Orthodontics in Obstructive Sleep Apnea Patients: A Guide to Diagnosis, Treatment Planning, and Interventions [1st ed. 2020] 978-3-030-24412-5, 978-3-030-24413-2

Table of contents :
Front Matter ....Pages i-vii
General Understanding of OSA as Orthodontists (Su-Jung Kim, Sung-Wan Kim)....Pages 1-13
Orthodontic Evaluation and Diagnostic Workflow for OSA Patients (Su-Jung Kim, Ki Beom Kim)....Pages 15-27
Therapeutic Pathway for Orthodontic Intervention (Su-Jung Kim, Patricia Pigato Schneider, Ki Beom Kim)....Pages 29-40
Craniofacial Growth Modification for OSA Children (Su-Jung Kim)....Pages 41-58
Craniofacial Orthopedics for Postadolescent OSA Patients (Su-Jung Kim)....Pages 59-64
Surgical Maxillary Expansion for OSA Adults with Nasal Obstruction (Hyo-Won Ahn, Su-Jung Kim)....Pages 65-79
Maxillomandibular Advancement Surgery for Skeletal Class II OSA Patients (Jin-Young Choi, Seung-Hak Baek)....Pages 81-94
Modification of Orthognathic Surgery for Skeletal Class III OSA Patients (Takashi Ono)....Pages 95-107
Mandibular Advancement Device for Elderly OSA Patients (Su-Jung Kim, Young-Guk Park)....Pages 109-130
Oropharyngeal Exercise for OSA Patients (Kyung-A Kim, Su-Jung Kim)....Pages 131-141

Citation preview

Orthodontics in Obstructive Sleep Apnea Patients A Guide to Diagnosis, ­Treatment Planning, and Interventions Su-Jung Kim Ki Beom Kim  Editors

123

Orthodontics in Obstructive Sleep Apnea Patients

Su-Jung Kim  •  Ki Beom Kim Editors

Orthodontics in Obstructive Sleep Apnea Patients A Guide to Diagnosis, Treatment Planning, and Interventions

Editors Su-Jung Kim Orthodontic Department Kyung Hee University School of Dentistry Seoul Korea (Republic of)

Ki Beom Kim Orthodontics, Saint Louis University Orthodontics Saint Louis MO USA

ISBN 978-3-030-24412-5    ISBN 978-3-030-24413-2 (eBook) https://doi.org/10.1007/978-3-030-24413-2 © Springer Nature Switzerland AG 2020 This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed. The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. The publisher, the authors, and the editors are safe to assume that the advice and information in this book are believed to be true and accurate at the date of publication. Neither the publisher nor the authors or the editors give a warranty, expressed or implied, with respect to the material contained herein or for any errors or omissions that may have been made. The publisher remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. This Springer imprint is published by the registered company Springer Nature Switzerland AG The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland

Preface

Snoring and obstructive sleep apnea (OSA), as the common types of sleep-­disordered breathing (SDB), have increasingly caught the attention of dentists and orthodontists since they become greater public health issues than ever. Previously, SDB is mostly recognized and managed by sleep physicians since it is a chronic multifactorial medical disease and a potentially life-threatening disorder leading to serious medical complications. Currently, however, dental sleep medicine has been emerging to deal with SDB by means of providing critical roles in the diagnosis and treatment with various orthodontic tools in hands. This text is intended to be a reference handbook on the orthodontic approaches for the SDB patients. This handbook will help dental students, dentists, orthodontic residents, and clinicians to understand all the practical information on the SDB from orthodontic point of view. Moreover, this handbook will update the orthodontists by providing well-organized diagnostic and therapeutic protocols for the SDB patients based on the integration of sleep into orthodontic practice. This book comprises three parts of general understanding of SDB and medical approaches, orthodontic diagnostic workflow, and orthodontic treatment application. In particular, the treatment parts are subdivided into six chapters depending on the patient’s phenotype and age groups. The readers will come to realize how many modalities are available beyond the previously well-known options and how important orthodontic contributions are for the treatment of SDB patients. This handbook will be a valuable clinical guideline for both beginners and experts who are interested in expanding our aims and scopes towards preventing or managing the SDB simultaneously with correcting skeletal and dental malocclusion. The demand of sleep-related orthodontics is driven by the need of our societies and patients who are coming into our offices aware of OSA. Let us keep in mind that we are improving our patient’s life quality and general health through changing the bite, smile, breathing, and sleep. Seoul, Republic of Korea

Su-Jung Kim

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Contents

1 General Understanding of OSA as Orthodontists����������������������������������   1 Su-Jung Kim and Sung-Wan Kim 2 Orthodontic Evaluation and Diagnostic Workflow for OSA Patients����������������������������������������������������������������������������������������  15 Su-Jung Kim and Ki Beom Kim 3 Therapeutic Pathway for Orthodontic Intervention������������������������������  29 Su-Jung Kim, Patricia Pigato Schneider, and Ki Beom Kim 4 Craniofacial Growth Modification for OSA Children����������������������������  41 Su-Jung Kim 5 Craniofacial Orthopedics for Postadolescent OSA Patients������������������  59 Su-Jung Kim 6 Surgical Maxillary Expansion for OSA Adults with Nasal Obstruction��������������������������������������������������������������������������������������  65 Hyo-Won Ahn and Su-Jung Kim 7 Maxillomandibular Advancement Surgery for Skeletal Class II OSA Patients������������������������������������������������������������  81 Jin-Young Choi and Seung-Hak Baek 8 Modification of Orthognathic Surgery for Skeletal Class III OSA Patients������������������������������������������������������������������������������  95 Takashi Ono 9 Mandibular Advancement Device for Elderly OSA Patients���������������������������������������������������������������������������������������������� 109 Su-Jung Kim and Young-Guk Park 10 Oropharyngeal Exercise for OSA Patients���������������������������������������������� 131 Kyung-A Kim and Su-Jung Kim

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General Understanding of OSA as Orthodontists Su-Jung Kim and Sung-Wan Kim

Contents 1.1  A  natomy of Upper Airway 1.2  P  athophysiology of OSA 1.3  M  edical Approach for Diagnosis and Treatment of OSA 1.3.1  Medical Diagnostic Approach for OSA 1.3.2  Medical Therapeutic Approach for OSA 1.3.3  Treatment Modalities for OSA References

1.1

 1  2  3  3  8  10  12

Anatomy of Upper Airway

The respiratory tract from the nose to the lung is divided into the upper tract and lower tract, also known as upper airway (UA) and lower airway (LA). The UA comprises nasal cavity, pharynx, and larynx, while the LA involves trachea, bronchi, and lung. In spite of inconsistent definition and terminology regarding the subdivision of UA, pharyngeal airway can be divided into three regions to be relevant to orthodontics: nasopharynx, oropharynx, and hypopharynx (Fig. 1.1). • Nasopharynx extends from behind the nasal turbinates to the level of hard palate. Adenoids (pharyngeal tonsils) affect the nasopharyngeal patency.

S.-J. Kim (*) Department of Orthodontics, Kyung Hee University School of Dentistry, Seoul, South Korea e-mail: [email protected] S.-W. Kim Department of Otorhinolaryngology—Head and Neck Surgery, Kyung Hee University School of Medicine, Seoul, South Korea © Springer Nature Switzerland AG 2020 S.-J. Kim, K. B. Kim (eds.), Orthodontics in Obstructive Sleep Apnea Patients, https://doi.org/10.1007/978-3-030-24413-2_1

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S.-J. Kim and S.-W. Kim

Fig. 1.1  Anatomic definition of upper airway described in the lateral cephalometric (left) and CBCT images (right). NC Nasal cavity, NP Nasopharynx, VP Velopharynx, OP Oropharynx, HP Hypopharynx

• Oropharynx lies behind the oral cavity extending from the soft palate to the upper border of epiglottis. This can be subdivided into the retropalatal airway, which lies behind the soft palate extending from the hard palate to the caudal margin of the soft palate (which is called velopharynx), and the retroglossal airway, which extends from the caudal margin of the soft palate to the base of the epiglottis behind the tongue. Uvula, soft palate, palatine tonsils, and tongue posture may affect the oropharyngeal patency. • Hypopharynx (laryngopharynx) lies inferior to the epiglottis and extends to the diverged area into the larynx and esophagus. Tongue base and hyoid position may influence the hypopharyngeal patency. Whereas nasal cavity is a bony structure, pharyngeal airway is a soft tissue structure surrounded by muscles constricting or dilating the UA lumen. In terms of orthodontists, genioglossus muscles are important when considering the control of tongue and hyoid posture, and palatoglossus muscles are known to be communicating muscles between the soft palate and the tongue, which contributes to opening the UA. More importantly, it should be noted that lateral pharyngeal walls comprising palatopharyngeus, stylopharyngeus, salpingopharyngeus, and pharyngeal constrictors are the most dynamic and responsive areas to the physiologic function and therapeutic application [1].

