Normal sleep involves understanding the two distinct states of sleep.

These states are non-rapid eye movement (NREM) sleep and rapid eye movement (REM) sleep.

NREM sleep is divided into several stages, characterised by different brain wave patterns and physiological changes. Understanding the pathophysiology of these sleep states provides insight into the potential mechanisms underlying various sleep disorders. These stages can be distinguished by electrophysiological criteria using an electroencephalogram. In REM sleep, the brain activity is similar to a state of wakefulness. NREM sleep is divided into four stages.

Stages 3 and 4 represent a deeper level of sleep and are required to refresh the brain. REM and NREM sleep alternate cyclically through the night at 90–120 min intervals. In normal sleep, a person would progress from wakefulness to NREM to REM sleep state. Overall sleep at night comprises 75%–80% NREM and 20%–25% REM sleep.

Recently, the sleep staging has been revised and is as follows :

• 1.

  Stage W (Wakefulness)

• 2.

  Stage N1 (NREM 1)

• 3.

  Stage N2 (NREM 2)

• 4.

  Stage N3 (replaces NREM stages 3 and 4)

• 5.

  Stage R (REM)

These are described in Table 91.1 .

TABLE 91.1

Sleep stages

Sleep stage	Salient features	EEG recording
Wakefulness
Stage N1	• 2%–5% of sleep time • Drowsy or light sleep stage • It can be awakened easily • Sudden muscle contraction • Brainwave activity from rhythmic alpha waves to mixed waves
Stage N2	• 45%–55% of sleep time • Can be aroused, but more stimulus is required than N1 • Reduction in heart rate and body temperature • EEG will show K complexes and sleep spindles
Stage N3	• 13%–23% of sleep time • Slow-wave sleep, deep sleep or restorative sleep • Highest threshold for awakening
REM stage R	• 20%–25% sleep time • Each recurring REM is longer than the prior period • Increased heart rate, respiration, blood pressure and jerky eye movements • EEG is characterised by a saw-toothed wavy form, similar to wakefulness

The minimum sleep duration required for healthy living is 7–9 h. The number of hours of sleep considered to be optimal varies with age. Infants and young children need 12–14 h, preadolescents require 10–11 h, teenagers or young adolescents require 8–10 h and adults require 7–9 h.

The ventilatory activity of respiratory muscles, including the musculature of the upper airway, is reduced in sleep, leading to a fall in ventilation and an increase in upper airway resistance, leading to increased CO2 saturation. Ventilatory activity in sleep is stimulated by chemical drive from hypoxia and hypercapnia. During wakefulness, the behavioural drive also stimulates ventilatory activity.

During REM sleep, there is generalised inhibition of skeletal muscles, including intercostal accessory and pharyngeal dilators. Thus, ventilation during REM virtually depends on diaphragmatic function, and upper airway function is more precarious than during NREM. Sleep is a time of vulnerability for the respiratory system.

The system’s resistance is increased, and at the same time, both chemical and mechanical sensors are depressed. Considerable individual variation exists in the threshold for arousal in response to chemical and mechanical/behavioural drive. This variation in responsiveness may be a significant risk factor for OSA.

Although not fully understood, the pathophysiologic mechanism of snoring and OSA can be explained by either the obstacle theory or the Bernoulli theory. According to the obstacle theory, an increased negative pressure during inspiration retracts the structures of the pharynx. It makes them vibrate in the airflow, producing snoring and simulating OSA.

The Bernoulli theory assumes that according to Bernoulli’s principle, the velocity of streaming air is higher, and the pressure is lower at the constriction of a tube compared with a larger part. This may cause inward suction of the pharyngeal structures in a constricted area and cause snoring by the vibration of wall structures.

