The Clinician’s Handbook for Dental Sleep Medicine

Library of Congress Cataloging-in-Publication Data

Names: Berley, Ken, author. | Carstensen, Stephen, author.

Title: The clinician’s handbook for dental sleep medicine / Ken Berley and Stephen Carstensen.

Description: Batavia, IL : Quintessence Publishing Co., Inc, [2019] | Includes bibliographical references and index.

Identifiers: LCCN 2018057222 | ISBN 9780867158137 (softcover) | eISBN 9780867158571

Subjects: | MESH: Sleep Apnea Syndromes--therapy | Sleep Bruxism--therapy | Dentistry--methods

Classification: LCC RC737.5 | NLM WF 143 | DDC 616.2/09--dc23

LC record available at https://lccn.loc.gov/201805722

© 2019 Quintessence Publishing Co, Inc

Quintessence Publishing Co Inc

411 N Raddant Rd

Batavia, IL 60510

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All rights reserved. This book or any part thereof may not be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, or otherwise, without prior written permission of the publisher.

Editor: Leah Huffman

Design: Sue Zubek

Production: Angelina Schmelter

Printed in the USA

I remember the night like it was yesterday. The phone rings at 2:00 am, and through sobs I hear my mother say, “Ken, your father has had a stroke.” Everything else is a blur. My father had had a stroke in the middle of the night, and he was in a coma. For the next 48 hours, I watched him struggle to breathe. He was having one apneic event after another, and finally he passed away. I did not know at the time that all the men in our family were prone to obstructive sleep apnea (OSA), or that 90% of the time strokes are caused by OSA. My grandfather had died of a stroke in the middle of the night, and now my father had followed suit. We all knew that my dad was a horrific snorer and he made funny sounds when he was asleep, but I never dreamed that he had a serious medical condition. If I had known the warning signs of OSA, my father and grandfather could have been treated for this condition.

The Clinician’s Handbook for Dental Sleep Medicine is dedicated to my father, James A. Berley. This book is a product of his life. While I was unable to prevent his stroke, his passing sparked a passion to learn as much as possible about the treatment of sleep disorders. Today, I am the one with OSA, but unlike my father, I wear a mandibular advancement appliance each night to control the serious consequences of this disease.

—Ken Berley

This book was written to honor the many who have embodied the passion for teaching I aspire to emulate, none more so than Dr Keith Thornton, who pushed me to start treating sleep problems in my dental practice and continues to show me how to live Dr L. D. Pankey’s philosophy. I’m inspired by my wife, Midge, the world’s most dedicated dental hygienist who supports everything I do, and my father, Larry, who I’m fortunate to still have in my life, in no small part because he has used CPAP every night for these many years.

—Steve Carstensen

Foreword

Preface

1Clinical Guide for the Practice of Dental Sleep Medicine

2An Overview of Sleep & Sleep Disorders

3Dental Sleep Medicine Protocol and Practice

4Integrating Dental Sleep Medicine into Your Practice

5Treatment Decisions and Appliance Selection

6Delivery of a Custom MAD

7Complications of Oral Appliance Therapy

8Evaluating Therapy and Ongoing Care

9The New Reality

10Legal Issues Related to the Practice of Dental Sleep Medicine

11Medical Insurance and Medicare

12Pediatric Airway Problems

Sleep Medicine Terminology

Recommended Materials

Index

The Clinician’s Handbook for Dental Sleep Medicine by Ken Berley and Steve Carstensen is a unique and timely contribution by two renowned experts in dental sleep medicine. More than a “how-to” manual, the book is also a concise and thorough review of knowledge in the field. It will find a welcome home chairside, as a practical reference, and bedside for thoughtful perusal.

Late one night 40 years ago, I stood beside a sleeping obese gentleman observing his breathing and blood oxygen. Aghast, I watched the blood oxygen plummet repeatedly to catastrophic levels despite his vigorous but unsuccessful efforts to breathe. His throat air passage, the pharynx, was completely blocked. This dreadful situation persisted until he aroused from sleep and took a few breaths. Returning to sleep, he was again unable to breathe because his pharynx was completely obstructed.

