**3. OSA pathophysiology**

In recent years, the understanding of the pathophysiology of sleep-breathing disorder has improved. Central nervous system regulation of breathing is now recognized as a significant contributor to the pathogenesis of OSA. To understand the pathophysiologic mechanisms that contribute to OSA, an overview of anatomical and physiological aspects of upper airway is in order.

#### **3.1. Upper airway anatomy and physiology**

The upper airway is a complex, multifunctional, and dynamic neuro-mechanical system. It is defined as the passageway for gas and food, beginning at the mouth and nose and ending at the epiglottis and vocal cords. It is composed of bony structures (maxilla, mandible and hyoid bone) and soft tissues (tonsils, soft palate, tongue, uvula, pharyngeal muscle, para-pharyngeal fat pads and lateral wall of the pharynx). The mandible and hyoid bone are the principal craniofacial bone structures that determine the dimensions of the upper airways. Soft tissues form the walls of the upper airways and they are supported by bone structures.[1, 25] The upper airways are typically divided into three segments: The nasopharynx (end of the nasal septum to the margin of the soft palate), the oropharynx (free margin of the soft palate to the tip of the epiglottis), divided into the retropalatal and retroglossal regions, and the hypophar‐ ynx (tip of the epiglottis to the vocal cords) (Figure 4).

The pharynx has several functions that enter into competition with each other; it requires patency and closure.[1, 4] It serves the neurological (speech, taste, smell), but also gastrointestinal and respiratory system (chewing, swallowing, breathing).Speech and swallowing

**Figure 4.** Sagittal magnetic resonance imaging of airway and division of oropharynx. (Clete A. Kushida)

require that the upper airway be collapsible. However, during breathing, the pharynx must remain patent.

Oropharynx and hypopharynx compose the collapsible portion of the pharynx. Due to the absence of bone and cartilage in these segments, their lumen patency, during awakening and sleep, depends heavily on muscle activity and intrinsic airway collapsibility, which is dictated by a combination of passive mechanical properties and active neural mechanisms.

During inspiration, negative intra-thoracic pressure is transmitted to the upper airways, resulting in a reduction in the transverse area of the pharynx. [25] The permeability of the upper airways is maintained through the balance between opposing forces from factors that collapse the airway and those that promote its patency. This is called "the balance of pressure concept" and involves the following determinants (Figure 5): [1,4, 26]


**•** The positive extra-luminal pressure from the abduction force of the pharyngeal dilator muscles, which is directed outwards, and functions to increase cross-sectional area.

Pharyngeal dilating muscles can be divided into four groups: [1, 4]


In normal individuals in awake state, the upper airway dimensions remain practically constant throughout inspiration by neuromotor mechanisms, like reflex muscle activation in response to stimuli such as sub-atmospheric pressure and hypercapnia. However, during sleep, neuromotor tone decreases and upper airway resistance increases considerably especially in sleep onset and REM stages. These physiologic variations are counteracted by a reduction of diaphragm and intercostal muscles activity and thus a decrease in inspiratory pressure. This tendency for the human upper airway to collapse predisposes it to abnormal deformation during sleep, mainly in susceptible individuals. [1,4, 27]

OSA results from a combination of structural upper airway narrowing and abnormal upper airway neuromotor tone. It is believed that the upper airways collapse more easily in OSA patients and occurs at slightly negative intra-thoracic pressures or even positive pressures. [27] Narrowing can occur in more than one site. The retropalatal or velopharyngeal region is the most common site; but the collapse usually extends to other locations. Since REM sleep is associated with greater muscle hypotonia compared to non-REM sleep, sleep-breathing disorder is more likely to occur during REM sleep. [13] In addition, the sleep-awake state in the pathogenesis of OSA is important to highlight. OSA patients, even with the most severe apnea, have generally no respiratory dysfunction during wakefulness through compensatory systems. [28]

