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The Role of a Dentist in Sleep Apnea

Serving Park City and Salt Lake City, Utah and surrounding areas

James F. Garry, DDS

Sleep is now regarded as an active and complex state; hence we use the term “sleep architecture” to describe the stages of sleep and their interrelationships.

Stages of Sleep

The average adult sleeps 7.5 hours per night. There are two kinds of sleep: non-rapid eye movement and rapid eye movement. There are four stages of NREM sleep recognized in humans:

Stage 1 or Twilight Sleep – reactivity to outside stimuli is diminished. College students with their eyes taped open would no longer see, remember or recall pictures presented to them. Stage 1 last from thirty seconds to seven minutes.
Stage 2 – contains sleep spindles and K complexes (Figure 1, page 2). This is the first true stage of sleep and makes up 50% or more of night sleep. This stage contains mundane and fragmented thoughts.
Stage 3 & 4 – distinguished by slow delta waves and therefore called “delta sleep”. Typically the deepest stages of sleep and therefore contains any parasomnias such as sleep walking or night terrors.

REM sleep alternates with NREM sleep at about 90 minute intervals in adults (60 min in infants). In about 80% of REM sleep awakenings, people recall dreams whereas only 5% in NREM sleep. Over a period of 7 to 8 hours, REM sleep occupies 1.5 to 2 hours. The first REM periods last approximately 10 minutes with a progressive lengthening and an EEG pattern that looks much like that during wakefulness. Electromyographic recordings (EMG) show hypoactivity of muscles except for the eye muscles and diaphragm. REM sleep occurs primarily in the last sleep cycles while delta sleep occurs primarily in the first couple of sleep cycles. When a person’s sleep is adequate, that person should feel alert throughout the day.

Sleep Disorder Centers

Sleep Disorder Centers are springing up throughout the country to record physiological parameters of sleep if a sleep disorder is suspected. The recordings are usually done on an outpatient basis.

Polysomnograph

In order to identify and classify sleep, it is necessary to record the electrical activity of three systems: the brain, the eyes, and the muscles. Small electrodes are attached to the face and head area and bilateral recordings are recorded on the polygraph.

EEG or electroencephalogram records brain activity. These recordings verify the stage of sleep in which the patient is being recorded at any specific hour.
EOG or elctro-oculogram records eye movement. The eyes are like small batteries that get a difference in electrical potential between the cornea and retina whenever the eyes move.
EMG or electromyogram records the electrical potential generated in muscle fibers corresponding to movement.

Other recordings that aid in diagnosing a patient’s physiologic parameters of sleep include nasal and oral airflow which is monitored with a temperature-sensitive flow thermistor. Thoracic and abdominal effort is measured with strain gauges which provide movement tracings during respiration. Oxygen saturation is measured by a finger or ear oximeter which measures changes in arterial oxygen tension or saturation and an electrocardiogram measures cardiovascular abnormalities during sleep.

Nosology

The American Sleep Disorder Association (ASDA) has published a sleep disorders nosology that basically recognizes four types of sleep disorders:

Narcolepsy

A disorder of excessive daytime somnolence and can be confused with sleep apnea because hypersomnolence is a common feature of both disorders. The four clinical symptoms associated with narcolepsy are:

The diagnosis of narcolepsy is made by finding at least two REM periods at sleep onset. The sleep attacks are usually short and the patient feels refreshed after the naps. Patients with Obstructive Sleep Apnea (OSA) usually take longer naps that fail to refresh.

Sleep Apnea

Special emphasis will be placed on Obstructive Sleep Apnea (OSA) which is classified a DOES associated with sleep-induced respiratory impairment. Sleep apnea is defined as 30 or more apneic episodes (cessation of airflow at the nose and mouth for more than 10 seconds) occurring during seven hours of nocturnal sleep. The condition is classified into three types: obstructive, central, and mixed. In central apnea, airflow and respiratory movements temporarily cease although the airway may remain open, owing to a disordered regulation of respiration. When more than 55% of events are central in nature, the form of apnea is defined as central. In obstructive sleep apnea thoracic and abdominal respiratory efforts continue however there is no effective airflow due to an obstruction or collapse in the upper airway. In mixed apnea, some apneic periods begin with a central process and become obstructive. Many patients have all three events. Some also manifest hypopnea which is a decreased tidal volume with associated oxygen desaturation. Apnea termination is usually accompanied by evidence of arousal on the sleep EEG with the patient unaware. A patient can have as many as 500 apneic episodes per night each lasting 10 to 120 seconds. Oxygen saturation may reach the lower limits of reliable measurement with an ear oximeter (50%-60%). In men typically, the muscles of the upper airway over relax during sleep so when the diaphragm drops to pull air into the lungs, it is like pulling it through a wet straw. Sleep related relaxation of the genioglossus muscles occurs which pulls the anterior one third of the tongue forward out of the oropharynx. Thus, sleep appears to predispose to airway obstruction by depressing airway maintaining musculature.