I had stumbled upon a new disease that night and referred to it as obstructive sleep apnea, ie, a cessation of breathing caused by pharyngeal obstruction, and showed that the fundamental abnormality was an anatomical narrowing of the pharynx that increased its collapsibility. We soon learned that obstructive sleep apnea was a common and a “bad” disease; 20% to 30% of adults have it, and it is a risk factor for cardiovascular disease and premature death. This is a health problem of significant proportions.

The medical profession responded to this new disease and its health implications by forming a new medical specialty and proclaiming that one of its specialists must see anyone suspected of having sleep apnea. This is, in my opinion, an absurd and unfeasible idea given the nature and prevalence of the disease and the limited availability of such specialists. Typically, the specialist uses a cumbersome, overnight diagnostic test and treats the patient by applying air pressure to the nose during sleep. This approach has been a failure, as only a modicum of sleep apneics have yet been diagnosed and treated. We obviously need more efficient and convenient methods in the hands of a large cadre of health care professionals.

We now stand on the cusp of a more fruitful approach to the health care and public health challenges posed by obstructive sleep apnea. Simple diagnostic testing in the home is now available, and new therapies are more acceptable. For instance, oral appliance therapy involves placing a piece of plastic on the teeth at night. This enlarges and stabilizes the pharynx and often eliminates sleep apnea. Consequently, a need emerges for dentists with competence in the new field of dental sleep medicine. The Clinician’s Handbook for Dental Sleep Medicine will play a key role in meeting this need. The timeliness and relevance of the book cannot be overemphasized.

The book is essentially without precedent; while others have offered a comprehensive review of the field of dental sleep medicine, none have provided the practical “hands-on” information that is found herein. This book represents a pioneering effort to supply a seamless hybrid of the basic concepts that form the knowledge foundation of the field together with the practical details that dental therapists might want at their fingertips. For this, the authors deserve hearty congratulations.

Another outstanding feature of the book is its comprehensiveness; all aspects of the field find careful treatment here. For example, the thorough presentation of sleep physiology and the review of the pathophysiology of sleep-related breathing disorders in the early chapters is counterbalanced by information on legal issues and practical aspects of medical billing and reimbursement in the final chapters. Likewise, the age scope is broad, with the principal focus of the book being on adults, followed by an authoritative treatment of pediatric dental sleep medicine in the final chapter.

A cautionary note for the newcomer: Remember that oral appliance therapy is not always efficacious. You must anticipate the unhappy prospect of having invested time and money to no avail in some patients. We can avoid this; a validated method for prospectively selecting favorable candidates for oral appliance therapy is now available (MATRx plus, Zephyr Sleep Technologies).

Never forget that obstructive sleep apnea is a bad disease. Many of your patients have, or are at risk of having, serious cardiovascular disease. You will need fluid, collegial interactions with your medical counterpart.

John E. Remmers, MD

Professor of Internal Medicine
University of Calgary

These are exciting times in dental sleep medicine (DSM). While still in its infancy, DSM is the fastest-growing discipline in dentistry. Many dentists are partnering with our colleagues in sleep medicine to provide therapy for patients suffering from the devastating effects of obstructive sleep apnea (OSA). DSM has blossomed to the point that it is truly a divergent medical discipline. OSA directly or indirectly affects many biologic systems within the human body; therefore, numerous medical disciplines are involved in the treatment of a patient with OSA. A dentist trained in DSM is a vital member of the multidisciplinary team of health care professionals necessary for the effective control of this deadly disease.

The majority of individuals with sleep complaints do not present to their physicians for treatment. Only 6% of patients who experience sleep issues have complained to their treating physicians. Sadly, sleep disorders are associated with significant morbidity and mortality rates. OSA predisposes patients to cardiovascular and cerebrovascular disorders. OSA has been shown to increase mortality for all causes and has been directly linked to sudden death during sleep. Excessive daytime sleepiness, which is frequently associated with OSA, has been linked with motor vehicle and industrial accidents. Mass transit and the trucking industries have both been adversely affected by OSA. Reports of accidents caused by or associated with sleep disruption abound. The Exxon Valdez ship accident in Alaska, the Chernobyl nuclear power station accident, the Space Shuttle Challenger, and the New Jersey mass transit train accident are all examples of major industrial accidents that were caused by sleep-related disturbances or OSA.