According to recent studies on OSA pathophysiology, anatomical factors are not the whole story. The coordination between collapsing and dilating forces is an important concept and there is increasing evidence that the quantity and pattern of ventilation plays a substantial role in airway collapse [29] as well as the presence of upper airway neuropathology. [28] In addition, not all individuals with OSA have the same anatomical features. Thus, OSA patho‐ physiological factors are usually divided into three categories, whose complex interplay may explain the variable response to treatment:

**1.** Anatomic factors that effectively reduce airway caliber;

require that the upper airway be collapsible. However, during breathing, the pharynx must

Oropharynx and hypopharynx compose the collapsible portion of the pharynx. Due to the absence of bone and cartilage in these segments, their lumen patency, during awakening and sleep, depends heavily on muscle activity and intrinsic airway collapsibility, which is dictated

During inspiration, negative intra-thoracic pressure is transmitted to the upper airways, resulting in a reduction in the transverse area of the pharynx. [25] The permeability of the upper airways is maintained through the balance between opposing forces from factors that collapse the airway and those that promote its patency. This is called "the balance of pressure

**•** The baseline pharyngeal area, determined by both craniofacial and soft tissue structures;

**•** The negative intraluminal pressure within the airway (intraluminal pressure), transmitted from inspiratory muscles (the diaphragm, the external intercostal muscles....), that tends to

**•** The pressure acting on the outside surface of the pharyngeal wall (tissue pressure), which also tends to collapse the airway such as compression by the lateral pharyngeal and

submandibular fat pad and a large tongue confined to a small oral cavity;

by a combination of passive mechanical properties and active neural mechanisms.

**Figure 4.** Sagittal magnetic resonance imaging of airway and division of oropharynx. (Clete A. Kushida)

concept" and involves the following determinants (Figure 5): [1,4, 26]

**•** The compliance or collapsibility of the airway;

366 A Textbook of Advanced Oral and Maxillofacial Surgery Volume 2

narrow the airway;

remain patent.


**Figure 5.** Determinants of upper airway caliber. PL = intraluminal pressure; Ptis = pressure in the tissues surrounding the pharyngeal wall; Pmusc = pressure exerted by the pharyngeal dilating muscles; V = change in volume; P = change in pressure. [1, 26]

#### **3.2. Anatomic factors in OSA**

There have been a number of studies comparing anatomic features of OSA patients and normal individuals. Upper airway imaging techniques such as cephalometry, acoustic reflection, nasopharyngoscopy, computed tomography and magnetic resonance imaging, have greatly improved the understanding of OSA biomechanical aspect, and guided treatment modalities.

Over the past several decades, many studies have demonstrated that patients with OSA have significant craniofacial and upper airway abnormalities when compared with age matched and sex matched controls. [17, 30]

Typical abnormalities include retroposition of the mandible and maxilla, shorter mandibu‐ lar body length, longer anterior facial height, steeper and shorter anterior cranial base.... [1, 4, 13, 17]

However recent studies have shown no strong evidence for a direct causal relationship between sagittal and vertical craniofacial features and sleep-breathing disorder. In contrast, transverse width in the maxilla has a real impact with strong support for a narrow maxilla in OSA patients. [31]-[32] In addition, there is theoretical evidence that the size and the shape of the upper airway are also important and influence upper airway collapsibility.[4, 13] Imaging studies have shown reduced nasopharyngeal and oropharyngeal sagittal dimensions in OSA cases, associated with longer soft palate and longer airway. Indeed, the upper airway long axis of OSA patients is likely to be oriented transversely compared to the wide, elliptically shaped airway of normal controls.[33]-[35]

Lung volume is also reported to influence upper airway caliber and compliance.[13, 29] Decreased lung volume results in a caudal traction effect, which decreases the pharynx area and increases its resistance and its collapsibility due to a loss of tracheal tug.