1.2

Pathophysiology of OSA

Physical obstruction of UA, due to the abnormal surrounding structures or to inadequate motor tone of the tongue and/or airway dilator muscles, prevents normal air passage. UA obstruction leads to hypoxia and hypercapnia. With oxygen desaturation, the heart rate and blood pressure rise with a ventilatory effort and sympathetic hyperactivity to stimulate pharyngeal dilator muscles. The airway opens and there

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is a correction of blood gases to normal, but sleep becomes fragmented as the cycle repeats. As such, main symptoms include loud snoring, witnessed apnea, and excessive daytime sleepiness (EDS). Consequently, the sequela of cardiovascular, cerebrovascular, and metabolic comorbidities, and all-cause mortality pose a significant public health problem [2]. OSA occurs as a result of anatomical and functional abnormalities of the UA that compromise airway space and increase pharyngeal collapsibility during sleep. Although alterations in neuromuscular and ventilatory control mechanisms can contribute to the reduced airway patency underlying OSA, anatomical abnormalities play a primary role in the development of OSA.  Anatomical risk factors for OSA include obesity, excess regional adipose tissue, enlarged upper airway soft tissues, and craniofacial skeletal abnormalities. The interactions between these anatomical factors, together with patient’s demographics and symptoms, are the main determinants of the likelihood and severity of OSA in the majority of patients. In this context, orthodontic treatments that may reduce oral cavity and tongue space have been in the debate issue whether they are significant risk factors of OSA or not. We sometimes recognize the narrowed pharyngeal airway spaces in the X-ray images after excessive anterior retraction with premolar extraction or mandibular set-back surgery. However, recent consensus is that not all these patients complain about respiratory discomforts. Actually, four different responses to the decreased UA dimension are observed clinically (Fig. 1.2): (1) no significant influence on the respiratory function and occlusion even maintaining the narrowed dimension; (2) compensatory adaptation of the UA to restore original dimension without leading to any problem; (3) respiratory dysfunction like snoring or OSA affected by decreased UA volume and subsequent increased pharyngeal collapsibility; (4) rebound of UA size resulting in occlusal relapse in relation to unfavorable tongue response. Evidence-based conclusion is still insufficient due to the limited number of studies and big heterogeneity among them [3]. There is no scientific evidence that decrease of UA dimension by orthodontic treatment, if any, would turn the airway more collapsible. The correlation between the UA dimensional change and respiratory functional change has not been clearly demonstrated. Nonetheless, we had better be cautious when we plan huge retraction of anterior teeth or jaw set-back surgery in the patients with already constricted UA.

1.3

Medical Approach for Diagnosis and Treatment of OSA

1.3.1 Medical Diagnostic Approach for OSA 1.3.1.1 Chief Complaint The most common complaint of OSA patients is loud snoring. Listening to the patient’s complaints beyond snoring may help the clinician in building up patient’s trust, which is crucial in starting patient-centered care.

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S.-J. Kim and S.-W. Kim Patient A; No significance influence on airway dimension and function

Patient B; Pharyngeal constriction inducing snoring

Patient C; Functional adaptation even with pharyngeal narrowing without relapse

Patient D; No functional adaptation to pharyngeal narrowing inducing relapse

Fig. 1.2  Various responses to the decreased upper airway dimension after premolar extraction treatment can be anticipated: Patient A, no significant influence on the airway dimension and function after treatment; Patient B, respiratory dysfunction like snoring after posttreatment pharyngeal narrowing; Patient C, compensatory functional adaptation to the pharyngeal narrowing without leading to any problem; Patient D, rebound of airway dimension in relation to occlusal relapse with unfavorable tongue response. There is no scientific evidence supporting that the patients treated with extraction treatment would have respiratory functional problems

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1.3.1.2 History Taking It is important to know other nighttime symptoms like witnessed apneas and daytime symptoms like excessive daytime sleepiness, morning headache, and difficult concentration. Sleep doctors firstly focus on some important factors such as average sleep time, sleep pattern, associated insomnia, and sleep habits. Asking about smoking and alcohol consumption are of a particular importance in OSA clinic. Social history and travel history may aid in understanding patients’ abilities or barriers toward some treatment lines. Past medical history (like history of depression disorder, uncontrolled hypertension, diabetes mellitus, cardiac diseases, etc.) and medications history (like antidepressants, hypnotics, etc.) are also important. 1.3.1.3 Questionnaire Some easy-to-use questionnaires have been developed as low-cost alternatives to PSG for detecting OSA: Berlin questionnaire [4], Epworth Sleep Scale (ESS) [5], and STOPBang [6]. ESS is a validated questionnaire that consists of eight items to discriminate the daytime sleepiness level of OSA patients from non-OSA patients (Table  1.1). The STOP-Bang questionnaire includes four sleep-related questions and four additional demographic queries, for a total of eight dichotomous (yes/no) questions: snoring, tiredness, observed apnea, high blood pressure, BMI, age, neck circumference, and gender) (Table 1.2). ESS and STOP-Bang scales are easily taken by dentists. 1.3.1.4 Polysomnography Polysomnography (PSG) is the gold standard for the diagnosis of OSA, but it is time-consuming and requires trained personnel. PSG is a noninvasive technique that involves overnight monitoring of several physiological variables including Table 1.1  Epworth sleepiness scales

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Table 1.2  STOP-Bang questionnaire

electroencephalography (EEG), eye movements (EOG), heart rhythm (ECG), and skeletal muscle activity (EMG) as well as respiratory effort, airflow, and oxygen saturation. Respiratory events can be quantified by overnight PSG study. An apnea is characterized by complete cessation of airflow for at least 10  s, and a hypopnea is defined as airflow reduction by 30% or greater lasting for 10 seconds or longer, or in case of associated oxygen desaturation by 3% or over. To grade the severity of sleep apnea, the number of apnea plus hypopnea per hour is reported as the apnea– hypopnea index (AHI). An AHI of less than 5 is considered normal. An AHI of 5–15 is mild; 15–30 is moderate; and more than 30 events per hour indicate severe sleep apnea. For children, an AHI in excess of 1 is considered abnormal due to the different physiology: 1–5, mild; 5–10, moderate; and 10 and over, severe. In addition to AHI, we have to think of respiratory disturbance index (RDI) and oxygen desaturation index (ODI) together to appreciate the severity of OSA. The RDI means the average number of apnea, hypopnea, and respiratory-effort-related arousals (RERAs) per hour of sleep. The ODI is the number of times per hour of sleep that the blood’s oxygen level drop by 3% from baseline.

1.3.1.5 Home Sleep Test with Portable Monitoring Device Home sleep test (HST) using a portable monitoring device can be an alternative to PSG for the diagnosis of OSA, due to the convenience, expedited diagnosis, and no need of hospitalization. It seems attractive to the dentists; however, it should be

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Table 1.3  Classification of sleep-monitoring system Category Type I Type II Type III Type IV

Definition Attended in-laboratory studies with full sleep staging, including EEG, EOG, ECG, EMG, respiratory efforts, airflow, pulse oximetry, and additional channels for CPAP levels (Full PSG). Unattended home studies without a technologist, recording the same variables as Type I PSG (Embletta ×100). Unattended home studies with a minimum of four channels: respiratory movement, airflow, cardiac variables, and oxygen saturation. RERAs and RDIs cannot be detected (Apnealink Plus™). These devices are called dual bioparameter devices. They record only airflow and arterial oxygen saturation.

EEG Electroencephalography, EOG Eye movements, ECG Heart rhythm, EMG Skeletal muscle activity, CPAP Continuous positive airway pressure, PSG Polysomnography, RERAs Respiratory-­ effort-­related arousals, RDIs Respiratory disturbance index.

performed only in conjunction with a comprehensive sleep evaluation by certified practitioner, since the sensor application, scoring, and interpretation of the collected data must be correctly set to assure accuracy and reliability. It is essential to recognize several inherent limitations when we use the HST [7]. First, HST does not record sleep but yields information regarding the number of disordered breathing events per hour. Second, disordered breathing events associated with arousals but without sufficient oxyhemoglobin desaturation cannot be assessed, leading to an underestimation of disease severity. Third, sensor failure or drop-out during the night can lead to suboptimal recordings. Fourth, the selection of specific sensors and the scoring methodology for portable monitoring are not as well formulated as they are for PSG.  Lastly, due to the different sensor mechanisms, comparisons of the disordered breathing measures among devices are difficult to make. According to American Academy of Sleep Medicine (AASM)’s guideline in 2017 [8], HST is recommended only to the uncomplicated adult patients presenting with signs and symptoms of moderate-to-severe OSA.  HST can also be used to evaluate the efficacy of oral appliance or surgical treatment. We should be aware of the type of HST device before use it (Table  1.3), considering the possibility of underestimation and misinterpretation.

1.3.1.6 Nasopharyngoscopy Nasopharyngeal endoscopy, nasopharyngoscopy, is the examination of the internal surfaces of the nose and throat by inserting a thin, flexible, usually fiber-optic instrument called nasopharyngoscope to detect and diagnose abnormalities in the nose and nasopharyngeal area. 1.3.1.7 Müller’s Maneuver This technique is designed to see the collapsed sites of upper airway during the inspiration with closed mouth and nose leading to the negative pressure in the chest and lungs. Introducing a flexible fiber-optic scope into the hypopharynx to obtain a view, the examiner may witness the collapse and identify weakened sections of the airway. However, the sites of obstruction with Müller's maneuver do not represent reliably the sites of obstruction during sleep.

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Nasal Valve Area

10.0

Septum

Area (cm2)

Inferior Turbinate

Nose tip

Nasal Valve

Turbinates

Nasal cavity

Right 1.0 Left

0.1 -6.0

-2.0

2.0

6.0

10.0 Distance (cm)

Nose tip

Nasal Valve

Turbinates

Nasal cavity

Fig. 1.3  Acoustic rhinometry to measure the nasal cavity geometry and nasal airflow change through acoustic reflection

1.3.1.8 Acoustic Rhinometry Acoustic rhinometry (AR) is a simple, fast, and noninvasive diagnostic tool measuring nasal cavity geometry and nasal airway change through acoustic reflection (Fig. 1.3). The size and the pattern of the reflected sound waves provide information on the structure and dimensions of anterior and middle parts of nasal cavity including nasal valve area, which shows the greatest nasal airflow resistance. 1.3.1.9 Dynamic Sleep MRI Dynamic sleep MRI has advantages of dynamic nature, the ability to evaluate the airway in a multiplane fashion, and more realistic information obtained in the sleeping state or a simulated sleep state. Although currently used in the research setting, these approaches may help further our understanding of levels of obstruction and impact of various treatments. 1.3.1.10 Drug-Induced Sleep Endoscopy (DISE) Drug-induced sleep endoscopy (DISE) has been introduced as an alternative to conventional endoscopy for more accurately representing patterns of collapse during the sleeping state. DISE brings us closer to understanding the dynamic airway during sleep. It seems that awake endoscopy and DISE detect retropalatal collapse equally well, but DISE may identify retrolingual, hypopharyngeal collapse more often, and also lateral pharyngeal wall collapse more specifically. Despite some shortcomings, more and more data are emerging about patterns of collapse on DISE that predict success with various surgical interventions.