Depending on the studies and projections cited, OSA may affect between 25 and 50 million Americans; 24% of men and 9% of women likely suffer from this devastating disease. Additionally, it has been estimated that at least 10% of all children may suffer from sleep apnea. These children struggle with a host of developmental and social issues.

It is estimated that 85% to 90% of all patients who suffer from OSA remain undiagnosed. It is also estimated that each dental office in the United States may have as many as 500 or more patients with undiagnosed OSA currently being treated for dental-related concerns. Therefore, dental professionals have never been presented with a better opportunity to positively impact the health of our patients.

Each day practicing dentists evaluate numerous patients in their offices who suffer from OSA. Some of these patients have been diagnosed and are successfully being treated with continuous positive airway pressure (CPAP); however, many of our dental patients who suffer from some form of sleep-disordered breathing are either undiagnosed or noncompliant with CPAP therapy. This presents a great opportunity for the dental professional. Dentists are now part of the medical team who can screen for OSA and provide life-saving therapy. Statistics show that dentists routinely evaluate approximately 50% of the American population each year. Using these statistics, one can surmise that as many as 25 million patients visited a dentist in the United States last year with undiagnosed or uncontrolled sleep-disordered breathing.

Unfortunately, a majority of dentists are not well versed in sleep medicine and sleep-related disorders. Studies have consistently shown that many dentists are unable to recognize systemic and oral risks of OSA. This educational deficiency must be corrected. Dentists trained to screen for snoring and OSA can provide a life-changing service to their patients. Fortunately, in addition to screening for OSA, properly trained dentists can provide a mandibular advancement device (MAD) to assist in treatment for patients who are unable to utilize CPAP. MADs are approved by the US Food and Drug Administration for the treatment of OSA and therefore can be billed to medical insurance and Medicare, if certain criteria are met. The treatment of OSA with MADs can also provide an additional income stream for offices wishing to expand their services. Many practitioners who provide oral appliance therapy are routinely billing medical insurance for payment. Dentists can now register as Medicare durable medical equipment providers and provide oral appliance therapy for their eligible Medicare patients.

This book was written as a reference for the dentist with little or no experience in DSM. Great effort has been directed to providing introductory-level material as well as advanced theories. Additionally, an exhaustive terminology section has been included for easy reference. This book will be your guide through the maze of protocols, rules, and regulations that frequently sabotage unwary dentists wishing to incorporate DSM into their practices. If the techniques and protocols outlined in this book are followed, readers should be able to easily incorporate the practice of DSM into their daily office routine. All aspects of the practice of DSM are discussed in depth. Care has been taken to present examples that are easily understood. Office-management systems are presented, risk-management issues are discussed, and readers are instructed on how to file medical insurance as well as Medicare.

This textbook will open the door to the fascinating world of DSM, providing the tools and techniques needed to successfully treat patients with sleep-disordered breathing. However, the reader is cautioned that OSA is a deadly disease. Many of the patients we treat for OSA are very sick. It is incumbent on every dentist practicing DSM to become well versed in the processes and protocols of treatment. Your patient’s life could depend on it.

As stated earlier, these are exciting times to be a dentist. Although DSM remains in its infancy, the profession has made great strides toward acceptance and respectability. Join us on this incredible journey. Help save the lives of many of your patients by providing oral appliance therapy to prevent snoring and treat OSA. This journey will change your life!

The woods are lovely, dark and deep.
But I have promises to keep, and miles to go before I sleep.

