential complications of OSA.

Evaluation. Patients who express concern about related symptoms should be offered evaluation of suspected OSA. Evaluation tools include the Berlin Questionnaire¹⁸ (Box 2), which was developed to identify sleep apnea in the primary care setting,⁴ and the STOP-Bang (snoring, tiredness, observed apnea, high blood pressure, body mass index [BMI], age, neck circumference, and male gender) questionnaire, which is more widely used in the clinical setting to screen for OSA despite being developed and validated for preoperative surgical patients.¹⁹ The Epworth Sleepiness Scale²⁰ is not specific for OSA and should not be used in the evaluation process in this population.

Many items on the Berlin Questionnaire are based on the epidemiologic distribution of risk factors associated with OSA. Other items, such as about snoring and fatigue, may be part of a patient’s history. The prevalence of OSA is greater in men than in women and increases with BMI and with age, especially after age 50 years.⁹ Clinical suspicion of OSA increases as the number of risk factors increases. A higher clinical probability of OSA is seen for patients with OSA symptoms and with 2 or more criteria of the STOP-Bang questionnaire.¹⁹

No specific physical examination can confirm OSA, but an examination may reveal anatomic variants such as tonsillar hypertrophy, retrognathia, and macroglossia.⁴ Attention should also be paid to the fit of dentures. A nasal examination should be performed as several treatable anatomic variants or pathologies, including rhinitis, nasal polyps, or septal deviation, can obstruct airflow.

Diagnosis. Polysomnography (level 1) is the accepted standard for the evaluation of sleep-disordered breathing, including OSA. The presence and severity of OSA are determined by the apnea-hypopnea index (AHI), which expresses the number of events per hour. However, the AHI does not accurately account for ventilatory deficits. Both the Canadian Thoracic Society^6,14 and the American Academy of Sleep Medicine (AASM) have proposed criteria and definitions for sleep apnea or hypopnea, although physicians use the AASM^21,22 criteria in the clinical setting (Table 1). Such criteria are not sufficient to assess health risks, and a complete assessment of the patient’s quality of life, occupation, and cardiovascular and metabolic risks is warranted.

Portable monitors, with high sensitivity (79%) and specificity (79%), allow for in-home sleep testing,⁴ which is frequently used for first-line diagnostic testing. Level 1 is reserved for severe cases or for patients with critical comorbidities. For patients with a high pretest probability, a negative home sleep test result should be followed by level 1 polysomnography, if available, or repeated in-home testing.^4,23 In the case of a negative result on subsequent or repeat testing, another diagnosis should be considered. In the case of a marginally positive test result (or inconclusive evaluation), a CPAP trial should be considered to guide next steps based on symptom response. Sleep tests may need to be repeated, particularly if symptoms change, which can happen with age, development of new comorbidities or worsening of existing ones, and changes in weight.

Management. Modifying risk factors can help control OSA (Table 2).^24-29 Obesity and overweight status in the adult population have been associated with OSA severity.^24,25 Weight control is of utmost importance in the patient-centred approach to OSA management. Multimodal strategies including dietary approaches, exercise, bariatric surgery, and treatment with glucagon-like peptide-1 (GLP-1) agonists may help achieve weight control most effectively, although GLP-1 agonist treatment has not been approved for OSA management in Canada. Clinicians should inform patients that achieving optimal weight and using a CPAP or mandibular advancement device (MAD) can contribute to reducing their health risk and improving their quality of life and of sleep. However, mild to moderate residual apnea and hypopnea may persist.

Behavioural intervention management. Behavioural interventions include weight loss, aerobic exercise, and alcohol abstinence.⁴ Weight loss, which the American Thoracic Society recommends as part of its clinical practice guideline, is associated with improvements in OSA severity, cardiometabolic comorbidities, and quality of life.³⁰ Physical activity independent of weight loss is also associated with improvements in OSA.^5,26

Whether patients should wear their dentures at night is a common and important question in the context of OSA. The current literature tends to support that such a decision should be made on an individual basis, with some recent data showing no major overall difference.³¹ However, sleeping with dentures was associated with greater daytime sleepiness for some, while for others, sleeping without dentures was associated with better breathing, probably due to a different anatomic airway configuration and length, as shown by 3-dimensional imaging.^31,32 More research is needed to reach a conclusion on this issue. In addition, the ability to properly use CPAP or MAD in an aging population is a crucial factor to consider.³³