1.3.2 Medical Therapeutic Approach for OSA 1.3.2.1 Traditional Concept 1: PAP or Non-PAP approach (Table 1.4) According to the European Respiratory Society task force report in 2011, continuous positive airway pressure (CPAP) has proven to improve OSA as the first-line of

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Table 1.4  Grade of recommendation (A>B>C>D) in case of CPAP intolerance

treatment, and other treatment options (non-CPAP treatments) can be considered only as an alternative in case of CPAP intolerance. The grade of recommendation (A>B>C>D) was given to each non-CPAP therapy as compared to the CPAP efficacy (Table 1.4). Here, mandibular advancement device (MAD) and maxillomandibular advancement (MMA) surgery were included in this report with grade A and B, respectively. This traditional approach has a limitation of nonselective application of CPAP regardless of patients’ phenotypes.

1.3.2.2 Traditional Concept 2: Phased Approach (Fig. 1.4) The original phase I and phase II Stanford protocol [9] is described in Fig.  1.4. Nonsurgical conservative treatment was firstly considered, and phase I surgical procedures were applied according to the main obstruction sites. Only when phase I alone was not successful in achieving surgical success, the sleep surgeon could proceed to phase II surgical protocol encompassing MMA. This approach has been advocated to minimize morbidity while maximizing opportunity for successful outcomes. Here, MMA could not be considered as a primary option regardless of severe craniofacial abnormality. 1.3.2.3 Current Concept: Precision One-Step Approach Stanford treatment protocol has evolved to play a role in collaboration with medical therapies in place of sleep surgeons aiming at providing a range of therapeutic options to best suit the patient’s goals for treatment [10]. This revised protocol in 2019 is defined by precision in patient selection, procedural selection, and

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Fig. 1.4  Original Stanford sleep surgery protocol. CPAP Continuous positive airway pressure, MAD Mandibular advancement device, OP Oropharynx, HP Hypopharynx, UPPP Uvulopalatopharyngoplasty, UPF Uvuolpalatal flap, GA Genioglossus advancement, HMS Hyoid myotomy and suspension, TBR Tongue base reduction, PSG Polysomnography, MMA Maxillomandibular advancement (Adapted from Riley RW, Powell NB, Guilleminault C. 1993 J Oral Maxillofac Surg.)

procedural accuracy. Here, MMA surgery can be considered as a primary option for OSA patient with definite dentofacial deformity and/or with complete concentric collapse of lateral pharyngeal wall in DISE, as well as secondary option for the patients who failed to other therapies. In addition, they introduced another orthodontic option of surgical maxillary expansion, called distraction osteogenesis maxillary osteotomy (DOME), for the patients with nasal obstruction. With increasing demand of orthodontist’s roles, we need our precision protocol not only to decide primary intervention but to participate in multiprofessional team better. This will be presented in Chap. 3.

1.3.3 Treatment Modalities for OSA 1.3.3.1 Lifestyle Modification: Weight Loss and Sleep Hygiene Sleep hygiene is the recommended behavioral and environmental practices, which are necessary to promote quality of nighttime sleep and daytime alertness. Clinicians assess the sleep hygiene of OSA patients who present with insomnia or depression, and offer recommendations based on the assessment. Sleep hygiene recommendations include establishing a regular sleep schedule, using naps with care, not exercising physically or mentally too close to bedtime, limiting worry, limiting exposure to light in the hours before sleep, getting out of bed if sleep does not come, not using bed for anything but sleep and sex, avoiding alcohol as well as nicotine, caffeine, and other stimulants in the hours before bedtime, and having a peaceful, comfortable, and dark-sleep environment.

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1.3.3.2 Positional Therapy Positional therapy uses devices like backpack, pillow, tennis balls attached to the night suit, or electrical sensors with alarm, that help patients to sleep on their side. The AASM task force recommends positional therapy as an effective secondary therapy for patients with positional OSA (defined as supine AHI>2×AHI). The European Respiratory Society task force on non-CPAP therapies in OSA states that positional therapy can yield a moderate reduction in AHI score, with a grade C recommendation (Table 1.4). 1.3.3.3 Positive Airway Pressure (PAP) Continuous positive airway pressure (CPAP) has been the first-line treatment for OSA due to the high efficacy in reducing sleep-disordered breathing events. In spite of the development of automatic positive airway pressure (APAP), however, lots of patients who try CPAP therapy are either completely intolerant or only partially adherent. Nowadays, the prescription of PAP to all OSA patients as a primary option is not necessary any more based on the novel concept of OSA phenotyping. If the patient has nonanatomical phenotypic causes in a progressive state of OSA, PAP would be an inevitable sole option or can be combined with other treatment modality allowing lower pressure. Otherwise, optimal treatment option needs to be considered based on the differential diagnosis of OSA phenotype. 1.3.3.4 Oral Appliance (OA) Patients mostly prefer oral appliance (OA) to CPAP despite less reduction of AHI, due to the portability, ease of use, and better comfort. OA includes tongue-retaining device (TRD) and mandibular advancement device (MAD). Although TRD directly pulls the tongue forward during sleep to open oropharynx, it is not currently used because of tissue irritation, discomfort, and limited effect. MAD can be prescribed by any sleep specialist, but should be adjusted and managed by qualified dentists. MAD will be discussed in detail in Chap. 9. 1.3.3.5 Surgical Interventions • Tracheostomy bypasses the upper airway and is thus nearly universally successful in managing OSA. However, the significant morbidity associated with tracheostomy limits its application in the OSA population. • Bariatric surgery is a primary surgical option in patients with morbid obesity. • Tonsillectomy with adenoidectomy is the first-line surgical therapy for children with OSA without craniofacial anomalies. • Nasal surgery may play a role in OSA management by improving nasal airflow. Although isolated nasal surgery is unlikely to lead to resolution of severe OSA, it may increase CPAP use and MAD adherence. • The most common palatal surgery is uvulopalatopharyngoplasty (UPPP), which involves removal of the tonsils, uvula, and posterior velum. Multiple variations of UPPP have been described. Due to the low success rate of 33%, UPPP is not recommended by the American Academy of Sleep Medicine (AASM) as a sole procedure for treating moderate-to-severe OSA [11].

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• Tongue base reduction surgery involves partial glossectomy or various ablative techniques to volumetrically reduce the tongue. • Genioglossal advancement (GA) involves advancement of the genial tubercles, and may be accompanied by hyoid suspension. • Multilevel surgery is acknowledged as an acceptable option for patients with multisite obstruction, reported surgical success rates vary widely from 22% to 78% [12]. • Hypoglossal nerve stimulation is a relatively new addition to the array of surgical options for treatment of OSA, and is applied to the patients with poor neuromuscle responsiveness. • Maxillomandibular advancement (MMA) is the most successful surgical intervention for OSA aside from tracheostomy. MMA has been equated to CPAP in terms of outcomes. This procedure involves advancement of both jaws and addresses airway obstruction at multiple levels; airway collapsibility decreases due to advancement of its skeletal framework.

Clinical Pearls in Understanding SDB and OSA

• The natural development of sleep disordered breathing (SDB) goes from normal to obstructive hypoventilation syndrome (OHS), passing through persistent snoring, upper airway resistance syndrome (UARS), and obstructive sleep apnea (OSA) between them. • In this chapter, anatomic limits of upper airway and pathophysiology of OSA were explained in terms of orthodontists with orthodontic approaches in mind. • Orthodontists should be well informed of medical approaches for the diagnosis and treatment of OSA patients for intimate collobaration.

References 1. Park JG, Ramar K, Olson EJ.  Updates on definition, consequences, and management of obstructive sleep apnea. Mayo Clin Proc. 2011;86:549–54. 2. Epstein LJ, Kristo D, Strollo PJ, et al. Clinical guideline for the evaluation, management and long-term care of obstructive sleep apnea in adults. J Clin Sleep Med. 2009;5(03):263–76. 3. Hu Z, Yin X, Liao J, et al. The effect of teeth extraction for orthodontic treatment on the upper airway: a systematic review. Sleep Breath. 2015;19(2):441–51. 4. Netzer NC, Stoohs RA, Netzer CM, et al. Using the Berlin Questionnaire to identify patients at risk for the sleep apnea syndrome. Ann Intern Med. 1999;131(7):485–91. 5. Johns MW. A new method for measuring daytime sleepiness: the Epworth sleepiness scale. Sleep. 1991;14(6):540–5. 6. Chung F, Yegneswaran B, Liao P, et al. Stop questionnaire a tool to screen patients for obstructive sleep apnea. Anesthesiology. 2008;108(5):812–21. 7. Punjabi NM, Aurora RN, Patil SP. Home sleep testing for obstructive sleep apnea: one night is enough! Chest. 2013;143(2):291–4.