ROBERT FROST

From the dawn of modern civilization, man has cherished and worshiped sleep. Sleep was deified by the Greeks and the Romans, resulting in their gods of sleep, Hypnos and Somnus. Yet today, a good night’s sleep has never been harder to achieve. Sadly, many of the reasons people are having trouble sleeping are self-inflicted. Today we are hyperconnected with a growing array of computer-driven screens and glowing devices. We now have the ability to work anywhere on the face of the planet and have constant contact with anyone in the world. The health-conscious person striving for a good night’s sleep must be very disciplined in light of this sensory onslaught.

In addition to the societal and entertainment choices that rob us of sleep, our ability to sleep is directly affected by certain physiologic characteristics or anatomical deficiencies. These physical characteristics that alter our ability to sleep can give rise to insomnia, an altered arousal threshold, asphyxia, and sleep fragmentation that can result in excessive daytime sleepiness (EDS) and contribute to a host of comorbid diseases. Fortunately, with the help of trained professionals, our sleep can be improved. By modifying or enlarging a patient’s upper airway with the assistance of either continuous positive airway pressure (CPAP), surgery, orthodontics, or a mandibular advancement device (MAD), nocturnal oxygenation may be increased, thereby improving the quality and quantity of sleep. Dental sleep medicine (DSM) was founded on the principle that the movable mandible can be supported during sleep to maintain an open airway. This simple act of holding the mandible in a stable or slightly protruded position during sleep may be adequate to prevent or mitigate the physiologic consequences of airway obstruction and the resultant nocturnal hypoxemia. There is an ever-increasing number of MADs that are cleared by the US Food and Drug Administration (FDA) to treat sleep-related breathing disorders (SRBDs), including snoring and obstructive sleep apnea (OSA). This fact has allowed properly trained dentists to become an integral partner in the treatment of SRBDs.

THE RISE OF DENTAL SLEEP MEDICINE

This is an exciting time to be a dentist. The field of DSM is exploding. This is primarily due to the fact that the majority of individuals with sleep disorders do not present to their physicians for treatment of their sleep issues.¹ These patients typically seek medical care for treatment of the comorbid diseases that are directly associated with sleep-disordered breathing, in particular hypertension, fatigue, stroke, cardiovascular disease, and diabetes. Sadly, most physicians do not screen for SRBDs, and the precipitating factors contributing to the patient’s chief complaint frequently go undiagnosed.² However, many of these patients who suffer from sleep issues will present for routine dental examinations and care. A dentist who is properly trained to recognize the signs and symptoms of sleep-disordered breathing can potentially provide life-saving referrals and MAD therapy for their sleep-deprived patients. Fortunately, patients with sleep-disordered breathing exhibit identifiable intraoral signs and symptoms as well as physical and social symptoms. With the appropriate training, dentists are well situated to screen and treat many of these patients.

The screening and treatment of our dental patients who have OSA has led to the birth of DSM. While still in its infancy, DSM is the fastest-growing discipline in dentistry. Screening and treating patients with SRBDs can greatly improve the health of these patients and potentially add a significant source of income to your dental practice.

ADA policy statement on SRBDs

In 2017, the American Dental Association (ADA) voted to approve a policy statement on dentistry’s role in the treatment of SRBDs.³ This policy places SRBDs firmly within the scope of practice of every dentist. While dentists are not obligated to provide treatment for SRBDs, dentists are now required to screen all patients for SRBDs and document the results in each patient record. When the screening is positive, the patient must be informed of the possibility of sleep-disordered breathing and referred to a sleep physician for appropriate diagnosis and therapy.

FIG 1-1 Patient during a PSG.

TERMINOLOGY

Sleep-related breathing disorder

A sleep-related breathing disorder is a chronic disease caused by repeated upper airway collapse during sleep resulting in recurrent nocturnal asphyxia, fragmented sleep, major fluctuations in blood pressure, and increased sympathetic nervous system activity.⁴ Readers should be aware that while OSA is also generally referred to as SRBD, in reality SRBD is a much broader term that includes a spectrum of breathing anomalies ranging from chronic or habitual snoring (resulting in airflow limitations) to upper airway resistance syndrome (UARS) to frank OSA, central and complex apnea, or in some cases, Cheyne-Stokes respiration and obesity hypoventilation syndrome.