Nasal airway pressure required to maintain airway patency is defined as the critical closing pressure (Pcrit). [4] It has been demonstrated that Pcrit is related to anatomical features and lung volumes, and shown to correlate with soft palate length in obese patients and airway length and hyoid-mandibular distance in non-obese patients [13]

On the other hand, the magnitude of extra luminal tissue pressure depends on the interaction of the upper airway soft tissues and the bony compartment size (Figure 6).[36] According to this model, soft tissues excess like in obesity, or restriction in bony compart‐ ment size such as retrognathia or both can lead to tissue pressure increase, thereby reducing airway caliber and predisposing to OSA. Soft tissues excess can be seen in case of tongue, soft palate and pharyngeal wall volume augmentation; but also in adenoids and tonsils lymphoid tissue hypertrophy.

**3.2. Anatomic factors in OSA**

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in pressure. [1, 26]

and sex matched controls. [17, 30]

4, 13, 17]

There have been a number of studies comparing anatomic features of OSA patients and normal individuals. Upper airway imaging techniques such as cephalometry, acoustic reflection, nasopharyngoscopy, computed tomography and magnetic resonance imaging, have greatly improved the understanding of OSA biomechanical aspect, and guided treatment modalities. Over the past several decades, many studies have demonstrated that patients with OSA have significant craniofacial and upper airway abnormalities when compared with age matched

**Figure 5.** Determinants of upper airway caliber. PL = intraluminal pressure; Ptis = pressure in the tissues surrounding the pharyngeal wall; Pmusc = pressure exerted by the pharyngeal dilating muscles; V = change in volume; P = change

Typical abnormalities include retroposition of the mandible and maxilla, shorter mandibu‐ lar body length, longer anterior facial height, steeper and shorter anterior cranial base.... [1,

However recent studies have shown no strong evidence for a direct causal relationship between sagittal and vertical craniofacial features and sleep-breathing disorder. In contrast, transverse width in the maxilla has a real impact with strong support for a narrow maxilla in OSA patients. [31]-[32] In addition, there is theoretical evidence that the size and the shape of the upper airway are also important and influence upper airway collapsibility.[4, 13] Imaging

**Figure 6.** Figure 6: OSA pathophysiology: schematic explanation for anatomic factors interaction to regulate extralumi‐ nal tissues pressure (Ptissue) [36]

Despite the relationship between structural features and function, some patients with OSA do not have clear anatomic abnormalities. Evidence for a direct causal relationship between craniofacial structure and OSAs has yet to be elucidated because several methodological deficiencies in the literature and lack of research standardization methods and treatment success definitions have been highlighted.

#### **3.3. Non-anatomic factors**

This category includes all factors underlying collapsibility. They are divided into pure mechanic and neurologic factors. In OSA patients, airway dilation appears less coordinat‐ ed than normal subjects and intrinsic mechanical properties of airway tissues are altered (Figure 7). [30, 37]

The respiratory control pattern generator responsible for automatic control ventilation is located into the brainstem. Respiratory rhythm is regulated by chemoreceptors and neural input from the upper airway and lungs to the brainstem neuronal network.[4] Instability of ventilatory control contributes to OSA pathophysiology by leading to periodic breathing and compromising airway patency during the ventilatory cycle. [28] It has also been suggested that upper airway inflammation and trauma caused by snoring and the hypoxia caused by intermittent upper airway collapse may impair the sensory pathways (upper airway mucosa) and the activation of neuromuscular reflexes (pharyngeal dilator muscles) rendering the upper airway prone to collapse. [38]

Other factors that may contribute to OSA pathophysiology include head posture, vascular supply to the mucosa and tissues surrounding the airway and arousal threshold.

Strohl et al. (2012) [39] reported that changes in blood pressure and/or pharyngeal muscles vascularity could affect airway stability and patency. Mucosal blood flow may either help resist distortion or contribute to narrowing if engorged.