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8. Kapur VK, Auckley DH, Chowdhuri S, et al. Clinical practice guideline for diagnostic testing for adult obstructive sleep apnea: an American Academy of Sleep Medicine clinical practice guideline. J Clin Sleep Med. 2017;13(03):479–504. 9. Riley RW, Powell NB, Guilleminault C. Obstructive sleep apnea syndrome: a surgical protocol for dynamic upper airway reconstruction. J Oral Maxillofac Surg. 1993;51(7):742–7. 10. Liu SY-C, Awad M, Riley R, Capasso R. The role of the revised Stanford protocol in today’s precision medicine. Sleep Med Clin. 2019;14(1):99–107. 11. Aurora RN, Casey KR, Kristo D, et al. Practice parameters for the surgical modifications of the upper airway for obstructive sleep apnea in adults. Sleep. 2010;33(10):1408–13. 12. Kezirian EJ, Goldberg AN. Hypopharyngeal surgery in obstructive sleep apnea: an evidence-­ based medicine review. Arch Otolaryngol Head Neck Surg. 2006;132(2):206–13.

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Orthodontic Evaluation and Diagnostic Workflow for OSA Patients Su-Jung Kim and Ki Beom Kim

Contents 2.1  History Taking 2.1.1  Medical History 2.1.2  Simplified Questionnaire 2.2  Clinical Examination of Risk Factors 2.2.1  Physical Factors 2.2.2  Behavior Factors 2.2.3  Craniofacial Anatomic Factors 2.3  Lateral Cephalometric Analysis 2.3.1  Significance of Cephalometric Analysis 2.3.2  Cephalometric Definition and Measurements of Upper Airway 2.4  CBCT Volumetric Analysis 2.5  Functional Evaluation on Respiration and Sleep 2.5.1  Mouth Breathing 2.5.2  Bruxism 2.6  Diagnostic Workflow for SDB Patients in Orthodontic Clinic References

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S.-J. Kim Department of Orthodontics, Kyung Hee University School of Dentistry, Seoul, South Korea e-mail: [email protected] K. B. Kim (*) Department of Orthodontics, Center for Advanced Dental Education, Saint Louis University, Saint Louis, MO, USA e-mail: [email protected] © Springer Nature Switzerland AG 2020 S.-J. Kim, K. B. Kim (eds.), Orthodontics in Obstructive Sleep Apnea Patients, https://doi.org/10.1007/978-3-030-24413-2_2

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2.1

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History Taking

2.1.1 Medical History After apprehending patient’s chief complaint, orthodontic diagnosis of OSA begins with a sleep history and related medical history. The representative OSA symptoms, which should be initially evaluated, include severe snoring, witnessed apnea, sleep fragmentation, excessive daytime sleepiness (EDS), distraction, and morning headache. The presence of comorbidities such as cardiovascular and cerebrovascular diseases with medication history needs to be check. Social or behavioral history including alcohol, smoking, exercise, and travel frequency should be checked.

2.1.2 Simplified Questionnaire The representative questionnaires for the suspected OSA patients such as Berlin questionnaire, Epworth Sleep Scale (ESS), and STOP-Bang can be introduced in orthodontic clinics [1]. Instead, as a routine health maintenance evaluation including respiration and sleep functions, five questions can be simply applied to every patient not only to diagnose OSA but to prevent OSA after any orthodontic treatment: (1) Is the patient obese? (2) Is the patient retrognathic? (3) Does the patient complain of daytime sleepiness? (4) Does the patient snore? (5) Does the patient have hypertension?

2.2

Clinical Examination of Risk Factors

2.2.1 Physical Factors Firstly, obesity should be checked at the time when the patient comes in the clinic. According to the recent review articles suggesting clinical prediction models [2], the best indicator for the presence of OSA are body mass index (BMI) and neck circumference. BMI can be calculated as a person’s weight in kilogram divided by the square of height in meters (kg/m2). BMI is a simple measure of body fat based on weight and height; however, it is not always correct, since the weight covers muscles as well as fat.

2.2.2 Behavior Factors Habitual head and neck posture, lip posture in rest position, breathing pattern, and the presence of daytime sleepiness need to be observed during the clinical examination.

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2.2.3 Craniofacial Anatomic Factors In order to check if craniofacial anatomic factors contribute to OSA, facial and chin profile, facial height ratio (posterior/anterior, lower/total), and midfacial width should be basically evaluated. More in details, facial and intraoral evaluating points, which are more critical to OSA patients than regular orthodontic patients, can be suggested as follows. Here are the essential roles of the orthodontists in diagnosing OSA.

2.2.3.1 Facial Examination: Facial Triads Retruded chin has been widely known to be the most common facial features of OSA patients. However, the patient with protruded chin sometimes reveals OSA symptoms especially in case with obesity. Therefore, facial characteristics related to obesity should be carefully checked as well as chin profile and facial proportion. Throat length, cervico-mental angle, and neck circumference can be facial triads to be examined together (Fig. 2.1). Short throat length and obtuse cervicomental angle are characteristic regardless of mandibular body length in OSA patients in relation to wide neck circumference over 17 inches and submental fat deposition. 2.2.3.2 Intraoral Examination: Intraoral Triads Dental Class II malocclusion with large overjet and arch constriction appears consistent to give strong consideration in the pathogenesis of OSA; however, this consensus exists in the studies on the Caucasian OSA population. When considering multifactorial causes including genetics and ethnicity, however, vertical and transverse malocclusions such as anterior openbite and posterior crossbite seem to be more associated with the high incidence of OSA than sagittal malocclusion like Class I, II, and III.  Thus, intraoral triads to be specifically evaluated for OSA patients can be suggested as (1) narrow and deep palatal arch; (2) tongue position-related structures like large tongue, tongue tie, and tori; and (3) enlarged palatine tonsils with flabby uvula in the mouth (Fig.  2.2). To classify the degree of tonsillar hypertrophy and posterior oropharyngeal tissue collapse, Friedman classification and modified Mallampati test can be used, respectively (Fig. 2.3). These scorings will alert the dentists to identify the oropharyngeal soft tissue problems and further to predict the presence and the severity of OSA. The tonsil grading depicts the ratio of pharyngeal lateral dimension occupied by the hypertrophic tonsils (Fig. 2.3, left). With a high tonsil grading of III or IV, a patient with OSA has a better chance to improve by tonsillectomy with UPPP. The modified Mallampati scale shows the disproportion between soft tissue volume and the size of oral cavity (Fig. 2.3, right).

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3

2

1

3

2

1

1, throat lenght; 2, cervicomental angle; 3, neck circumference

Fig. 2.1  Facial triads in clinical examination of OSA patients: (1) throat length, (2) cervico-­ mental angle, (3) neck circumference. Left patient showing short throat length with retruded chin, obtuse cervico-mental angle, and normal neck circumference indicates nonobese OSA patients with craniofacial phenotype of retruded mandible. In contrast, right patient showing short throat length despite protruded chin, obtuse cervico-mental angle, and long neck circumference indicates obese OSA patients with no definite craniofacial risk factors

1. Palatal vault

2. Tori & Tongue tie

3. Tonsils & Uvula

Fig. 2.2  Intraoral triads in clinical examination of OSA patients: (1) palatal vault (left), (2) tori and tongue-tie (middle), (3) uvula and palatine tonsils (right). The presence of narrow and high palate, lingual tori, heavy lingual frenulum, flabby and long uvula, and hypertrophic tonsils can be risk factors of SDB

2.3

Lateral Cephalometric Analysis

2.3.1 Significance of Cephalometric Analysis Lateral cephalometric analysis has fundamental limitations to evaluate upper airway and diagnose OSA patients. First, it is a static image taken in an awake upright position, which can hardly characterize the asleep airway function. Second, it is a two-dimensional image, where lateral pharyngeal wall collapse linked to more severe OSA than retropalatal and retrolingual collapse (as assessed with dynamic MRI) would not be noted [3]. Third, the image is

2  Orthodontic Evaluation and Diagnostic Workflow for OSA Patients Friedman Tonsils classification

0 Surgically removed tonsils

I Tonsils hidden with tonsil pillars

II Tonsils extending to the pillars

III IV Tonsils extending 3/4 Tonsils completely of the way to midline obstructed (Kissing tonsils)

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Modified Mallampati classification

II I Tonsils, pillars, soft palate Uvula, pillars, upper pole are clearly visible are visible

III Only part of soft palate is visible

IV Soft palate is not visible

Fig. 2.3  Friedman classification to check tonsillar hypertrophy (left) and modified Mallampati scoring for visualization of the oropharynx based on soft palate-uvula-pillars-tongue base relationship in the mouth (right). (Cited from Friedman M et al. Clinical predictors of obstructive sleep apnea. Laryngoscope. 1999 Dec;109(12):1901–7.)

inconsistently obtained depending on the head and tongue posture or the time of imaging. Also, airway images change throughout the respiratory cycle, so any measurement should be taken at a standardized point in the cycle. Fourth, no consensus exists on the most useful landmarks, measurements, and numeric norms to evaluate the pharyngeal airway. Nonetheless, lateral cephalometric analysis is worthy of a basic screening tool to determine the need for more rigorous ENT follow-up for the following reasons [4]. 1 . It is the most hand-handled analyzing tool in a daily orthodontic clinic. 2. It is useful for screening the main site of pharyngeal narrowing or obstruction as an adjunctive airway assessment. 3. The pharyngeal dimension can be evaluated in relation to the craniofacial and para-pharyngeal soft tissue abnormalities as a whole. 4. A meta-analysis in 2019 [5] suggested that the lateral cephalogram exhibited very good diagnostic accuracy for the diagnosis of adenoid hypertrophy and posterior upper airway obstruction, although the rate of false-positive diagnosis should be considered. 5. It is useful to predict treatment response initially, to quantify the airway changes in relation to skeletal change after intervention, and to compare the airway changes among groups. Thus, lateral cephalometric airway assessment should be well informed of in order to understand most of the literatures and studies dealing with the prediction and treatment responses of upper airway.

