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128

S.-J. Kim and K. B. Kim

. Table 9.1 Timeline of normal development and craniofacial alteration resulting in abnormal respiratory function

Critical time point 5–6y 7–9y 12–15y 15–18y

Main growth event Neural growth ends

(~95%): from cranial to facial dynamics 1st molar eruption

Normal growth and development

Main

skeletal

growth

site

Pharyn-

geal soft

tissue

Cranium 1. Basicranial exion

→ Dolicho/Brachy pattern → Affects facial depth,

width, height

2. Cranial base lengthening → Displaces maxilla forward

3. Mid- cranial fossa development

→ Displaces glenoid fossa

Nasomaxillary complex (NMC)

Mandible and hyoid

Adenoid tonsils soft palate

Tongue 1. Tongue development

1. Displacement by ACB growth (*) & circum-maxillary sutural growth

2. Nasal septal cartilage

→ Nasal cavity development → Push midface forward

3. Additional surface remodeling

1. AP growth>vertical growth

→ Rate body length>ramus

2. Hyoid triangle established (~4–5y)

1. Airway dimension is mostly established and substantially maintained afterwards

ends

→ Affects mandibular development

2. Backward and downward displacement toward oropharynx

Benchmark of midface growth Juvenile mandibular growth spurt

1. Residual growth of ACB length: frontal sinus development

2. SES ossied

→ Affects facial height

1. Forward and downward displacement by sutural growth (*)

→ Width, depth height growth

2. Downward drift of palate (PNS)

→ Palatal depth remodeling → Soft palate uprighting → Nasal cavity increase

1. Juvenile growth spurt– mandibular internal rotation

→ Gonial angle decrease → Determines mandibular shape

1. Enlargement

→ No inuence on retropalatal airway width: maxillary forward growth and palatal bone drift → Upright soft palate and increase nasopharyngeal airway → Compensate enlarged A&T

1. Increase m tongue size

→ Transient decrease of retroglossal airway

PHV (puberty) permanent dentition

1 Post-cranial base

growth

→ SOS starts ossied → Increases maxillary

depth → Affects mandible position

1. Maxillary width and depth growth decreased

2. Active maxillary height growth and palate remodeling

1. Mandibular growth spurt-vertical growth of condyle and ramus

→ CCW external rotation and surface remodeling

2. Second puberty of hyoid growth → consistent mandiblehyoid-cervix relationship

1. Reduction of A&T size

1. Tongue moves lower

→ Upright soft palate → Increases retroglos-

sal airway

2. Increase of retroglossal airway by mandible growth

Post-adolescence growth decelerates/ends

1. PCB growth ends: SOS closed

1. Midpalatal suture ossied

2. Maxillary growth ends

1. Residual growth of mandible

2. Stable hyoidcervical relationship maintaining UA patency

1. Later

development of lingual tonsils → Affects retroglossal airway

Craniofacial Morphology Related to Obstructive Sleep Apnea: Growth of Craniofacial Bones…

. Table 9.1 (continued)

Critical time point 5–6y 7–9y 12–15y 15–18y

Craniofacial alteration affected by abnormal respiratory function

Critical inuencing factor on craniofacial growth

1. Extended head posture

→ Inhibit cranial exion → Dolichocephalic pat-

tern → Post. positioning of MC fossa → Protruded maxilla and retrognathic mandible

2. Low posterior tongue posture

→ Decent hyoid → Impairs mandibular

forward G. and affects symphysis growth (by extended suprahyoid m.)

1. Nasal obstruction → Inhibits maxillary forward/lateral G.

2. Abnormal habit causing impaired palatal bone drift

→ Deep palatal vault, narrow arches, and narrow nasal cavity → Decient constricted maxilla (CIII)

3. Excessive ATH

→ Retropalatal obstruction– Mouth breathing → Poor mandibular internal rotation → Increases mandibular divergency

4. Low tongue posture

→ Retroglossal obstruction → Hyperdivergency, long symphysis

1. Persistent ATH → Retropalatal obstruction mouth breathing → Increases maxillary height, increase of palatal depth, decrease of palatal width and Mandibular CW rotation long face and ant. openbite