On the other hand, flexion and extension of the neck affect the mechanics of the upper airway because the axis of rotation for extension and flexion is behind the airway. Thus, altered sleep position, mainly supine, may increase upper airway collapsibility and predispose to OSA particularly in adults because of tongue base prolapse. [40] In contrast, OSA children breathe better in the supine than in the prone position; this may be true because obstruction in children occurs usually at the level of the adenoids or soft palate rather than at the level of the tongue [1]

Although arousal is known to reinstate ventilation and thus to be protective in OSA, it is not essential to terminate an obstructive event. Low arousal threshold can exacerbate instability and worsen OSA.[1, 41] However, some authors who believe, that poor sleep is a secondary cause of OSA have rejected this claim. [29]

OSA has been shown to aggregate significantly within families. Genetic factors are likely to determine upper airway anatomy, neuromuscular activity and ventilatory control stability; these factors produce the phenotype of the OSA syndrome.[1, 4, 25, 42].

In sum, it is probably reliable to conclude that, in OSA individuals, there is a multiplicity of coexisting factors interacting to varying degrees at night; and everyone has biological sus‐

**Figure 7. Schematic model proposed by Isono et al., 1997 <sup>30</sup> and explaining pharyngeal airway patency: When a wake, upper airway (UA) muscle activity compensates the depression forces exerted by the air, both in normal subjects (A) and the OSA (B) for which activity is most important. During sleep, activity decrease generates too much imbalance in the apneic and causes collapse (D). In panels B and D (subject with OSAS) the fulcrum that Figure 7.** Schematic model proposed by Isono et al., 1997 [30] and explaining pharyngeal airway patency: When a wake, upper airway (UA) muscle activity compensates the depression forces exerted by the air, both in normal subjects (A) and the OSA (B) for which activity is most important. During sleep, activity decrease generates too much imbal‐ ance in the apneic and causes collapse (D). In panels B and D (subject with OSAS) the fulcrum that represents intrinsic properties of the pharynx, is to the right of the normal subject (A and C)

ceptibility and responds differently to environmental predisposing factors. Because OSA is a public health problem, its treatment should target the specific pathophysiologic processes that contribute to the collapse of the upper airway, in an attempt to alleviate symptoms and modify the long-term health consequences. **represents intrinsic properties of the pharynx, is to the right of the normal subject (A and C)** Other factors that may contribute to OSA pathophysiology include head posture, vascular supply to the mucosa and tissues surrounding the airway and arousal threshold.

Strohl et al. (2012) <sup>39</sup> reported that changes in blood pressure and/or pharyngeal muscles vascularity could affect

Although arousal is known to reinstate ventilation and thus to be protective in OSA, it is not essential to terminate an obstructive event. Low arousal threshold can exacerbate instability and worsen OSA. 1, 41However, some authors

OSA has been shown to aggregate significantly within families. Genetic factors are likely to determine upper

In sum, it is probably reliable to conclude that, in OSA individuals, there is a multiplicity of coexisting factors interacting to varying degrees at night; and everyone has biological susceptibility and responds differently to

airway anatomy, neuromuscular activity and ventilatory control stability; these factors produce the phenotype of the

environmental predisposing factors. Because OSA is a public health problem, its treatment should target the specific pathophysiologic processes that contribute to the collapse of the upper airway, in an attempt to alleviate symptoms

Aimed at maximal standardization and better care of patients, a task force of the American Academy of Sleep Medicine (AASM) has recommended terminology and standards of practice for recording sleep and breathing, and assigned evidence‐based definitions for abnormal events, parameters and disorders. <sup>43</sup> These definitions are still

**Apnea** is defined as cessation of airflow at the nose and mouth for 10 seconds or more with an arterial oxygen desaturation of 2% to 4%. Apnea is central, obstructive or mixed. The distinction between central and obstructive apnea is essential in determining the most appropriate treatment. During obstructive apnea, patients display

#### **4. OSA diagnosis** airway stability and patency. Mucosal blood flow may either help resist distortion or contribute to narrowing if

#### **4.1. Definitions** On the other hand, flexion and extension of the neck affect the mechanics of the upper airway because the axis of

and modify the long‐term health consequences.

**3.1.1. Respiratory events:**

engorged.

OSA syndrome. 1, 4, 25, 42.

**3. OSA Diagnosis** 

valid today.