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2.3.2 C  ephalometric Definition and Measurements of Upper Airway (Fig. 2.4) Here, we suggest a simplified clinical guideline of cephalometric analysis of UA as briefly explained in the Chap. 1 (Fig. 1.1). Despite the limited availability and wide variation of cephalometric measurements as mentioned above, the repetitive measuring procedure is recommended to the beginners in order to raise their appreciation ability to grasp the upper airway and craniofacial complex at a glance. Firstly, draw a line of palatal plane passing through ANS and PNS (line 1, upper limit of oropharynx). Then, draw two parallel lines to the line 1 passing through the tip of soft palate (line 2, lower limit of velopharynx) and tip of epiglottis (line 3, lower limit of oropharynx). And draw another line from PNS to the midpoint of Sella-Basion line (line 4, upper limit of nasopharynx). With these four lines, we can

Fig. 2.4  Definition of anatomical limits of upper airway (left) and the landmarks and measurements of pharyngeal airway (right) in the lateral cephalogram. Se Sella, Ba Basion, AD1 Adenoid point 1 (adenoid tissue on the PNS-Ba line), AD2 Adenoid point 2 (adenoid tissue on the midpoint between sella and basion to PNS line), Go Gonion; ANS, anterior nasal spine, PNS Posterior nasal spine, Me Menton, Rg Retrognathion, Sp Tip of soft palate, Eb Base of epiglottic fold, Hy hyoidale (the most antero-superior point on the body of the hyoid bone), (1) PNS-AD2, upper nasopharyngeal airway space (width of airway along PNS-R line); (2) PNS-AD1, lower nasopharyngeal airway space (width of airway along PNS-Ba line); (3) SPAS, superior posterior airway space (width of airway behind soft palate along parallel line to palatal plane); (4) MAS, middle airway space (width of airway along parallel line to palatal plane through Sp); (5) IAS, inferior airway space (width of airway along parallel line to palatal plane through epiglottis tip); (6) SPL, soft palatal length (PNS-P); (7) MPT, maximum palatal thickness measured on-line perpendicular to PNS-P; (8) SPI, soft palate inclination (angle between ANS-PNS line and PNS-P line); (9) TGL, tongue length (Eb to tip of tongue); (10) TGH, tongue height (longest distance from Eb-tongue tip line to tongue dorsum); (11) MPH, the shortest distance from mandibular plane (Me-Go) to hyoidale; dashed triangle means the hyoid triangle

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easily assort different pharyngeal areas and their adjacent structures. Figure  2.4 shows how to measure the pharyngeal airway, soft palate, tongue, and hyoid using minimum landmarks and reference lines.

2.4

CBCT Volumetric Analysis

The use of cone-beam computed tomography (CBCT) for the airway analysis may be criticized for additional radiation exposure and high cost when thinking of the similar limitations to lateral cephalometric analysis mentioned above. Besides, CBCT has different anatomic boundaries of UA, which are more difficult to be defined, and little is known about the CBCT parameters, which can predict treatment success and their normative values. However, the addition of the third dimension offers an advantage over traditional plain films, as follows (Fig. 2.5):

Fig. 2.5  CBCT image analysis of upper airway. (a) Lateral volumetric image; (b) lateral sectional image encoded by color-scale; (c) frontal volumetric image; (d) frontal sectional image showing relative transverse dimension of nasal cavity, maxillary base, and mandibular base

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1 . Three-dimensional airway shape as well as total volume can be assessed. 2. Site-specific information can be obtained through manual or automatic airway segmentation. 3. The most useful thing is that the minimal cross-sectional area (cm2), which is more pathophysiologically relevant than volume, can be identified in relation to surrounding structures. 4. The presence and the origin of nasal cavity obstruction can be assessed in relation to transverse maxillary constriction. 5. Change of airway length can be noted with the displacement of hyoid bone in space. 6. Computational fluid dynamics (CFD) can be utilized to assess theoretical airway flow and resistance but still has limitation to represent real functional problem.

2.5

Functional Evaluation on Respiration and Sleep

2.5.1 Mouth Breathing Mouth breathers do not usually realize that they breathe through the mouth especially while sleeping. Instead, they complain about the symptoms like dry mouth, gingival or periodontal inflammation, halitosis, snoring, chronic fatigue, and excessive sleepiness. Mouth breathing is more often observed in children, when the parents should look for the signs of slow growth rate, irritability, crying episode at night, and behavioral and cognitive problems. Mouth breathing influences underdeveloped midface, transverse maxillary deficiency, high and deep palatal vault, and long face in children. In earlier stage of growth under the age 5–6, mouth breathing with extended head/neck postures, and lowered jaw/tongue postures, may disturb the mechanism of cranial base flexion, resulting in dolichocephalic pattern with narrow facial width and innate mandibular retrusion (Fig.  2.6), creating a vicious cycle between mouth breathing and craniofacial abnormalities. On the other hand, skeletal Class III pattern with strong potential of mandibular growth can be deteriorated by serious mouth breathing passing through the pubertal growth peak period, as seen in Fig. 2.7. The underlying causes of mouth breathing are adenotonsillar hypertrophy, nasal obstruction, and severe skeletal discrepancy to structurally prevent lip sealing, and poor habits. The dental office is in the best position to diagnose mouth breathing and to lead the therapy by addressing each of these causative areas. From orthodontic point of view, mouth breathing can be classified into three types: obstructive type, structural type, and habitual type (Fig. 2.8). For the obstructive type of mouth breathers, nasal obstruction caused from allergic rhinitis, septal deviation, or nasal polyps should be treated firstly, and hypertrophic adenoids and tonsils need to be removed if indicated. We need to refer the obstructive type of mouth breather to the ENT doctors. For the structural type of mouth breathers who have severely retruded chin, excessive lower facial height, constricted maxillary

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Fig. 2.6  Two cephalograms taken at different head and neck postures at the same day. Extended head posture (left) was changed into extended neck posture (right) to secure the upper airway obstructed by hypertrophic adenoids and tonsils

Fig. 2.7  An example of skeletal Class III patients with serious mouth breathing. Skeletal Class III with strong mandible, hyperdivergent pattern, anterior openbite, and maxillary arch constriction were deteriorated after pubertal growth, and the pharyngeal constriction was not improved even with mandibular overgrowth, creating the vicious cycle

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1. Obstructive MB

→ Adenotonsillectomy

2. Structural MB

→ Growth modification

3. Habitual MB

→ Myofunctional theraphy

Fig. 2.8  Three types of mouth breathing requiring different treatment approach

arch and nasal cavity, skeletal modification treatment should be considered to change the structure to allow natural lip sealing and nasal breathing. For the habitual or residual mouth breathers, active myofunctional therapy should be recommended after checking the presence of tongue tie or tori.

2.5.2 Bruxism Bruxism is divided into awake bruxism and sleep bruxism. Sleep bruxism is a sleep-­ related movement disorder that is associated with SDB. Sleep bruxism is defined as “repetitive jaw muscle activity characterized by clenching or grinding of the teeth and/or bracing or thrusting of the mandible.” [6] Diagnostic criteria for sleep bruxism include regular or frequent tooth grinding sounds along with the presence of either abnormal tooth wear or transient morning jaw muscle pain or fatigue, and/or jaw locking on awakening. Sleep bruxism peaks during childhood and decreases with age. The pathophysiology of sleep bruxism is not well understood and multifactorial in nature. Current literature [7] suggests that it is regulated centrally (pathophysiological and psychosocial factors) and not peripherally (morphological factors), implying that no effective treatment that cures or stops it permanently. Definitive diagnosis of sleep bruxism is only achieved using electrophysiological tools, and management is usually directed toward tooth protection using occlusal splint, reduction of muscle activity using botox (BTX-A) injection, or pain relief.

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Mandibular advancement device (MAD) has shown better results to decrease muscle activity than occlusal splint [8, 9], and could be a promising alternative treatment for sleep bruxism with OSA.

2.6

 iagnostic Workflow for SDB Patients D in Orthodontic Clinic

In summary of diagnostic overview from orthodontic perspectives, we suggest a diagram of diagnostic workflow for the referred or suspected SDB (snoring and OSA) patients whom we will see in the orthodontic clinic (Fig. 2.9). Beforehand, we emphasize two points related to diagnosis and treatment planning of SDB patients. First, orthodontic professionals should be qualified for the differential diagnosis and selective application of orthodontic modalities toward active cooperation with sleep specialist for SDB patients. Second, orthodontists should be more alert to evaluate the respiratory function whenever we evaluate and treat the regular orthodontic patients.