2. Sagittal mandible growth is controversial

129

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Orthodontics andSleepDisordered Breathing

KiBeomKim andSu-JungKim

Contents

10.1 The Diagnostic Value ofCephalometrics forAirway Evaluation– 136

10.2 Relationship Between Craniofacial Characteristics andOSA–137

10.2.1 Cephalometric Characteristics ofAdult OSA Patients – 138

10.2.2 Cephalometric Characteristics ofPediatric OSA Patients – 140

10.3 Relationship Between Craniofacial Characteristics andOSA–141

10.3.1 Maxillary Expansion – 141

10.3.2 Orthodontic Extraction andtheRisk ofOSA – 148

10.3.3 Headgear andRisk ofOSA – 149

10.3.4 Protraction Headgear forOSA – 150

10.3.5 Chin Cup andOSA – 151

10.3.6 Functional Appliances Treatment forClass II Malocclusion andOSA–151

135

References – 155

136

K. B. Kim and S.-J. Kim

The topics of disturbed sleep and the airway have drawn interest among orthodontists since the beginning of the profession. In fact, these issues were discussed more than a century ago in the very rst issue of the American Journal of Orthodontics & Dentofacial

Orthopedics in 1915 (then The International Journal of Orthodontia), in which physician Daniel M’Kenzie dis-

cussed their potential relation with craniofacial structure and malocclusion [1]. As discussed in the previous chapter (7 breathing, and other related issues are surmised to have some effect on craniofacial growth, malocclusion, and respiration. Many orthodontists have taken a general interest in these issues and their potential relationship with obstructive sleep apnea (OSA). This chapter focuses on an evidence-based discussion regarding these topics as they relate to OSA.

Chap. 9), adenoid hypertrophy, mouth-

10.1 The Diagnostic Value

ofCephalometrics forAirway Evaluation

The lateral cephalogram is the part of the standard orthodontic records and the most commonly used imaging modality. Because the diagnostic process using cephalometric radiographs and cone beam computed tomography (CBCT) was discussed in the previous chapter, evaluation of adenoid hypertrophy and obstruction in the nasopharyngeal airway using lateral cephalography will be discussed in this chapter. The relationship between facial growth and breathing has been a subject of controversy in orthodontics, particularly relating to how adenoid tissue and mouth- breathing affect craniofacial growth. A variety of imaging techniques have been used to diagnose adenoid hypertrophy [2–7].

Nasal endoscopy is the most common method in otolaryngology to evaluate adenoid hypertrophy and nasopharyngeal airway obstruction [8–12]. In addition, rhinomanometry [13, 14], acoustic rhinometry [15], uoroscopy [12], computed tomography (CT) [16], cone- beam computed tomography (CBCT) [17–21], and magnetic resonance imaging [22, 23] have been used as well. Besides cephalometrics and CBCT, however, the remaining imaging techniques are not commonly used in orthodontics because of their invasiveness, high radiation, and cost.

Many researchers have used cephalometrics to identify key craniofacial characteristics of OSA patients, and several studies have investigated its diagnostic value in identifying adenoid hypertrophy and upper respiratory tract obstruction [24–29]. In 1979, Fujioka etal. [4] introduced the adenoid-nasopharynx (A/N) ratio

to determine adenoid size using cephalometrics. Its advantage is the assessment is not impacted by changes in horizontal or vertical position of the patient [30]. McNamara’s analysis, or McNamara’s line, has become one of the most important and common analytical tools for orthodontists to evaluate and describe structural relationships that affect the airway and is fundamental for diagnosis of many conditions, including adenoid hypertrophy [28]. (See .

Figs.10.1, 10.2, and 10.3).

Caylakli etal. [8] reported on the reliability of the A/N ratio calculated by a lateral cephalogram (evaluated by a blinded author) and nasal endoscopy for measuring the size of adenoid tissue. A total of 85 patients (52 males, 33 females; mean age: 5.0±2.2years; range: 2–12years) with a suspected prediagnosis of adenoid hypertrophy between June 2007 and March 2008 were included. The average A/N ratio was 0.87±0.1, which was reported to have a statistically signicant Pearson correlation with nasal endoscopy (r=0.511; P<0.0001). However, Feres etal. [31] questioned the value of the lateral cephalography regarding detection of adenoid hypertrophy and nasopharyngeal obstruction in their systematic review, citing spectrum bias in the evaluation of patients with the disease and those without. They noted that the study by Caylakli etal. was the only one among all studies citing the A/N ratio that recruited patients with suspected adenoid hypertrophy, whereas the other four studies [6,

15, 32] included patients with an previously conrmed

diagnosis.