**3.1. Definitions:**

Despite the relationship between structural features and function, some patients with OSA do not have clear anatomic abnormalities. Evidence for a direct causal relationship between craniofacial structure and OSAs has yet to be elucidated because several methodological deficiencies in the literature and lack of research standardization methods and treatment

This category includes all factors underlying collapsibility. They are divided into pure mechanic and neurologic factors. In OSA patients, airway dilation appears less coordinat‐ ed than normal subjects and intrinsic mechanical properties of airway tissues are altered

The respiratory control pattern generator responsible for automatic control ventilation is located into the brainstem. Respiratory rhythm is regulated by chemoreceptors and neural input from the upper airway and lungs to the brainstem neuronal network.[4] Instability of ventilatory control contributes to OSA pathophysiology by leading to periodic breathing and compromising airway patency during the ventilatory cycle. [28] It has also been suggested that upper airway inflammation and trauma caused by snoring and the hypoxia caused by intermittent upper airway collapse may impair the sensory pathways (upper airway mucosa) and the activation of neuromuscular reflexes (pharyngeal dilator muscles) rendering the upper

Other factors that may contribute to OSA pathophysiology include head posture, vascular

Strohl et al. (2012) [39] reported that changes in blood pressure and/or pharyngeal muscles vascularity could affect airway stability and patency. Mucosal blood flow may either help resist

On the other hand, flexion and extension of the neck affect the mechanics of the upper airway because the axis of rotation for extension and flexion is behind the airway. Thus, altered sleep position, mainly supine, may increase upper airway collapsibility and predispose to OSA particularly in adults because of tongue base prolapse. [40] In contrast, OSA children breathe better in the supine than in the prone position; this may be true because obstruction in children occurs usually at the level of the adenoids or soft palate rather than at the level of the tongue [1] Although arousal is known to reinstate ventilation and thus to be protective in OSA, it is not essential to terminate an obstructive event. Low arousal threshold can exacerbate instability and worsen OSA.[1, 41] However, some authors who believe, that poor sleep is a secondary

OSA has been shown to aggregate significantly within families. Genetic factors are likely to determine upper airway anatomy, neuromuscular activity and ventilatory control stability;

In sum, it is probably reliable to conclude that, in OSA individuals, there is a multiplicity of coexisting factors interacting to varying degrees at night; and everyone has biological sus‐

these factors produce the phenotype of the OSA syndrome.[1, 4, 25, 42].

supply to the mucosa and tissues surrounding the airway and arousal threshold.

success definitions have been highlighted.

370 A Textbook of Advanced Oral and Maxillofacial Surgery Volume 2

**3.3. Non-anatomic factors**

airway prone to collapse. [38]

distortion or contribute to narrowing if engorged.

cause of OSA have rejected this claim. [29]

(Figure 7). [30, 37]

Aimed at maximal standardization and better care of patients, a task force of the American Academy of Sleep Medicine (AASM) has recommended terminology and standards of practice for recording sleep and breathing, and assigned evidence-based definitions for abnormal events, parameters and disorders. [43] These definitions are still valid today. rotation for extension and flexion is behind the airway. Thus, altered sleep position, mainly supine, may increase upper airway collapsibility and predispose to OSA particularly in adults because of tongue base prolapse. <sup>40</sup> In contrast, OSA children breathe better in the supine than in the prone position; this may be true because obstruction in children occurs usually at the level of the adenoids or soft palate rather than at the level of the tongue <sup>1</sup>

who believe, that poor sleep is a secondary cause of OSA have rejected this claim. <sup>29</sup>

#### *4.1.1. Respiratory events*

**Apnea** is defined as cessation of airflow at the nose and mouth for 10 seconds or more with an arterial oxygen desaturation of 2% to 4%. Apnea is central, obstructive or mixed. The distinction between central and obstructive apnea is essential in determining the most appropriate treatment. During obstructive apnea, patients display respiratory effort without being able to ventilate because of upper airway obstruction, whereas central apnea occurs in the absence of ventilatory effort. Mixed apnea is initially started without ventilatory effort (as a 'central' pattern), and ends as obstructive with resumption of ventilatory efforts.