Fig. 2.9  Diagram of diagnostic workflow for OSA patients who are referred from sleep specialists or who visit orthodontic clinic

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For the referred OSA patients from sleep specialists: • Based on the review of chief complaint, medical history, and PSG report, orthodontists should grasp the severity of OSA and medically related factors. • Clinical examination and imaging analysis can assist orthodontists in assessment of main obstruction site in relation to craniofacial contributing factors. • Functional examination on the stomatognathic system (bruxism and temporomandibular disorders) as well as sleep function can support the phenotypic causes of OSA. • Differential diagnosis on the craniofacial anatomical phenotyping of OSA will guide orthodontists to determine whether to intervene with orthodontic modalities or not. • Titration PSG is recommended to confirm the treatment efficacy after orthodontic intervention. Unless it is successful, more aggressive surgical intervention can be considered, or PAP may be highly recommended again. For the orthodontic patients who might have risks of OSA: • Medical history and sleep questionnaire need to be enquired to the orthodontic patient population for recognizing the present SDB or the risk of SDB after orthodontic treatment. History taking should not be ignored even in the patients who have no craniofacial discrepancy, keeping the possibility of nonanatomical phenotype of OSA in mind. • Clinical examination and imaging analysis allow orthodontists to identify the anatomical risk factors of OSA. • Functional examination not only on the stomatognathic system but also on sleep and respiration can be implemented in the case of suspected SDB patients, by using HSTs or by referring to the sleep laboratory for the PSG. According to the AASM, no treatment should be rendered without definite diagnosis through PSG. • Following the collaborative differential diagnosis of the SDB, orthodontists can play a primary role in the treatment of craniofacial phenotypes, or should be able to refer the patients with nonanatomical phenotype to the sleep specialists for collaboration. If the patient has no SDB at present but has some risks of SDB after orthodontic treatment with obesity, orthodontists need to change the orthodontic treatment planning to minimize airway dimensional constriction. • Titration HST or PSG is helpful for the evaluation of treatment efficacy. If the primary orthodontic intervention is not effective, referral to the sleep specialists should be suggested.

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Clinical Pearls in Orthodontic Diagnosis of OSA

• Orthodontic diagnostic workflow for the referred OSA patients includes consultation about the chief complaint, history taking, clinical examinations, radiographic image analysis, and functional analysis. • Whenever we evaluate and diagnose the regular orthodontic patients, dimensional and functional analyses on the upper airway and respiration are important to recognize the hidden SDB or to prevent SDB after orthodontic treatment. • Clinical examination comprises physical, behavioral, facial, and intraoral evaluations. • Two- or three-dimensional radiographic image analysis provides the upper airway morphometry and the main obstruction site in relation to the craniofacial skeletal pattern and para-pharyngeal soft tissues at a glance. • Respiration or sleep-related functional evaluation such as mouth breathing, tongue posture, bruxism, and home sleep test, if available, should be integrated with the morphometric evaluation. • Final diagnosis of SDB should be reserved for the sleep specialists, however dentists play a crucial role in evaluating patients with SDB for the suitability of various orthodontic modalities.

References 1. Netzer NC, Stoohs RA, Netzer CM, et al. Using the Berlin Questionnaire to identify patients at risk for the sleep apnea syndrome. Ann Intern Med. 1999;131(7):485–91. 2. Sutherland K, Lee RW, Cistulli PA.  Obesity and craniofacial structure as risk factors for obstructive sleep apnoea: impact of ethnicity. Respirology. 2012;17(2):213–22. 3. Hong S-N, Won T-B, Kim J-W, et al. Upper airway evaluation in patients with obstructive sleep apnea. Sleep Med Res. 2016;7(1):1–9. 4. Major MP, Flores-Mir C, Major PW. Assessment of lateral cephalometric diagnosis of adenoid hypertrophy and posterior upper airway obstruction: a systematic review. Am J Orthod Dentofacial Orthop. 2006;130(6):700–8. 5. Duan H, Xia L, He W, et al. Accuracy of lateral cephalogram for diagnosis of adenoid hypertrophy and posterior upper airway obstruction: a meta-analysis. Int J Pediatr Otorhinolaryngol. 2019;119:1–9. 6. Lobbezoo F, Ahlberg J, Raphael K, et al. International consensus on the assessment of bruxism: report of a work in progress. J Oral Rehabil. 2018;45(11):837–44. 7. Lobbezoo F, Naeije M. Bruxism is mainly regulated centrally, not peripherally. J Oral Rehabil. 2001;28(12):1085–91. 8. Landry-Schönbeck A, de Grandmont P, Rompré PH, Lavigne GJ.  Effect of an adjustable mandibular advancement appliance on sleep bruxism: a crossover sleep laboratory study. Int J Prosthodont. 2009;22(3):251–9. 9. Singh PK, Alvi HA, Singh BP, et  al. Evaluation of various treatment modalities in sleep bruxism. J Prosthet Dent. 2015;114(3):426–31.

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Therapeutic Pathway for Orthodontic Int ervention Su-Jung Kim, Patricia Pigato Schneider, and Ki Beom Kim

Contents 3.1  Phenotype-Based Orthodontic Intervention 3.2  Orthodontic Treatment Protocol for SDB Adults 3.3  Life-Long Craniofacial Management for OSA Patients 3.4  Case Examples of Various OSA Phenotypes References

3.1

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Phenotype-Based Orthodontic Intervention

Traditionally, treatment modalities for OSA adult patients represented a stepwise phased approach starting from conservative therapy such as behavioral or lifestyle modification, continuous positive airway pressure (CPAP), and oral appliance. According to the American Academy of Sleep Medicine, CPAP is the first-line treatment of OSA, and should be recommended as a primary option to all patients regardless of its severity. When the conservative therapy was not effective to improve

S.-J. Kim Department of Orthodontics, Kyung Hee University School of Dentistry, Seoul, South Korea e-mail: [email protected] P. P. Schneider Department of Orthodontics, School of Dentistry at Araraquara, UNESP Sao Paulo State University, Araraquara, Sao Paulo, Brazil K. B. Kim (*) Department of Orthodontics, Center for Advanced Dental Education, Saint Louis University, Saint Louis, MO, USA e-mail: [email protected] © Springer Nature Switzerland AG 2020 S.-J. Kim, K. B. Kim (eds.), Orthodontics in Obstructive Sleep Apnea Patients, https://doi.org/10.1007/978-3-030-24413-2_3

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patients’ symptoms, phase I soft-tissue surgery was suggested by sleep surgeon. Phase II skeletal surgery was considered only when the preceded procedures did not work based on the postoperative PSG evaluation. Decrease in the patient’s motivation going through these stepwise procedures was the biggest problem, so nowadays one-step target approach has been pursued. In this context, defining phenotypic causes of OSA is necessary to determine whether craniofacial orthopedic or surgical intervention is required to the OSA patient as a primary option. Eckert et al. [1] suggested a novel concept of phenotypic classification aiming at development of novel therapeutic approaches that target underlying mechanisms in individual patients with OSA. Key pathophysiologic causes include four factors: (1) anatomically collapsible UA (high critical closing pressure); (2) inadequate responsiveness of UA dilator muscles; (3) low respiratory arousal threshold; and (4) oversensitive ventilatory control system (Fig. 3.1). The PALM scale can be determined from data captured during PSG identifying (P)crit, (A)rousal threshold, (L)oop gain, and (M)uscle responsiveness, each of which represents a different etiology of OSA and responds to differing therapies. The PALM scale is expected to aid both physicians and dentists in directing optimal treatment and in avoiding much of the trial-and-error approach. For personalized phenotyping, orthodontists should integrate all information of respiratory parameters, race, gender, age, and hormone status with 3D imaging morphometric data. Despite multifactorial pathophysiology, pharyngeal collapsibility and its related anatomy is fundamental determinant of orthodontic intervention. When a patient shows moderately collapsible UA, which is primarily anatomically driven without nonanatomic vulnerabilities, anatomic intervention is likely to be effective.

(4) Oversensitive ventilator control system

(3) Premature arousal (low threshold)

(1) Anatomically collapsible UA (2) Poor pharyngeal dilator muscle responsiveness

Fig. 3.1  A novel concept of phenotypic classification aiming at therapeutic approaches that target underlying mechanisms of OSA. Key pathophysiologic causes include four factors: (1) anatomically collapsible UA (high critical closing pressure); (2) inadequate responsiveness of UA dilator muscles; (3) low respiratory arousal threshold; and (4) oversensitive ventilatory control system. Orthodontic intervention will be effective primarily to the patients with craniofacial anatomical phenotype (1)

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Especially in case of craniofacial skeletal discrepancy constricting the UA dimension, craniofacial modification treatment need to be primarily recommended to the patient.

3.2

Orthodontic Treatment Protocol for SDB Adults (Fig. 3.2)

Once orthodontic intervention is selected for the OSA patient with craniofacial anatomic vulnerability, proper orthodontic treatment modality is decided depending on the craniofacial target. The most frequent anatomic issue is retruded small mandible followed by narrow nasomaxillary complex. When a patient has retruded small mandible narrowing pharyngeal airway, mandibular advancement is required for upward and forward positioning of tongue base and hyoid to open the airway [2, 3]. If the patient shows normal or protruded maxilla with normal or flat occlusal plane, mandibular advancement surgery would be a good option [4, 5]. Advancing genioplasty can be combined as needed [6, 7]. Alternatively, temporary mandibular advancement device (MAD) can be recommended especially to elderly patients who tend to refuse skeletal surgery [8, 9]. If a patient has retruded maxilla and steep occlusal plane with retruded mandible, in contrast, maxillomandibular advancement (MMA) surgery is highly required for significant enlargement of overall pharyngeal airway [10, 11].

