Obstructive Sleep Apnea - An Underestimated and Overlooked Condition

Introduction

Sleep Disordered Breathing (SDB), is a term that encompasses simple snoring, upper airway resistance syndrome and sleep apnea. Among all the SDBs, sleep apnea is the most prevalent and it can be either central, obstructive or mixed type, mild, moderate or severe in intensity based on Apnea Hypopnea Index (AHI). Obstructive type of sleep apnea is the most common among sleep apneas.¹ Obstructive Sleep Apnea (OSA) is defined as sleep associated breathing disorder characterized by the absence of breathing for at least 10 seconds or more despite having a ventilatory effort.²

Epidemiology and Prevalence

A cross sectional study conducted in urban and rural Bengaluru concluded that 6.7% subjects in urban and 8.7% subjects in rural areas were at risk of OSA and the prevalence of OSA was 4.6% in urban and 3.7% in rural Bengaluru.³ Another STOP Bang-Questionnaire study which evaluated the prevalence of OSA in Odisha reported that the prevalence of OSA was highest in the age group of 50-59 years (21.7%) and least in the age group of 18-29 years (12.0%). OSA was more prevalent among males (14.8%) than females (12.9%).⁴

Pathophysiology and Predisposing Factors

OSA results from increased resistance in upper airway and closure of the airway which can be attributed to anatomic and/or physiologic factors that can further lead to impaired functioning of airway dilating muscles and thus increasing the chances of its collapsibility.² The neuromuscular tone of the group of muscles holds the pharyngeal tube in a patent state during breathing. An abnormal pharynx can be kept open during wakefulness by compensatory actions of dilatory muscles, but this fails during sleep and can result in apnea.⁵

Predisposing factors include obesity, BMI greater than 28 which is found to be associated with five times increased probability of moderate to severe OSA, tonsillar hypertrophy, neck circumference of ≥ 17 inches (men), ≥ 16 inches (females), nasal obstruction, Modified Mallampati Grade of III, IV, inferior position of hyoid bone, long soft palate. Other predisposing dento-skeletal features include macroglossia, micrognathia, mandibular retrognathia, narrow tapered and short maxillary arch.²

Genetic and familial predisposition also play an important role and it is stated that the first degree relatives have 1.5-2 times greater risk for developing OSA.^6,7 Positional factors are also known to exacerbate OSA, like supine position, that causes the gravitational forces to displace tongue as well as the soft palate posteriorly.²

Alcohol consumption, Benzodiazepines and other sedatives exacerbate OSA and medications causing weight gain such as anti-psychotics, anti-epileptics, hormones, sedative anti-histamines, highly active antiretroviral therapy (HAART) are also contributing factors to developing OSA.²

Diagnosis

Clinical diagnosis: Overnight polysomnography is the gold standard diagnostic tool for OSA, but clinical examination, thorough history regarding snoring, observed/self-reported cessation of breathing, choking episodes, daytime sleepiness, lack of concentration and fatigue, limited channel testing, split light testing, oximetry are helpful in establishing diagnosis of OSA.¹

Pre-treatment evaluation of pre-disposing factors and airway evaluation for tongue and tonsil size, Mallampati scoring, evaluation of nasal turbinates, using acoustic reflexion to evaluate the site of airway restriction and probable effect if the mandible is to be repositioned must be evaluated carefully.^1,2

Questionnaires and AHI: Various questionnaires like Epworth sleepiness scale which assess daytime sleepiness of the subjects, the Berlin questionnaire, STOP Bang questionnaire are helpful in the diagnosis of high risk OSA cases.⁸ AHI can also be helpful which is total number of apneas or hypopneas per hour of sleep. It also gives us an idea on the severity of OSA: AHI ≤ 4 - normal, AHI 5-15 episodes - mild OSA, AHI 15-30 episodes - moderate OSA, AHI ≥ 30 - severe OSA.⁵

Cephalometric evaluation: It is used as an important tool to assess airway dimensions, cranial and skeletal structures. As SNA, SNB angles and posterior airway space are reduced in OSA, PNS-B is increased.¹ Some of the other diagnostic parameters for OSA are reduced sPAS, elongated soft palate, reduced maxillary projection, reduced mandibular projection, reduced iPAS.² 

OSA patients also demonstrate high ANB angle, mandibular plane angle and lower anterior facial height.⁹ But the limiting factor in utilizing cephalometrics for diagnosis is lack of correlation between skeletal cephalometric analysis and severity of OSA in patients.² Cephalometric studies have shown that anatomical differences in patients with sleep disordered breathing groups place their entire facial complex closer to the cervical spine leading to reduced airway space. OSA patients also have an inferiorly placed hyoid bone.¹⁰