Snoring

Snoring is the lay term for obstructive breathing during sleep and it is almost exclusive to humans. Bulldogs and other brachycephalics can be strangled during sleep by their soft palate and uvula. The musculature fails to maintain normal tonus in the respiratory cycle to keep the airway open during inspiration. The condition is exaggerated when people consume alcohol, sedative-hypnotics, tranquilizers or antihistamines before bedtime. Nasal or septal deformity, nasal tumors and sinusitis with nasal polyps are also causes of snoring.

Classification of Severity of OSA

Lugaresi et al. compared the mortality of different patients and found it to be significantly higher in those with an apnea index greater than 20 (20 apneic events / hour).

Mild apnea – 5 to 15 episodes per hour
Moderate apnea – 15-25 episodes per hour
Severe apnea – 25 episodes per hour or more

The duration of each apneic episode similarly increases, lasting often as long as 15 to 25, or even 120 seconds.
Common Complaints of the Apneic Patient

It has been noted that, as the arousals occur, there is a transition into a lighter sleep resulting in increased sympathetic tone causing a more rapid heartbeat. Common complaints in children with OSA are frequent upper airway infections, earaches, enuresis, nocturnal mouthbreathing, snoring, restless sleep, apneic episodes, heavy sweating, nightmares, night terrors, and headaches. The child commonly exhibits a chronic runny nose (rhinorrhea) whereas the adult patient will complain of a stuffy nose.

Side Effects of Sleep Apnea

The most typical changes experienced in adults are depression and agitation and hyperactivity in children. Intellectual impairment is not uncommonly noted by the parents, teachers, and coworkers. A younger child may go through a developmental delay as a result of his condition. Obesity is typical but not required, and they are noisy breathers as well as mouthbreathers with a hyponasal quality to their voice. Eating patterns vary in children without obstruction of the pharyngeal passages. The obstructed youngster will select food that does not require prolonged chewing but allows them to simply swallow so they may resume breathing promptly.

Contributing Factors to Sleep Apnea

Any disorder that leads to muscular weakness can contribute to obstructive breathing: cerebral palsy, myasthenia gravis, polio, etc.

Hypothyroidism

Hypothyroidism is a common cause or contributing factor to snoring and OSA and must be considered even if the symptoms do not suggest a hypothyroid state. Hypothyroidism and sleep apnea both feature obesity, lethargy and somnolence.

Obesity and Sleep Apnea

In the obese patient who demonstrates a pendulous abdomen with an adipose laden chest, there is a perfusion mismatching the lung and hypoxemia occurs due to the weight distribution preventing the lungs from inflating completely in the supine position (atelectasis). The size of the resting lung (and airway) increases with weight loss which might explain why there is an improvement of apnea after weight reduction.

Sleep Position and Apnea

Patients with OSA associated with a supine sleep position found significant improvement when they alter their sleep position to a lateral decubitus posture. If the patient can only sleep supine, elevating the head of the bed 30 to 40 degrees reduces the gravitational pull on the mandible and tongue.

Sedative and Sleep Apnea

Alcohol, along with benzodiazepines and narcotics, have been shown to induce sleep apnea in snorers and worsen apnea and nocturnal hypoxemia in patients with preexisting sleep apnea.

Proteinuria and Sleep Apnea

Elimination of OSA reduces accelerated hypertension which has been associated with Proteinuria.

Angina Pectoris and Sleep Apnea

Heavy snorers, who usually develop sleep apnea, are more likely to develop angina pectoris than non-snorers with normal apneic episodes.

Nocturnal Gastroesophageal Reflux and Sleep Apnea

Factors that contribute to the competence of the gastroesophageal junction include intrinsic sphincter pressure, the angle of the cardioesophageal junction, and the action of the diaphragm. Allen and Newhouse found a relationship between chronic respiratory disease and GER (from the resuscitative effort of the diaphragm during apneic episodes).

Enuresis and Sleep Apnea

Frequent nocturnal voiding has been associated with OSA. It may be hypothesized that increased episodes of nocturnal hyperactivity can have an influence on the bladder incontinence in children.