Orthodontic protocol for SDB adults PAP Intolerance

Refer Nonanatomic vulnerability

Anatomic vulnerability Refer

Para-pharyngeal soft tissue abnormality

Craniofacial deformity

Narrow nasomaxilla

Retruded mandible Protruded Maxilla / Flat OP

MARPE DOME

Lateral pharyngeal walls

MAD

Mandibular surgery

Retruded Maxilla / steep OP

MMA

Fig. 3.2  A therapeutic pathway of phenotype-based precision protocol for the adult OSA patients from orthodontic point of view. PAP Continuous positive airway pressure, MARPE Microimplant-­ assisted rapid palatal expansion, DOME Distraction osteogenesis maxillary expansion, MAD Mandibular advancement device, MMA Maxillomandibular advancement, OP Occlusal plane

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When a patient has transverse skeletal discrepancy with maxillary constriction and nasal obstruction, nasomaxillary skeletal expansion is necessary for the enlargement of the nasal cavity to decrease nasal resistance affecting the pharyngeal collapsibility, as well as the oral cavity to guide the tongue-up posture [12, 13]. According to the age, different expansion modality is considered. Conventional rapid palatal expansion (RPE) can be applied for the growing children under 15 years old [14, 15], microimplants-assisted RPE (MARPE) is preferred for the post-adolescents or young adults [16, 17], and surgical removal of tissue resistance using corticotomy can be combined with MARPE for adult patients [18]. Sagittal skeletal correction is concomitantly performed depending on the pattern of sagittal discrepancy. Although a severe OSA patient belongs to the nonanatomic phenotype with lateral pharyngeal wall dysfunction, the patient can be referred to the orthodontists for consideration of salvage MMA surgery in case of PAP intolerance or surgical failure [19, 20]. When a referred OSA patient has no definite craniofacial risk factors, or when a patient who wants orthodontic treatment has OSA symptoms, orthodontists should be able to refer to the sleep specialists for collaboration.

3.3

 ife-Long Craniofacial Management for  L OSA Patients (Fig. 3.3)

In the past, craniofacial management could be accomplished by two-phase approach through the growth modification treatment before the peak height velocity (the first phase), and by the surgical reconstruction after the end of residual

Fig. 3.3  Life-long sequence of craniofacial modification by orthodontic, orthopedic, and surgical interventions for the expansion of upper airway as well as skeletal framework

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growth (the second phase). Nowadays, on the other hand, the craniofacial orthopedic treatment can be successfully achieved during the postadolescence up to young adult, which was the waiting period between the two phases, with the development of bone-anchored craniofacial orthopedic appliances. Recently, moreover, earlier orthopedic intervention during the preschool ages has been issued to secure nasal breathing as early as possible especially in the child with nasal obstruction [21]. Guilleminault et al. [22] found that abnormal breathing during sleep is related to intrinsic and extrinsic factors, which are present early in life and may induce progressive narrowing of the collapsible airway. Oronasal dysfunction should be recognized from infants for appropriate intervention to prevent OSA and secondary negative impacts on orofacial growth [23]. Further, surgically assisted orthodontic treatment for the osseopharyngeal reconstruction is being applied to no less than the elderly patients for functional improvement of sleep and respiration as well as esthetic improvement. In this context, life-long craniofacial management has been established to extend the roles of orthodontic specialists. More specific guideline of timely target intervention throughout the life will be explained in the following chapters.

3.4

Case Examples of Various OSA Phenotypes

Case 1: Anatomical Phenotype with Maxillary Constriction, Hypertrophic Adenoid, and Obesity A 29-year-old Caucasian woman sought for orthodontic treatment with a chief complaint of anterior open bite. She was obese with heavy submental fat tissues. Patient reported a medical history of OSA and chronic mouth breathing. Major findings noted during the extraoral clinical examination were concave facial profile with protruded chin and substantial lip incompetence, which contributes to the inability to produce full lip closure. The intraoral examination showed a bilateral Class III malocclusion, anterior open bite, severe maxillary transverse insufficiency with deep and high palatal vault, bilateral posterior cross bite, and mild-to-moderate tooth size arch length discrepancy (Fig.  3.4). Radiographically, skeletal Class III with strong mandible and hyperdivergent vertical pattern was seen. Due to the adenoid hypertrophy and elongated soft palate, nasopharyngeal and velopharyngeal airway spaces were narrowed, probably contributing to the OSA (Fig. 3.5). Conclusively, this young adult patient belongs to the anatomical phenotype of OSA with maxillary transverse constriction, hypertrophic adenoid and thick soft palate, and obesity. At the same time with weight loss and adenoidectomy, orthodontic treatment is recommended to expand the maxilla and intrude the posterior teeth for at last maintaining the facial height with closing the anterior openbite. Surgical maxillary expansion using microimplant-assisted device (distraction osteogenesis maxillary expansion) can be rendered.

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Fig. 3.4  Facial and intraoral photographs of an OSA patient with anatomical risk factors Measurement

Value

Norm

SNA (º)

77.7

82.0

SNB (º)

79.7

80.9

ANB (º)

-6.7

1.6

Wits (mm)

-7.2

-1.0

SN–GoGn(º)

35.3

32.9

FMA (º)

31.7

25.9

U1–NA (mm)

7.9

4.3

U1–SN (º)

110.9

103.1

L1–NB (mm)

3.2

4.0

L1–GoGn (º)

83.6

93.0

Fig. 3.5  Lateral cephalogram and the skeletal measurements of the OSA patient. In spite of prognathic mandible, naso- and velo-pharyngeal airway spaces were narrowed in relation to hypertrophic adenoid and thick soft palate

Case 2: Anatomical Phenotype with Mandibular Retrusion, Bi-Arch Constriction, and Obesity A 28-year-old Caucasian male patient was presented with chief complaint of OSA.  Patient’s physical characteristics noted were midrange obesity with BMI

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35

Fig. 3.6  Facial and intraoral photographs of an OSA patient with craniofacial anatomical risk factors Measurement

Value

Norm

SNA (º)

85.0

82.0

SNB (º)

78.4

80.9

ANB (º)

6.5

1.6

Wits (mm)

3.3

-1.0

SN–GoGn(º)

34.3

32.9

FMA (º)

31.2

25.9

U1–NA (mm)

3.3

4.3

U1–SN (º)

98.2

103.1

L1–NB (mm)

7.4

4.0

L1–GoGn (º)

97.1

93.0

Fig. 3.7  Lateral cephalogram and the skeletal measurements of the OSA patient. Retrognathic mandible, low hyoid position, and hypertrophic tonsils seem to be related to the constricted oropharynx and OSA

score of 28.7. The patient was seen by an ENT specialist who found enlarged tonsils and categorized the patient as Class III Mallampati score. Furthermore, the patient’s overall AHI was 12.5 and the lowest oxygen saturation level was 91% from the baseline. Facial evaluation showed convex profile with retruded small chin, short throat length, and obtuse cervicomental angle, and thick neck circumference

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(Fig.  3.6). Intra-arch evaluation showed compensated Class I relationship with severe tooth size arch length discrepancy in the mandibular arch, maxillary and mandibular arch constriction, and missing upper right first premolar and lower right first molar (Fig. 3.6). The lateral cephalogram presented skeletal Class II with retrognathic mandible, inferiorly displaced hyoid, and hypertrophic palatine tonsils, which might contribute to the narrow oropharyngeal space. (Fig. 3.7) In summary, this young adult male patient belonged to the typical craniofacial anatomical phenotype of OSA; therefore, maxillomandibular advancement surgery was considered for the primary treatment option. Concurrently, mandibular midline distraction osteogenesis with three-piece maxillary expansion was planned and tonsillectomy was recommended. Case 3: Complex Phenotype with Craniofacial Deformity and Nonanatomical Risk Factors A 55-year-old Caucasian female patient was referred to the orthodontic department. She had been diagnosed with severe OSA associated with poor neuromuscular responsiveness and obesity, and tried to use CPAP as a sleep physician’s prescription. Her AHI reading using CPAP was at 0.8, which indicates good control of OSA with CPAP. However, the patient was interested in seeking surgical options to treat her OSA permanently. She had a history of osteoarthritis and reported occasional soreness of the TMJ.  She showed a convex profile with retruded chin and heavy submental fat pads. Minimal gingival display (Fig.  3.8) was observed. Intraoral exam showed that she has Class I molar and Class II canine relationship, maxillary arch constriction with deep and high palatal arch, insufficient posterior buccal

Fig. 3.8  Facial and intraoral photographs of an elderly OSA patient with complex phenotype

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Fig. 3.9 Panorama and lateral cephalogram of the OSA patient. Retrognathic mandible, hyperdivergent vertical pattern, low hyoid position, long and flabby soft palate, and long and narrow oropharynx are observed

Fig. 3.10  CBCT volumetric and sectional images representing transversely as well as sagittally collapsed minimal cross-sectional area in the oropharyngeal level

overjet, moderate-to-severe tooth size arch length discrepancy, and anterior open bite. Analysis of cephalogram represented excessive lower facial height with high mandibular plane angle, Class II skeletal pattern with retrognathic mandible, inferiorly positioned hyoid bone, and constricted oropharyngeal airway (Fig. 3.9). CBCT volumetric images confirmed the transversely as well as sagittally collapsed pharyngeal airway. In terms of her TMJ, both the panoramic radiograph and CBCT imaging reveal “flattened-look” of both condyles and a noticeable osteophyte “beaking” on her right condyle (Fig. 3.10). For this elderly OSA patient with complex phenotype, CPAP is recommended for the first-line treatment and mandibular advancement device can be an alternative. Since she had TMD signs and symptoms and asked permanent osseopharyngeal reconstruction, MMA with advancing genioplasty was considered with extraction of the both mandibular first premolars to maximize mandibular advancement.