**Hypopnea** is defined as a decrease in airflow for 10 seconds or more with a concomitant drop in arterial oxygen saturation. AASM distinguish two situations of hypopnea events:


The exact magnitude of desaturation for a hypopnea varies in the literature. In routine clinical practice, it may not be necessary to differentiate apneas from hypopneas when both have similar pathophysiological consequences.[13] It is recommended to associate these two events in the form of an index of apnea / hypopneas (AHI).

#### *4.1.1.1. Apnea and Hypopnea Indices (AHI)*

This index, also termed respiratory disturbance index (RDI), refers to the total number of apnea and hypopnea episodes per hour of sleep. It is calculated by dividing the total number of apneas/hypopneas during a recording period by the total sleep time. AHI is usually employed to quantify OSA severity, but also to compare individual patient data with normative as well as pre-treatment and post-treatment values.

#### *4.1.2. Obstructive sleep apnea syndrome*

As noted previously, OSA is characterized by repeated partial or complete collapses of the upper airway during sleep, which precludes or reduces airway flow. It is associated with excessive daytime somnolence, sleep fragmentation and adverse sequelae attributable to frequent obstructive apneas or hypopneas during sleep. According to the AASM, OSA refers to an AHI ≥ 5 associated to one or both of these two criteria:


*4.1.1. Respiratory events*

372 A Textbook of Advanced Oral and Maxillofacial Surgery Volume 2

during sleep;

(> 3%) or an arousal. [4]

in the form of an index of apnea / hypopneas (AHI).

*4.1.1.1. Apnea and Hypopnea Indices (AHI)*

as pre-treatment and post-treatment values.

to an AHI ≥ 5 associated to one or both of these two criteria:

**•** Excessive daytime sleepiness (EDS) not explained by other factors

**•** Manifestation of at least two of following symptoms that should co-exist:

*4.1.2. Obstructive sleep apnea syndrome*

**•** Choking or suffocation during sleep

**•** Fragmented and non-restorative sleep

**•** Daily severe snoring

**Apnea** is defined as cessation of airflow at the nose and mouth for 10 seconds or more with an arterial oxygen desaturation of 2% to 4%. Apnea is central, obstructive or mixed. The distinction between central and obstructive apnea is essential in determining the most appropriate treatment. During obstructive apnea, patients display respiratory effort without being able to ventilate because of upper airway obstruction, whereas central apnea occurs in the absence of ventilatory effort. Mixed apnea is initially started without ventilatory effort (as

**Hypopnea** is defined as a decrease in airflow for 10 seconds or more with a concomitant drop

**•** A clear decrease (> 50%) from baseline in the amplitude of a valid measure of breathing

**•** Or an amplitude reduction (< 50%) associated with either an oxyhemoglobin desaturation

The exact magnitude of desaturation for a hypopnea varies in the literature. In routine clinical practice, it may not be necessary to differentiate apneas from hypopneas when both have similar pathophysiological consequences.[13] It is recommended to associate these two events

This index, also termed respiratory disturbance index (RDI), refers to the total number of apnea and hypopnea episodes per hour of sleep. It is calculated by dividing the total number of apneas/hypopneas during a recording period by the total sleep time. AHI is usually employed to quantify OSA severity, but also to compare individual patient data with normative as well

As noted previously, OSA is characterized by repeated partial or complete collapses of the upper airway during sleep, which precludes or reduces airway flow. It is associated with excessive daytime somnolence, sleep fragmentation and adverse sequelae attributable to frequent obstructive apneas or hypopneas during sleep. According to the AASM, OSA refers

a 'central' pattern), and ends as obstructive with resumption of ventilatory efforts.

in arterial oxygen saturation. AASM distinguish two situations of hypopnea events:

However, the presence of 15 or more obstructive respiratory events per hour of sleep in the absence of sleep related symptoms is enough proof for the diagnosis of OSA due to the greater association of this severity of obstruction with important consequences such as increased cardiovascular disease risk.[44] Two indicators must be taken into account for severity estimation of OSA: AHI and the importance of diurnal hyper-somnolence after exclusion of another cause of sleepiness. Patients in normal sleep have an AHI of 5 or less. Patients with mild sleep apnea have an AHI of 5 to 15, with moderate sleep apnea typically 15 to 30 events and severe apnea 30 or more events per hour.