Treatment Options for OSA Patients

Continuous Positive Airway Pressure (CPAP)

It acts as pneumatic splint to elevate and maintain a constant amount of pressure along the upper airway during breathing. CPAP leads to the enlargement of airway by dimensional changes of lateral pharyngeal wall. It also improves tonicity of upper airway dilator muscles, thus reducing chances of collapse. It is the most effective method to manage OSA. Two variations of CPAP are possible - bilevel CPAP and automated CPAP.²

Limitations of CPAP

Non-compliance to CPAP can be attributed to problems in tolerating it (dry mouth, rhinorrhea, pressure sores), inadequate instructions, psychological problems like claustrophobia and lack of follow-up.^2,11 At times CPAP can have dental implications as well like, reflection of muco-periostel flaps is contraindicated in patients undergoing nasal CPAP therapy as they are susceptible to develop sub-acute emphysema.¹²

Oral Appliance Therapy

These are more commonly employed in the treatment of mild-moderate OSA cases which are non-compliant to nasal CPAP. They are based on the ideology of increasing posterior pharyngeal airway spaces, thus reducing the airway collapsibility in sleep.²

The two main categories of appliances used are: Tongue retaining devices and mandibular repositioning devices.² Other appliances that can be used include soft palate lifters and tongue trainers.¹

Tongue retaining devices position the tongue anteriorly with a negative suction and are indicated in cases of macroglossia or in patients with few or no teeth. Mandibular repositioning devices reposition mandible, hyoid bone, tongue anteriorly, thereby increasing the antero-posterior and lateral dimensions of upper airway. Mandible can be advanced up to 80% of patient’s maximum protrusive capacity.²

Oral appliance can particularly help patients who suffer from high blood pressure as side effect from CPAP machine usage. There is no gold standard OA design to manage OSA and most commonly prescribed designs are the custom made titratable designs that restrict mouth opening, whereas the prefabricated designs have a poor fit and are not recommended.¹³

Limitations of oral appliance therapy

There are few limitations with OSA appliances like, reduced lateral jaw movements, pain and increased salivation, appliances being tightly retained to apply orthodontic forces which is undesirable. This can lead to a dose depended shift in occlusion and periodic maintenance is necessary as it can become loose or distort over a period of time.^1,13

Oral appliance for OSA is worn in non-growing adult patients with an average wear time of 6-8 hours per day, is considered as a lifelong treatment and thus the associated bite changes and shifts are also progressive. Reduction in overjet and overbite has also been reported as side effects in OSA patients undergoing OA Therapy.¹⁴

Medications

Modafinil, Armodafinil can be helpful in reducing daytime drowsiness in CPAP complaint patients and should not be prescribed in the non-complaint patients.²

Surgical Approach

Stage I surgery: It includes nasal surgery, uvulopalatophargoplasty, surgery of base of the tongue. The main indication for stage I surgery is a minimum respiratory disturbance index (RDI) of 15-20 and cases that are unsuccessful or intolerant to other conservative approaches.²

Stage II surgery: It includes upper airway reconstruction surgery, MMA (Maxillary-mandibular advancement) surgery. MMA increases antero-posterior and lateral dimension of upper airway, improves tension, reduces collapsibility of suprahyoid and velopharyngeal muscles. Tongue can be advanced more compared to stage I.²

Other surgical approaches include bariatric surgery, tracheostomy and non-airway surgery.²

Other Approaches

Oropharyngeal exercise, upper airway neuroelectrical stimulation.⁵

Applied Medical and Dental Aspects of OSA

There can repeated apneic episodes in known OSA patients under intra-venous sedation for dental procedures due to aggravation of compromised airway obstruction.¹ Diaphragmatic excursion increases in OSA cases to counteract airway obstruction during sleep, and this leads to gastroesohageal reflexes, which can lead to scaring of soft palate mucosa. This inflamed scar tissue can further progressively reduce the airway space, thereby increasing chances of aspiration and chemical pneumonitis.

OSA patients can report with altered swallowing reflexes which makes the recording of centric relation more difficult.

Xerostomia is one of the side effects of weight loss medications used in obese patients with OSA; so prescribing artificial saliva or saliva substitutes is important. Patients should be counseled on smoking as smoking is known to cause mucosal irritation leading to further secretions and resulting in aggravated obstruction of airway. Patients should be assessed for OSA prior to fabrication of occlusal splints/ night guards as they can lead to aggravated respiratory disturbances.¹

Conclusion

Dentists and physicians should have an updated knowledge regarding identification, definitive diagnosis and management of OSA. With the increasing number of cases being diagnosed, it is equally important to keep ourselves updated with the evolving treatment strategies for early and better management and prognosis of OSA patients.

Conflict of Interest

None