A´

. Fig. 10.1 A/N ratio. Adenoidal measurements (A): distance from

A′ point of maximal convexity, along inferior margin of adenoid shadow to line B, drawn along straight part of anterior margin of basiocciput. Nasopharyngeal measurement (N): distance between posterior nasal spine (PNS) and C, anteroinferior edge of sphenobasioccipital synchondrosis

PNS

Orthodontics andSleep-Disordered Breathing

Upper pharynx

width

Lower pharynx

width

. Fig. 10.2 McNamara Analysis. Airway widths according to

McNamara analysis, upper pharynx and lower pharynx widths

137

dene the relationship between adenoid hypertrophy and associated symptoms, afrming that this method was useful as a treatment planning tool. Kurien etal. [34] also evaluated the reliability of lateral cephalography in the diagnosis of adenoid hypertrophy and determine if exible nasopharyngoscopy validated ndings. They showed statistically signicant agreement was observed between the two techniques, although the accuracy of lateral cephalography was a suboptimal 65%.

Wang et al. [35] compared 109 patients evaluated with both nasal endoscopy and lateral cephalometrics, nding a highly signicant relationship (P < 0.0001) between both imaging methods. However, there was some disagreement between the two imaging methods. Notably, only 54% of patients who showed adenoid hypertrophy by lateral cephalography radiographs were conrmed by nasal endoscopy. In addition, radiographs revealed 25.4% of children had a large adenoid that nasal endoscopy could not conrm and, conversely, nasal endoscopy revealed a large adenoid in 13% of children that radiographs could not conrm.

Filho etal. [36] in 2001 reported that while lateral cephalography promised high sensitivity, specicity was low in the diagnosing hypertrophy of the inferior and middle turbinates vs. nasopharyngeal endoscopy. They suggested nasal endoscopy is a more suitable method for the diagnosis of diverse nasopharyngeal obstructions. Major etal. conrmed this in 2014. Even though lateral cephalography showed good to fair sensitivity, they found specicity widely varied, depending on the evaluation method used. Conversely, the clinical exam was found to yield poor sensitivity but good specicity [37].

Furthermore, cephalograms have many disadvantages, such as the use of ionizing radiation [38] and can only represent a 3D structure with a superimposed 2D image [39]. One 2006 systematic review by Major etal. [40] concluded that cephalograms can be used to evaluate adenoid hypertrophy, but they are less reliable for determining the size of the nasopharynx. They suggest lateral cephalography is best used as a screening tool for diagnosing obstructed upper airways before a more rigorous follow-up is performed.

. Fig. 10.3 Example of hypertrophic adenoid cephalometrics

Saedi etal. [33] evaluated the diagnostic efcacy by comparing patient’s symptoms with nasal endoscopy and lateral cephalometrics ndings. They found both cephalography and nasal endoscopy could adequately

10.2 Relationship Between Craniofacial

Characteristics andOSA

Some orthodontists have suggested that the soft tissue of the airway should be considered when establishing an orthodontic treatment plan to improve the likelihood of orthodontic and orthopedic stability [41, 42]. As previously discussed, there is controversy surrounding what specic morphology of the craniofacial structures, as well as nasal obstruction and mouth-breathing, impacts craniofacial growth. Linder-Aronson reported that

138

K. B. Kim and S.-J. Kim

hypertrophic adenoid tissue can cause the retrusion of maxilla and mandible relative to the cranial base, and can also cause narrow dental arches, posterior crossbite, retro-inclination of maxillary and mandibular incisors, short mandibular dental arches, increased facial height, and a low tongue position [43].