#### **4.2. OSA clinical approach**

Despite its high estimated prevalence, awareness of OSA remains insufficient in the commun‐ ity.[4] Health professionals, including orthodontists, should not disregard the risk factors of OSA and should detect and diagnose this disorder. OSA screening should be based on sleeporiented history and physical examination in conjunction with objective tests. When diag‐ nosed, OSA severity level must be determined for an effective treatment decision.[44]

#### *4.2.1. Physical examination*

According to the AASM, sleep history is sought to evaluate OSA symptoms and to determine patients who present high-risk levels. A sleep examination is directed at modifying the OSA probability based on the history, looking for associated or complicating disease, and excluding other potential causes for symptoms.

Clinical assessment must encompass all sleep and physical features of the patient that may provide helpful guidance for screening this condition such as:

#### *4.2.1.1. Excessive Daytime Sleepiness (EDS)*

EDS is caused by sleep fragmentation due to frequent arousals at night. It is still a very subjective symptom that overlaps significantly with other factors such as tiredness and lethargy. [4] Epidemiological studies estimate EDS prevalence at 8% to 30% in the general population. [45]Sleepiness may occur during "passive" conditions, such as watching television or, in severe forms, during "active" conditions, such as conversation or driving. Several instruments have been developed to measure EDS. Currently, the most useful instrument is the Epworth Sleepiness Scale.[46] This questionnaire provides sleep propensity measure and has good test–retest reliability. It should be described with regards to onset, situation, and chronicity of sleep problems (Figure 8). [45]Objective laboratory sleep tests, like multiple sleep latency test (MSLT) or maintenance of wakefulness test (MWT) are also used for EDS assess‐ ment, but their limits are principally related to their costs and duration.


**Figure 8.** Figure 8. 1997 version of Epworth sleepiness scale. [47]. A score > 10 is consistent with EDS, and a score >16 indicates a high level of EDS.

#### *4.2.1.2. Snoring and witnessed apneas with choking or gasping*

The presence of snoring alone is a poor predictor of OSA. Thus, it must be correlated with other accompanying clinical features. Similarly, snoring absence does not exclude OSA. If severe, snoring can affect social relationship and become one of the main complaints of patients. Talking to the partner and family members can be very helpful; they can often report signs, such as apnea or falling asleep unintentionally (that the patient may be unaware of or deny). Therefore, patients can report awakening during choking episodes. But this is less common among females. OSA can also be associated with array of noctur‐ nal and daytime symptoms that are not necessarily specific to this affection, but can complete its clinical pattern and give an idea about its impact on patients' functionalities. One can cite poor sleep quality, morning headaches, impaired memory, failed concentra‐ tion, nocturia, and depression....[4]

#### *4.2.1.3. Obesity*

Obesity is the main predisposing factor for OSA. It is usually quantified by BMI (Body Mass Index). Increased BMI is closely correlated to OSA likelihood and severity. [4, 13] Additionally, central obesity (i.e. fat around the neck and waist), evaluated by neck circumference and hip-to-waist ratio, is simple clinical measurements that seem most predictive for SDB. There is no evidenced threshold value for these measurements, but a BMI ≥ 30 kg/m2 and a neck circumference >17 inches in men and >16 inches in women are habitually used as critical values.[4] Moreover, a study found that waist-hip ratio is the most reliable correlate of OSA in both sexes; while neck circumference is an independent risk factor for males. [48]To establish OSA diagnosis, obesity indicators alone are not sufficient and further diagnostic testing is needed. [26]

#### *4.2.1.4. Craniofacial examination*

**Figure 8.** Figure 8. 1997 version of Epworth sleepiness scale. [47]. A score > 10 is consistent with EDS, and a score >16

indicates a high level of EDS.