Medical and noninvasive options. Positive airway pressure (PAP) therapy is recommended as first-line therapy for patients with OSA symptoms and polysomnograph findings showing an AHI greater than 5.^27,34 The AASM suggests using CPAP or autoadjusting PAP over bilevel PAP in the treatment of OSA.²⁷ The use of nasal devices, compared to oral interfaces, resulted in greater adherence to PAP therapies.³⁴ One study reported a statistically significant reduction in mean hourly use of CPAP compared to MAD at 30 days.³⁵

Using a MAD is the second choice after PAP therapy for patients with mild or moderate OSA or for those who cannot tolerate PAP therapy. Several randomized controlled trials have compared the efficacy of MAD to CPAP (as standard of care). A meta-analysis showed that both treatments decreased the AHI and the oxygen desaturation index compared to controls, although MAD was less effective than CPAP.²⁶ Nevertheless, using a MAD may be a reasonable alternative to PAP therapy because the higher adherence rates help achieve similar patient-oriented outcomes over time.³⁶ In the CHOICE (Adherence and Preference of Continuous Positive Airway Pressure vs Mandibular Advancement Splints in Obstructive Sleep Apnea Patients: A Randomized Trial) randomized clinical trial, 35 of the 64 participants (55%) preferred alternating between CPAP and MAD versus using only 1 or the other intervention, which suggests that a multimodal treatment improves patient-centred outcomes and therefore OSA management.²⁸

A review of prescribed drugs and adequate withdrawal of sleep-inducing medication, such as muscle relaxants and benzodiazepines, could help with excessive daytime sleepiness.

Surgical options and considerations. Otorhinolaryngologic evaluations to assess for nasal or pharyngeal obstruction are recommended. Surgical alternatives to PAP therapy are possible if adherence to or efficacy of CPAP is low. These include uvulopalatoplasty, nasal septoplasty, and treatment of nasal polyps. Other proposed surgical procedures include maxillary expansion, with the goal of reducing nasal resistance and improving nasomaxillary airway flow. The American Academy of Dental Sleep Medicine supports surgical approaches to maxillary expansion if orthodontic transverse discrepancy is present, but otherwise concluded there is insufficient evidence supporting the use of ablative procedures to prevent, manage, or cure OSA.²⁹

While behavioural interventions and lifestyle changes are preferable for controlling weight, options such as bariatric surgeries have shown promising results.³⁷ Three systematic reviews and meta-analyses reported that bariatric surgery did not resolve OSA.^38-40 While weight loss occurred after the intervention, the authors highlighted the absence of linear correlation between the decrease in both weight and AHI.^38,39

Prognosis. The prognosis of OSA depends on the severity of the condition and adherence to treatment. PAP therapy or MAD do not cure patients and only address the underlying biomechanical airway obstruction. Lifelong treatment is required unless sufficient weight loss or surgery results in disease remission.⁴ Treatment is important as patients who do not receive treatment or who experience nonadherence barriers are at increased risk of developing cardiovascular and cerebrovascular disease—especially those with more severe OSA, for whom treatment benefits are likely greater.^6,14 The daytime sleepiness associated with OSA also puts people at increased risk of motor vehicle accidents and work-related challenges.

Case resolution

The patient’s history showed a temporal association between the recurrence of his symptoms and the recent dental procedure. Investigations ruling out anemia and dysthyroidism suggested that decompensated OSA was likely. Considering the biomechanical impacts of the patient’s recent dental surgery, it was suspected that the new permanent implant-supported dentures reduced the overall volume of the oral cavity, probably causing the tongue to project posteriorly and in a downward position in the oropharyngeal space, thus exacerbating a previously compensated sleep apnea.

Following 10 days of CPAP use, the patient reported a return to baseline sleep and nocturia and a marked decrease in dizziness and daytime sleepiness. This clinically significant improvement strongly supports the biomechanical hypothesis of decompensated sleep apnea.

Conclusion

OSA has a range of signs and symptoms that affect quality of life and risk of additional comorbidities. While considering differential diagnosis, careful history-taking and understanding of the underlying biomechanical pathophysiology can orient physicians to consider OSA. Appropriate counselling should include regular use of CPAP or the use of removable dentures rather than a dental implant–supported solution.

Family physicians should motivate patients to regularly use CPAP, as treatment adherence is essential to obtain benefits. Personalized and interdisciplinary approaches adapted to the motor and cognitive changes related to aging are additional factors to consider when prescribing OSA treatment and at follow-up.