The upper airway is a non-rigid structure, which includes the hypopharynx, oropharynx, velopharynx and nasopharynx. During inspiration, the air pressure in the upper airway space becomes sub-atmospheric, caused by the diaphragm attempting to pull air through the airway and the walls of the airway resisting this airflow. The negative pressure tends to cause a change in the shape of the airway, which is resisted by the activity of tensor veli palatini and the genioglossus muscles. In an OSA patient, there is a reduction in the activity of these muscles that results in decreased airway space.

The man is the only mammal other than the English Bulldog that experiences OSA. OSA in humans has often been hypothesised as an anatomic illness caused by evolutionary changes. Natural selection, during the process of evolution, is believed to have resulted in bipedalism along with the migration of splanchnocranium (face) under and behind the neurocranium for locomotion and binocular vision and laryngeal descent with shortening of the palate for enabling the development of voice and speech. These adaptive changes, when compared to other primates, are considered the anatomic basis of OSA in humans.

• 1.

  Craniofacial anomalies observed in patients with OSA include a small mandible, retrognathia, hypoplastic maxilla or a combination of these, which can compromise the upper airway volume. In cases with a mandibular deficiency or functional retrusion, the tongue is held back in the mouth, compromising the airway patency. Figure 91.1 depict (A) Functional anatomy of the normal airway during sleep and (B) airway during OSA.

  

  (A) Functional anatomy of the normal airway during sleep. (B) Anatomy of the airway during OSA.

• 2.

  Patients with long face syndrome are found to be more susceptible to OSA.

• 3.

  Patients with craniofacial syndromes, like Pierre Robin and Treacher Collins, are prone to OSA.

• 4.

  Subjects with maxillary hypoplasia and increased nasal resistance in operated cleft patients and deficiency related to temporomandibular joint (TMJ) ankylosis are prone to developing OSA.

• 5.

  In dolichocephalism, there is a tendency towards mandibular retrusion and a convex profile; these cases have chances of developing SDB. These subjects exhibit an increase in lower anterior face height and steep mandibular plane angle. High arch palate and narrow maxilla have been observed in children with upper airway sleep disorders.

• 6.

  Maxillary deficiency can cause an approximation of the soft palate with the posterior pharyngeal wall, thus reducing the airway.

• 7.

  Other common causes of obstruction include adenoids, enlarged tonsils, deviated nasal septum, postnasal space tumours, retropharyngeal mass and short neck ( Fig. 91.2 ).

  

  Possible anatomical locations and factors contributing to a compromised airway and OSA.

• 8.

  Posterior and inferior placement of the hyoid bone is a contributory factor.

• 9.

  Obesity can compromise airway space, hence making a subject susceptible to breathing disorders.

• 10.

  Environmental factors like localised polyneuropathy could affect the small fibres of the soft palate. Untreated longstanding gastroesophageal reflux can progressively scar the soft palate and surrounding tissues. The scarring can decrease the size of the upper airway and thus proneness to OSA.

Specific cephalometric values indicative of craniofacial deformities have shown a strong association with OSA ( Fig. 91.3 ) and should be considered in the evaluation of OSA along with upper airway analysis ( Table 91.2 ). Significant cephalometric features suggestive of OSA:

• I.

  Increased anterior facial height

• II.

  Inferiorly and posteriorly positioned hyoid

• III.

  Short anterior cranial base angle

• IV.

  Decreased cranial base length

• V.

  Smaller maxillary length

• VI.

  Smaller mandibular length

• VII.

  Enhanced rotation of the mandible

• VIII.

  The mandible is held backwards

• IX.

  Short ramus height

Common cephalometric findings associated with obstructive sleep apnoea (OSA):

(i) increased anterior lower facial height and total facial height, (ii) inferior and posterior displacement of the hyoid bone, (iii) decreased cranial base angle, (iv) decreased cranial base length, (v) decreased maxillary length, (vi) decreased mandibular length, (vii) decreased posterior facial height, and (viii) decreased gonial angle (posterior rotation of mandible).