374 A Textbook of Advanced Oral and Maxillofacial Surgery Volume 2

Clinical examination should include anatomical features of craniofacial and oropharyngeal structures as they can compromise airway patency. Particular attention should be paid to upper airway narrowing signs such as tonsillar hypertrophy especially in children, nasal obstruction, macroglossia with dental impressions at the edge of the tongue, elongated uvula or soft palate inflammation. [44, 45] Oropharyngeal crowding can be assessed using the modified Mallampati classification designed originally by anesthetists to grade intubation difficulty (Figure 9). [49]

Other conditions that should be searched for when examining potential OSA patients are skeletal abnormalities because they are high risk factors among either obese or non-obese individuals. Actually, retrognathia, micrognathia, maxilla deficiency with high arched/narrow hard palate, longer anterior facial height, cranial base abnormalities or inferior hyoid bone position should be evaluated as they may suggest the presence of OSA. Cephalometric radiographs enable health professionals to obtain quantitative measures of these features. [50]

**Figure 9.** Modified Mallampati classification of oropharyngeal visualization. Class I: Soft palate, tonsils, pillars, and uvula, are clearly visible. Class II: Soft palate, pillars, and uvula are visible. Class III: only part of soft palate and base of uvula are visible. Class IV: Soft palate is not visible at all. 49

#### *4.2.1.5. Associated comorbidities*

A clinical examination should not ignore respiratory, cardiovascular, and neurologic systems. In this area, medication history must be taken into account especially with regard to drugs that are associated with OSA (Barbiturates, Benzodiazepines...), those that sedate and/or decrease respiratory drive (Antihistamines, Antispasmodics, Anxiolytics, Muscle relaxants...) and those that impair sleep onset or maintenance (Anticholesterol agents, Appetite suppressants, Benzodiazepines, Caffeine, Nicotine, Diuretics...). Furthermore, since hypertension is descri‐ bed as independently associated with OSA, blood pressure has been integrated into several clinical prediction rules for sleep apnea. [22, 44]

#### *4.2.2. Objective testing*

To establish OSA severity, objective testing is required. There are two accepted methods: laboratory polysomnography (PSG) and home testing with portable monitors (PM)

Polysomnography is the golden standard method for diagnosing OSA. It records sleepbreathing pattern and oxygen saturation overnight via a minimum of 12 channels of physio‐ logical signal such as electroencephalogram, electrocardiogram, electromyogram, oronasal airflow, electroocculogram, respiratory effort, body position and oxygen saturation. This examination provides AHI by monitoring apnea and hypopnea occurrence. Clinical interpre‐ tation of OSA severity is based, in addition to AHI, on factors like oxygen desaturation and sleep fragmentation degrees. In general, a single night PSG is sufficient to make an appropriate OSA diagnosis. However, some variability can be identified in recordings between the first and the second night of a PSG, a phenomenon known as the "first night effect". This may be due to factors such as sleep position and alcohol [44, 51]

Unlike PSG that is expensive and labor intensive, PM is performed at home and thus offers greater convenience for patients. Nonetheless, this procedure has some limits related to the lack of supervision, which can affect its reliability, but also to the impossibility to detect other sleep disorders such central apnea or nocturnal epilepsy. The choice between PSG and PM should take into consideration resource limitations and pre-test clinical evaluation. Thus, PSG could be performed if PM is technically inadequate or fails to establish OSA patients with a high pre-test probability.[44]

Furthermore, numerous imaging modalities are available for 2D or 3D craniofacial and airway study. They have potential usefulness in understanding the pathogenesis of sleep- breathing disorder, and planning of treatment (adenoidectomy, orthognathic surgery), but their routine use in the evaluation and diagnosis of OSA is limited. All diagnosis components previously studied (clinical examination and diagnostic testing) should be discussed with patients to establish a program including risk factors, consequences, but also treatment options/outcomes of OSA in the context of disease severity and patients' expectations.[44]