Hemodynamics and Ventilatory Changes in Sleep Apnea

During OSA, hypoxemia and hypercarbia develop, stimulating vagal tone, and bradycardia develops as the patient struggles to inspire against a collapsed pharyngeal airway. Systemic hypertension develops from the resulting sympathetic discharge and pulmonary hypertension occurs from hypoxia and academia. Upon resumption of breathing, the catecholamine surge and decreased vagal tone contribute to tachycardia, PVCs and can lead to V tach. In addition, catecholamines are aggregating agents for platelets increasing the susceptibility to atherosclerosis. Arterial BP has been found to rise as much as 20 to 30 mm Hg during apneic episodes. It does return to normal when ventilation resumes unless they occur in rapid succession. Wide swings in blood pressure can cause disruption of the vascular endothelium leading to adherence of platelets and prostaglandin release. Myocardial oxygen demand increases as a result of the increase afterload due to increased PVR and increased pulse rate.

Cardiovascular Consequences in Sleep Apnea

It becomes clear that when obstructive sleep apnea progresses there are physiologic consequences that have an impact on the cardiovascular system. Common signs and symptoms are that of right heart failure (right ventricular enlargement as revealed by EKG, peripheral edema, and an exaggerated pulmonic component of the second heart sound and hypertension. Cardiac arrhythmias are frequent and range from PVCs to AV block and sinus arrest. These complications are progressive unless sleep apnea is treated.

Choosing Therapy

It is essential that an upper airway evaluation be done once the patient has had an all night polysomnograph which documents episodes of OSA greater than 10 episodes / hr. If nasal and or pharyngeal obstruction is diagnosed, the patient may be a candidate for nasopharyngeal surgery. Prior to initiating additional aggressive therapy, the patient must be encouraged to:

Lose weight
Avoid CNS depressants
Change sleeping position to a lateral decubitus position
Elevate the head of the bed 30 degrees when sleeping supine
Reduce alcohol ingestion
Control Allergies
Insert a Mandibular Positioning Orthosis

Sleep causes a selective suppression of genioglossal activity which can induce OSA. A dentist has the capability of preventing distalization of the mandible during sleep and maintaining an optimal neuromuscular position relative to the skull. An additional approach is the use of a Continuous Positive Airway Pressure system or CPAP to keep the airway from collapsing. The problems with a CPAP are six fold:

Many surgical procedures have been advanced for the treatment of sleep apnea such as:

Uvulopalatopharyngoplasty (UPPP)
Maxillomandibular advancement
Partial resection of turbinate
Hyoid splitting
Tonsillectomy
Adenoidectomy or Tracheostomy
Partial glossectomy
Geniotomy advancement to advance the genioglossus

UPPP is effective for snoring but is only 50 percent effective in reducing or eliminating sleep apnea. To avoid the surgical and economic risks of surgery, the author feels that a reversible dental appliance should be utilized first as it is conservative and reversible.

Sleep Apnea and the Dentist

The tongue must have adequate three dimensional volume to avoid compaction in the hypopharynx. The dentist who understands and practices neuromuscular craniomandibular orthopedics knows that when the muscles of mastication relax, there is usually in increase in vertical dimension with a simultaneous antero-inferior translation of the condyles within the glenoid fossa. Initially an acrylic overlay orthotic can be constructed that will position the mandible optimally to the cranium. Treatment by a dentist may include:

Surgical or orthopedic advancement of the mandible in retrognathia
Arch development (widening)
A partial glossectomy in the neurologically impaired
Extrusion of posterior teeth
Orthodontics
Prosthodontics
A combination of orthodontics and prosthodontics

Since 1911, practitioners have been developing methods of fixing the tongue in a more anterior position by utilizing sutures or creating scar tissue. A dentist who understands how micrognathia occurs would correct any ongoing obstruction and then develop the arches with functional appliances.

Dentist Role in Treatment of OSA

Armed with a polysomnograph, an upper airway evaluation, and a medical history, the dentist can now proceed to construct a sleep apnea appliance. The patient suffering from sleep apnea should have a second polysomnograph after he or she has worn the sleep appliance for several days. This will verify whether the appliance has improved episodes of apnea, hypopnea, and or increased blood oxygen saturation. If not, the appliance therapy should be discontinued.

Dental Appliances

There have been many attempts to develop appliances to widen or expand dental arches in order to accommodate the tongue and improve upper airway competency. The first effective sleep apnea appliance that has adequate documentation was developed to hold the tongue in a forward position by suction. The most successful cases are those patients whose apnea is positional in nature, i.e. twice as severe when they are sleeping supine than when in a lateral decubitus position, and that such patients are not excessively obese. Dr. Garry at this point illustrates six appliances and their evolution to the current marketplace. With over 800 anti-snoring devices on the market, he states that there isn’t one that is superior to all others. In any case, the patient should be scheduled for a follow-up appointment to evaluate the fit of the appliance and also the compliance. If possible, the spouse should be present at the appointment to verify how the appliance has affected both snoring and OSA episodes.