TABLE 91.2

Parameters used in cephalometric analysis for upper airway

S.no.	Parameter	Description	Value mean
1.	NAS	Measured from PNS to the upper pharyngeal wall along the palatal plane	25.9 ± 2.6 mm (M); 24.1 ± 2.3 mm (F)
2.	VAS	A horizontal distance from the tip of the soft palate to the pharyngeal wall	9.9 ± 2.8 mm (M); 9.9 ± 2.4 mm (F)
3.	PAS/oropharyngeal airway space	Horizontal distance from the posterior margin of the tongue to the pharyngeal wall measured on the Go-B line	10.1 ± 3.1 mm (M); 10.0 ± 2.8 mm (F)
4.	HAS	Minimum horizontal distance in the hypopharyngeal area measured from point V (intersection of tongue and epiglottis)	18.7 ± 2.6 mm (M); 16.5 ± 3.1 mm (F)
5.	Hyoid distance (MP-H)	The perpendicular distance from the mandibular plane (Go-Gn) to the anterior superior aspect of the hyoid	15 mm
6.	Hyoid angle	The angle from the mandibular plane (Go-Gn) to the superior aspect of the hyoid	25.42 ± 7.48
7.	Hyoid, C3 vertebrae and menton relationship	The perpendicular distance from H to the line joining inferior-anterior tip of cervical third vertebrae (C3) to the menton	H point should be on or above the line
8.	Length of soft palate	PNS to tip of the soft palate	34.3 + 3.9 mm (M); 30.6 + 3.7 mm (F)
9.	Soft palate thickness	Maximum thickness of soft palate measured perpendicular to PNS–P line	10.1 + 1.4 mm (M); 8.9 + 1.2 mm (F)
10.	Length of tongue (VT)	Measured from vallecula (V) to tip of tongue (T)	72.0 + 4.1 mm (M); 64.8 + 4 mm (F)
11.	Height of the tongue	Measured as the perpendicular distance from H to VT line (H—the highest point on the superior part of the tongue)	36.9 + 3.9 mm (M); 32.9+ 3.9 mm (F)

HAS, Hypopharyngeal airway space; NAS, nasopharyngeal airway space; PAS, posterior airway space; PNS, posterior nasal spine; SAS, superior pharyngeal airway space; VAS, velopharyngeal airway space.

Based on the cephalometric and morphometric analyses, patients with upper airway sleep disorders can be grouped into three major categories:

• 1.

  Non-obese with craniofacial abnormalities:

  • Retroposed mandible, narrow posterior airway space, enlarged tongue and soft palate, lowered hyoid bone, and retro-positioned maxilla are considered significant risk factors for sleep apnoea in non-obese individuals.

• 2.

  Obese with craniofacial abnormalities as above.

• 3.

  Obese with normal craniofacial anatomy where bone structures are well placed. These patients have truncal obesity and enlarged neck circumferences.

Snoring is a common sleep disorder that occurs when the base of the tongue or soft palate or both come close to the posterior wall of the pharynx, resulting in an acoustical phenomenon. This obstruction usually happens when a patient falls asleep in the supine position, causing the oropharyngeal musculature to relax, which leads to a decrease in airflow. As a result, the patient tries to increase the speed of airflow to maintain the required oxygen saturation. The vibration of soft tissue is caused by increased airflow velocity, which leads to snoring sounds. ^{, ,} Obesity, enlarged tonsils and adenoids are contributing factors to snoring. A polysomnogram (PSG) is necessary to diagnose intractable snoring before treatment. Snoring may indicate a serious health condition.

• Apnoea is defined as a cessation of airflow during sleep that lasts for at least 10 s, with oxygen desaturation of more than 3% and/or is associated with arousal.

• Hypopnoea is a reduction in airflow amplitude of greater than 50% of the baseline measurement for at least 10 s with accompanying oxygen desaturation of at least 3% and/or associated with arousal. These apnoeic/hypopnoea spells last for 10–30 s.

• Obstructive sleep apnoea (OSA) refers to the occurrence of at least five apnoeas or hypopnoeas per sleep hour (AHI > 5/h), which results in sleep fragmentation and decreased oxygen saturation.