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Case 4: Adolescent OSA Patient with Obese Phenotype A 13-year-old Black male patient was referred from pediatric ENT department. His medical records showed a BMI of 35 indicating high obesity, attention deficit hyperactivity disorder (ADHD), ongoing nocturnal enuresis, and OSA.  Tonsillectomy and adenoidectomy had been performed, but OSA symptoms persisted. The patient was using a full-face CPAP, but despite the efforts, the AHI reading was less than optimal at 1.6. Furthermore, due to his persistent loud snoring, his CPAP pressure gage was increased from 6 to 14 cm H2O pressure to 11 cm H2O. Major orthodontic findings upon facial examination were protruded lips with well-developed chin, but almost flat cervicomental angle due to the heavy submental

Fig. 3.11  Facial and intraoral photographs of an adolescent OSA patient with obese phenotype

Fig. 3.12  Panorama and lateral cephalogram of the OSA patient. Skeletal Class III with prognathic mandible and normal vertical divergency is found, which implies no craniofacial anatomical phenotype of OSA

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fat pad. Intraoral examination showed bilateral Angle Class I malocclusion, generalized spacing, normal maxillary arch, and wide mandibular arches creating bilateral posterior cross-bite in relation to the thrusting habit of large tongue (Fig.  3.11). Tongue thrusting habit might be caused to secure the patency of narrow pharyngeal airway. Lateral cephalogram represented skeletal Class III tendency with strong mandible, which might not contribute to the OSA directly, but long, thick, and retroclined soft palate made the velopharyngeal airway space narrow in association with low tongue posture, low hyoid position, and heavy fat tissues (Fig. 3.12). For this patient, growth modification treatment would not be available to treat OSA.  Weight loss should be strongly recommended considering the bariatric surgery to avoid the CPAP treatment.

Clinical Pearls in Therapeutic Decision of Orthodontic Intervention

• Phenotype-based orthodontic intervention: Not all SDB patients will respond to the orthodontic intervention successfully even though they have been referred from sleep clinic to the orthodontists. OSA phenotyping is important to decide whether to orthodontically intervene or not, and craniofacial phenotyping is necessary to decide how to treat the SDB patients orthodontically. • Orthodontic precision protocol: An updated therapeutic pathway for the SDB patients is established from orthodontic point of view on the basis of target-based selective application of various orthodontic modalities. • Life-long craniofacial management: Orthodontic, orthopedic, and surgical craniofacial managements for the SDB patients with craniofacial skeletal risk factors can be timely applied throughout the life.

References 1. Eckert DJ, White DP, Jordan AS, et al. Defining phenotypic causes of obstructive sleep apnea. Identification of novel therapeutic targets. Am J Respir Crit Care Med. 2013;188(8):996–1004. 2. Riley RW, Powell NB, Guilleminault C. Obstructive sleep apnea syndrome: a surgical protocol for dynamic upper airway reconstruction. J Oral Maxillofac Surg. 1993;51(7):742–7. 3. Li KK. Maxillomandibular advancement for obstructive sleep apnea. J Oral Maxillofac Surg. 2011;69(3):687–94. 4. Dalla Torre D, Burtscher D, Widmann G, et al. Long-term influence of mandibular advancement on the volume of the posterior airway in skeletal Class II-patients: a retrospective analysis. Br J Oral Maxillofac Surg. 2017;55(8):780–6. 5. Chan AS, Sutherland K, Schwab RJ, et al. The effect of mandibular advancement on upper airway structure in obstructive sleep apnoea. Thorax. 2010;65(8):726–32. 6. Camacho M, Liu SY, Certal V, et al. Large maxillomandibular advancements for obstructive sleep apnea: an operative technique evolved over 30 years. J Craniomaxillofac Surg. 2015;43(7):1113–8.

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7. Singhal D, Hsu SSP, Lin CH, et al. Trapezoid mortised genioplasty: a further refinement of mortised genioplasty. Laryngoscope. 2013;123(10):2578–82. 8. Marklund M, Verbraecken J, Randerath W. Non-CPAP therapies in obstructive sleep apnoea: mandibular advancement device therapy. Eur Respir J. 2012;39(5):1241–7. 9. Canadian Agency for Drugs and Technologies in Health (CADTH). Oral appliances for treatment of snoring and obstructive sleep apnea: a review of clinical effectiveness. CADTH Technol Overv. 2010;(1):e0107. 10. Fairburn SC, Waite PD, Vilos G, et al. Three-dimensional changes in upper airways of patients with obstructive sleep apnea following maxillomandibular advancement. J Oral Maxillofac Surg. 2007;65(1):6–12. 11. Kim T, Kim H-H, Hong S, et al. Change in the upper airway of patients with obstructive sleep apnea syndrome using computational fluid dynamics analysis: conventional maxillomandibular advancement versus modified maxillomandibular advancement with anterior segmental setback osteotomy. J Craniofac Surg. 2015;26(8):e765–70. 12. Baratieri C, Alves M Jr, de Souza MMG, et al. Does rapid maxillary expansion have long-­ term effects on airway dimensions and breathing? Am J Orthod Dentofacial Orthop. 2011;140(2):146–56. 13. Gordon JM, Rosenblatt M, Witmans M, et  al. Rapid palatal expansion effects on nasal airway dimensions as measured by acoustic rhinometry: a systematic review. Angle Orthod. 2009;79(5):1000–7. 14. Haas A.  Long-term posttreatment evaluation of rapid palatal expansion. Angle Orthod. 1980;50(3):189–217. 15. Ballanti F, Lione R, Baccetti T, et  al. Treatment and posttreatment skeletal effects of rapid maxillary expansion investigated with low-dose computed tomography in growing subjects. Am J Orthod Dentofacial Orthop. 2010;138(3):311–7. 16. Carlson C, Sung J, McComb RW, et  al. Microimplant-assisted rapid palatal expansion appliance to orthopedically correct transverse maxillary deficiency in an adult. Am J Orthod Dentofacial Orthop. 2016;149(5):716–28. 17. Brunetto DP, Sant’Anna EF, Machado AW, Moon W.  Non-surgical treatment of transverse deficiency in adults using Microimplant-assisted Rapid Palatal Expansion (MARPE). Dental Press J Orthod. 2017;22(1):110–25. 18. Jang H-I, Kim S-C, Chae J-M, et al. Relationship between maturation indices and morphology of the midpalatal suture obtained using cone-beam computed tomography images. Korean J Orthod. 2016;46(6):345–55. 19. Mehra P, Downie M, Pita MC, Wolford LM.  Pharyngeal airway space changes after counterclockwise rotation of the maxillomandibular complex. Am J Orthod Dentofacial Orthop. 2001;120(2):154–9. 20. Liu SY, Awad M, Riley R, Capasso R. The Role of the Revised Stanford Protocol in Today’s Precision Medicine. Sleep medicine clinics. 2019;14(1):99–107. 21. Monini S, Malagola C, Villa MP, et  al. Rapid maxillary expansion for the treatment of nasal obstruction in children younger than 12 years. Arch Otolaryngol Head Neck Surg. 2009;135(1):22–7. 22. Guilleminault C, Sullivan SS, Huang Y-S. Sleep-disordered breathing, orofacial growth, and prevention of obstructive sleep apnea. Sleep Med Clin. 2019;14(1):13–20. 23. Guilleminault C, Huang Y-S. From oral facial dysfunction to dysmorphism and the onset of pediatric OSA. Sleep Med Rev. 2018;40:203–14.

4

Craniofacial Growth Modification for OSA Children Su-Jung Kim

Contents 4.1  M  ajor Differences in Pediatric OSA 4.1.1  Different Diagnostic Criteria 4.1.2  Different Subjective Symptoms 4.2  Early Intervention: Why? 4.3  Early Intervention: How? 4.3.1  Phenotype-Based Patient Selection 4.3.2  Target-Based Treatment Selection 4.3.3  Timely Target Application of Appliances 4.4  Cases References

4.1

 41  41  42  43  43  43  44  45  50  58

Major Differences in Pediatric OSA

Pediatric OSA differs from adult OSA in both diagnosis and management. Pediatric OSA is more difficult to be correctly diagnosed than adult OSA due to less available PSG finding, less sensitive HST finding, less reliable questionnaire, limited information from lateral cephalometry, and uncommon application of CBCT to the growing patients. Different diagnostic criteria and subjective symptoms need to be contemplated.

4.1.1 Different Diagnostic Criteria Overnight PSG is the gold standard for diagnosing OSA in children as in adults. However, AHI as specific criterion of OSA severity is provided differently from that S.-J. Kim (*) Department of Orthodontics, Kyung Hee University School of Dentistry, Seoul, South Korea e-mail: [email protected] © Springer Nature Switzerland AG 2020 S.-J. Kim, K. B. Kim (eds.), Orthodontics in Obstructive Sleep Apnea Patients, https://doi.org/10.1007/978-3-030-24413-2_4

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in adults (Table 4.1). Poor availability of pediatric sleep laboratories for overnight PSG has prompted a search for alternative diagnostic screening tools including a combination of history and physical examination findings.

4.1.2 Different Subjective Symptoms Pediatric OSA can be undiagnosed, since the symptoms are different from adults. The main differences between children and adults are compared in Table 4.2 [1]. The chief complaint of OSA children is snoring or labored breathing during sleep, and mouth breathing is frequently observed during the examination time. The most common cause is known to be adenotonsillar hypertrophy, followed by nasal obstruction. Obesity contributes to the pediatric OSA less than the adult OSA. Since sleep fragmentation, witnessed apnea, arousal, and excessive daytime sleepiness, which are very common in adult OSA, are not usually detected, it is hard to recognize OSA in children. Cardiovascular and neurovascular comorbidities rarely occur, instead, irreversible disturbances such as psychosocial and behavioral problems, neurocognitive deficits, learning disorder, physical and facial growth disturbances make serious concerns. The behavioral problems represent various aspects across ages: attention deficit hyperactivity disorder (ADHD)-like behavior in the early childhood, in contrast, depression in adolescence [2]. As a simple screening instrument of pediatric OSA, BEARS (B, Bedtime; E, Excessive daytime sleepiness; A, night Awakenings; R, Regularity and duration of sleep; S, Snoring) has been used in primary care settings [3].

Table 4.1  Different objective criteria of OSA severity between children and adults

OSA severity Mild Moderate Severe

Children 1 ≤ AHI  5, RDI > 30, LSaO2