Yamada et al. [44] suggested that nasopharyngeal respiratory obstruction is associated with downward and backward rotation of the mandible, upward and backward growth of the condyle, a divergent gonial angle, and anterior open bite. They suggested that permanent craniofacial deformities form because of a nasopharyngeal obstruction that existed prior to and during puberty, causing a skeletal open bite. Trotman etal. [45] suggested different craniofacial morphological associations for lip posture, sagittal airway, and tonsils. However, there is a controversy surrounding the relationships between head posture and/or facial patterns in children with different malocclusions and structures of the pharyngeal airway [46–48].

Other studies report other issues may be related to respiratory problems, such as a lower facial height, a retruded mandibular position, a deep palatal vault, and a posterior crossbite [45, 49, 50].

Martin et al. conducted a study with Class I ideal occlusion patients without OSA, suggesting that different skeletal patterns have different airway dimensions [51]. Freitas etal. [52] evaluated 80 untreated adolescent patients initially divided into two equal groups (Class I and Class II), then separately dividing these groups on the basis of normal and vertical growth patterns. Patients with Class I and Class II malocclusions and vertical growth patterns are known to have signicantly narrower upper pharyngeal airways than those with Class I/II malocclusions and normal growth patterns. However, malocclusion type does not appear to inuence upper pharyngeal airway width, nor do malocclusion type and growth pattern inuence lower pharyngeal airway width.

Similarly, other research reports that Class II patients and hyperdivergent patients had smaller airway size dimensions [53]. Sagittal malocclusion type does not appear to inuence upper pharyngeal width; however, hyperdivergent subjects have statistically signicant narrower upper pharyngeal width when compared to normodivergent and hypodivergent vertical patterns [54].

Muto et al. [55] reported that the diameter of the anteroposterior pharyngeal airway was largest in a patient group with mandibular prognathism, followed by groups of normal mandible and mandibular retrognathism. They suggested that the anteroposterior dimension of the PAS is affected by different skeletal patterns of the mandible. Adult OSA patients have been characterized by a retrognathic mandible, maxillary hypoplasia, inferior position of the hyoid bone, a greater exion of the cranial base, with an elongated soft palate [56].

However, one study that employed CBCT imaging showed that patients with different anteroposterior jaw relationships varied in airway volumes and shapes; furthermore, while airway shape differs in various vertical jaw relationships, volume does not [57]. However, one study that evaluated 276 healthy adult subjects 17–27 years of age with CBCT found that SNB (the angle between the anterior cranial base [SN] and the NB line) and oropharyngeal airway volume had a weak statistical correlation with minimum cross-sectional area. Despite this, the authors concluded that craniofacial morphology does not appear to have a big impact on upper airway dimensions [58].

It is difcult to conclude that there is an increased risk of OSA just by observing decreased airway dimensions in cephalography and/or CBCT. A more comprehensive appraisal of OSA risk should be attempted that includes a clinical examination accompanied with a polysomnogram, as well as cephalometrics and/or CBCT examinations.

The 2014 systematic review by Indriksone etal. [48] concluded that there is insufcient evidence to prove that the dimensions of the upper airway differ in various sagittal skeletal patterns. Many studies have tried to elucidate how head and tongue posture affects pharyngeal airway dimension and shape. Furthermore, there have been methodological concerns in studies in which the posture of the head and tongue was not standardized during image acquisition [59–70]. For instance, a standardized posture might be to position the head naturally and then capture the image after the patient has swallowed and while the patient is holding their breath. However, it is still questionable if this method will reliably show airway dimensions.

10.2.1 Cephalometric Characteristics

ofAdult OSA Patients

The following craniofacial characteristics are reported to be different between normal, healthy adults and adult individuals with OSA.

10.2.1.1 Cranial Base

Some studies reported that the cranial base length is larger than the control for an OSA patient [71, 72], but others showed that there was a signicantly shorter cranial base length [73–83]. (See . Figs.10.4 and 10.5).

According to a meta-analysis by Neelapu et al. [84] reported that SN length in adult OSA patients was

2.25mm shorter than normal [84]. The authors concluded that a decrease in cranial base length strongly suggests shorter dimensions of the anteroposterior cranium, ultimately expressed as bimaxillary retrusion and a relatively smaller pharyngeal airway.

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