• Sleep apnoea is classified as central, obstructive and mixed sleep apnoea.

  • •

    Central sleep apnoea occurs when the respiratory muscles do not attempt to breathe due to a central nervous system (CNS) disorder. Orthodontists have no role in these cases.

  • •

    Obstructive sleep apnoea (OSA) is characterised by repetitive upper airway obstruction during sleep, resulting in episodic hypoxaemia and arousal. In OSA, the respiratory muscles attempt to breathe. However, they are characterised by repetitive episodes of complete or partial upper airway obstruction, leading to diminished or absent airflow to the lungs ( Fig. 91.1 ). Sleep physicians may refer these cases to the orthodontist for craniofacial and upper airway evaluation on a lateral cephalogram and fabrication of suitable oral appliances.

  • •

    Mixed sleep apnoea : A patient with a combination of central and OSA is said to have mixed apnoea. Oral appliances alone cannot address mixed apnoea effectively.

All cases of OSA elicit snoring, but all snoring cases need not have OSA.

The OSA team is usually led by a respiratory physician or a pulmonologist, who often work with dedicated in-house facilities or outsourced PSG (polysomnography) services. Since these patients have several comorbidities, additional investigations related to diabetes, cardiac illnesses, and systemic diseases may also be required alongside PSG.

• 1.

  PSG is considered the gold standard test for diagnosis of OSA.

  • The test involves recording sleep, breathing patterns and oxygenation overnight. The study records apnoea, oxygen saturation, body position, change in heart rate, snoring, desaturation relations and sleep staging. The recordings include electroencephalography (EEG), electrooculography (EOG), electromyography (EMG) and electrocardiography (ECG).

  • PSG provides the AHI scores, which estimate apnoea–hypopnoea episodes per hour of sleep. Also, respiratory effort-related arousals (RERA) could be evaluated using a full PSG, which helps estimate the respiratory disturbance index (RDI) based on the AHI scores.

  • OSA severity is grouped into four categories:

    • a.

      Normal (AHI <5/hour)

    • b.

      Mild OSA (AHI 5–15/hour)

    • c.

      Moderate OSA (AHI 16–30/hour)

    • d.

      Severe OSA (AHI >30/hour)

  • Based on the recorded channels and data analysed, sleep studies are classified into four levels. PSG in the sleep laboratory remains the gold standard, although home or portable sleep studies are increasingly accepted. Different levels of sleep study are as follows:

    • •

      Level 1: Gold standard, attended PSG and intervention is possible.

    • •

      Level 2: Unattended full PSG, with the same parameters as level 1 and intervention is not possible.

    • •

      Level 3: A cardiorespiratory study with only four parameters: airflow, SpO ₂ , respiratory effort and EEG.

    • •

      Level 4: Only one or two parameters, namely airflow and SpO ₂ .

• Imaging modalities for upper airway:

  • Various imaging modalities can be effectively used to assess the upper airway. All the imaging modalities have their advantages and limitations ( Table 91.5 ).

    TABLE 91.5

    Imaging modalities for OSA and their advantages and disadvantages

    Imaging modality	Description	Advantages	Limitations
    Lateral cephalogram	Provides a 2D evaluation of the profile	• Helps identify adenoid hypertrophy • Airway assessment in sagittal plane possible • Hyoid bone position can be analysed	2D representation of a 3D structure. It provides a limited use for UA assessment, as the mesiolateral direction is not evaluated
    Computed tomography (CT)	3D evaluation	• One of the best imaging modalities for evaluating the nasal cavity and paranasal sinus geometry • 3D reconstruction possible	• Functional evaluation not possible • Objective criteria is lacking • High doses of radiation
    Cone beam computed tomography (CBCT)	3D evaluation	• Good to evaluate smaller regions • Volumetric analysis possible • Smaller doses of radiation as compared to CT	• Functional evaluation not possible • Objective criteria is lacking
    Magnetic resonance imaging (MRI)	Easy method to evaluate soft tissue in 3D	• Accurate in measuring the soft tissue lining, fat pad and surrounding structures of the airway in 3D • Good to visualise the airway lumen	Metals may interfere with images
    Nasoendoscopy	UA obstruction can be diagnosed reliably	Real time, direct and functional view of the airway	There is no objective grading. Depends on an understanding of the observer
    Acoustic rhinometry (AR)	Uses sonar technology and acoustic impedance during function	It is a simple, rapid and non-invasive technique. It proves clinically valuable and highly reliable, particularly when assessing the anterior and middle sections of the nasal cavities	Reduced accuracy in the posterior part of the nasal cavity
    Acoustic pharyngometry	Sonar waves are used for acoustic reflection during function	The exact location of the obstruction can be determined, and non-invasive pre- and post-therapy assessment possible	Accuracy is questionable, and applicability needs evidence
    Ultrasonography	Assessment with ultrasound	Dynamic assessment can be done during function	Needs professional expertise for evaluation

  • I.

    A two-dimensional (2D) lateral cephalogram helps examine the upper airway and the craniofacial and soft tissue profile ( Table 91.2 ). The lateral cephalogram should be standardised and recorded at end expiration, not at deglutition, because the respiratory cycle affects upper airway calibration.

  • II.

    The critical cephalometric measurements include posterior airway space, the length of the soft palate and the distance of hyoid measurement perpendicular to the mandibular plane. ^{, ,} A comprehensive airway analysis concerning the upper airway, hyoid position, soft palate and tongue is handy for diagnosis and treatment planning ( Table 91.2 ). A recent systematic review and meta-analysis of cephalometric studies concerning craniofacial and upper airway morphology in OSA patients has concluded that ‘There is strong evidence for reduced pharyngeal airway space, inferiorly placed hyoid bone and increased lower anterior face height in OSA patients than controls’. Cephalometric analyses are a valuable tool to understand the anatomic basis of the aetiology of OSA, which would help plan appropriate intervention.

  • III.

    Cone beam computed tomography (CBCT)/computed tomography (CT) and magnetic resonance imaging (MRI):

    • The upper airway is a three-dimensional (3D) collapsible tube, which limits the benefits of 2D imaging. CBCT permits 3D airway assessment and volumetric analysis supported by advanced software functions. High-quality evidence supporting its use for OSA airway assessment is lacking. The airway is a dynamic structure, and the position and posture of many craniofacial structures affect its patency and dimensions. Guijarro-Martínez and Swennen noted inconsistencies and discrepancies in the technique of imaging acquisition. There are limitations in studies on the use of CBCT for airway assessment. Many of these studies did not control factors such as respiratory phase, mandibular position and tongue position, all of which can affect airway dimensions. Additionally, most CBCT scanners acquire images in an upright position, which can impact airway analysis for patients with OSA.

    • The opinions regarding positional changes in the airway during the acquisition of CBCT are divided. A study comparing airway dimensions in upright and supine positions while acquiring CBCT concluded that upright CBCT airway dimensions may not apply to supine cross-sectional imaging. On the contrary, a recent meta-analysis concluded that a supine or standing position does not significantly affect volumetric airway assessment during CBCT acquisition.

    • Patients with OSA showed smaller upper airway measurements in the upright (volume) and supine (lateral dimension) positions. The anteroposterior dimension was also reduced in patients with OSA compared to the control group.

    • Nevertheless, CBCT can be used to compare airway dimensions pre- and post-treatment ( Fig. 91.6 ). The need for norms for volumetric and area assessment of the airway using CBCT is greatly warranted. Dynamic MRI and CT scans are helpful imaging aids to investigate the upper airway in snoring and sleep apnoea patients ( Fig. 91.7 ).

      

      Pre-and post-mandibular advancement device (MAD), volumetric and area assessment of airway on CBCT.

      Note improvement of airway dimensions post-MAD.

      

      MRI scan of an 18-year-old patient with bilateral TMJ ankylosis and severe OSA.

      Characteristic features to be noted are severe mandibular hypoplasia, collapsed upper airway due to tongue being placed posteriorly and hyoid being placed downwards and far away from the lower border of the mandible.

  • IV.

    Acoustic pharyngometer : The acoustic pharyngometer is a rather new induction in the clinical practice of otorhinolaryngology to assess the oropharyngeal airway. Acoustic pharyngometry is a non-invasive procedure based on acoustic reflection technology, similar to the ship’s sonar. Sound waves are projected down the airway and reflected back out so that pharyngometer software can analyse and quantify changes in the airway cross-sectional area. It allows users to quickly and easily measure a patient’s pharyngeal airway size and patency from the oropharyngeal junction to the glottis. The accuracy and reproducibility of the acoustic reflection technique in measuring airway dimensions have been validated. The technique has also demonstrated excellent agreement between glottis area measurements of the pharyngeal cross-sectional area measured acoustically compared to those obtained through CT. Eccovision acoustic pharyngometer is the propriety of Sleep Group Solutions, Florida 33020, USA. The procedure involves making the patient rest and acclimatise for 15–20 min. The patient is asked to be seated on a straight back chair. The patient should be informed of the nature of the test and the clicking noise emanating from the wave tube during the procedure. Proper positioning of the mouthpiece (tongue under, teeth touching and lips around) and proper execution of breathing trials (slow exhale, with external nose compression) should be demonstrated to the patient. The positioning should be checked before each trial. Patients are instructed to avoid nasal breathing as the opening of the velopharyngeal space during nasal breathing increases the calculated volume. The patients should be asked to pronounce ‘pooh’ in the mouthpiece of the pharyngometer without actually producing the sound with the nostrils closed and should also be instructed to look forward at a fixed point during the test ( Fig. 91.8 A). The mean airway volume, area and mean airway will be calculated in minutes. A phonogram of a patient is depicted in Fig. 91.8 B.

    

    Acoustic pharyngometry set up and phonogram generated by acoustic pharyngometry.

    (A) Equipment used and (B) phonogram of a 58-year-old male patient of OSA. The X-axis depicts airway distance calculated in cm from the tip of the incisors and Y-axis depicting area in cm ² . The oropharyngeal junction is approximately 8–10 cm on X-axis.

Includes behavioural modifications, sleep position changes and weight control by lifestyle modification. Definite modalities include continuous positive air pressure (CPAP), surgery to enlarge the upper airway and orthognathic surgery for bringing the mandible and maxilla forward.

• 1.

  Behaviour modification includes body weight control, sleep position changes, stopping the use of sedatives and limiting or stopping alcohol consumption.

  • a.

    Increasing body weight compromises the diameter of the upper airway because fat deposits accumulate in the walls around the pharynx. Obese patients should be encouraged to lose weight and reach a BMI of 25 or close to it.

  • b.

    Patients may be asked to lie on their side and place a pillow behind them so they cannot roll onto their back to a supine position during sleep. Another alternative is to sew a tennis ball in the centre of the back of the pyjamas to serve the same purpose.

  • c.

    The elimination of alcohol and sedatives at least 3 h before sleep has been recommended because of the depressant effect of the drugs on the central nervous system (CNS).

• 2.

  Oral appliances are useful in mild to moderate OSA. Complete dentures for edentulous patients help restore face height and better lower jaw control, thereby helping normal breathing. The treatment protocol for the management of SDB or OSA in children would be different from those in adults. It is based on prevention, growth modification, adenotonsillectomy, correcting breathing patterns and RME in children. The algorithm for management for adults and children is depicted in Figs 91.9 and 91.10 , respectively.

  

  Treatment algorithm for mild to moderate OSA in adults.

  SARPE : surgically assisted rapid palatal expansion; MARPE : miniscrew assisted rapid palatal expansion.

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