Polysomnography

A polysomnogram (PSG), also called a sleep study, is a test used to diagnose sleep disorders. A PSG provides a continuous recording of specific physiologic markers and variables over a full night of sleep that helps to identify and diagnose various sleep disorders (Fig 1-1). Typically, a PSG records changes in brainwaves (via electroencephalogram [EEG]), eye movements (via electrooculogram [EOG]), muscle tone (via electromyogram [EMG]), respiration (via nasal flow sensor and effort belts around the chest), heart rate (via electrocardiogram [ECG]), and leg movements (via EMG).

Obstructive sleep apnea

Obstructive sleep apnea is the most common type of apnea and is characterized by repetitive episodes of partial obstruction or complete obstruction of the patient’s airway during sleep, despite the effort to breathe, and is usually associated with a reduction in blood oxygen saturation (SaO₂). Repetitive reduction of airflow is termed hypopnea, and complete cessation of airflow is termed apnea. These episodes of decreased breathing, called apneas (literally meaning “without breath”), typically last 20 to 40 seconds.⁵ The level of OSA is described by the Apnea-Hypopnea Index (AHI), a count of respiratory events divided by the time of the testing.

Common symptoms of OSA include the following⁶:

●Unexplained daytime sleepiness, restless sleep, and loud snoring (with periods of silence followed by gasps); the severity of EDS does not correlate closely with AHI

●Attention deficit and/or hyperactivity in children

●Trouble concentrating; mood changes such as irritability, anxiety, and treatment-resistant depression and forgetfulness

●Temporomandibular disorder symptoms, sleep bruxism

●Decreased sex drive, sexual dysfunction, and heavy night sweats

Some OSA patients may experience additional symptoms⁷:

●Restless leg syndrome/periodic limb movements

●Restless or fragmented sleep and lack of dreams

●Increased heart rate and/or blood pressure (systemic hypertension), ischemic heart disease, congestive heart failure

●Decline in performance at work

●Dry mouth/throat sensations upon awakening

●Fatigue

●Gastroesophageal reflux disease (GERD)

●Impaired cognition (memory and concentration)

●Insomnia and parasomnias (confusional arousals and sleep-related eating disorders)

●Morning headaches

●Nocturia

●Witnessed apnea

●Nonrestorative or unrefreshing sleep

●Repeated awakenings with gasps or choking

Other medical problems common with patients with OSA include stroke or other ischemic cerebrovascular disease and diabetes and/or insulin resistance. They may experience unexplained weight gain. Drowsiness in the daytime can result in increased industrial and automobile accidents. Some research is linking OSA to cognitive decline such as dementia.⁷

HOW BIG IS THE PROBLEM?

In spite of the severe societal and health consequences of SRBDs, a surprisingly small number of studies have been conducted using PSG to determine the prevalence of OSA in the general population. Most studies performed to date simply extrapolate the data to derive an estimate of SRBD prevalence. It has been estimated that 20 million Americans suffer from moderate to severe OSA and at least one person in five (65 million Americans) has mild OSA. In the late 1980s and early 1990s, three large cohort studies were done in the United States: the Wisconsin Sleep Cohort,⁸ the Sleep Heart Health Study,⁹ and the Penn State Cohort.¹⁰ Based primarily on these three studies, the prevalence of SRBDs was estimated to be between 6.5% and 9% in women and between 17% and 31% in men. However, these prevalence estimates were subsequently revised to 34% in men aged 30 to 70 years and 17% in women aged 30 to 70 years.¹¹ All of these studies are somewhat flawed in that the prevalence of SRBDs was not measured directly by sleep studies but was derived from statistical calculations. Nonetheless, it is conservatively estimated that 52 million Americans have clinically significant OSA.¹²

In 2015, the HypnoLaus Study was published in Lancet and reported a significantly higher incidence of OSA.¹³ In this study, 2,121 citizens of Lausanne, Switzerland, were diagnosed after a full-night PSG (via home sleep apnea testing [HSAT]). Of the participants, 1,024 (48%) were men, and 1,097 (52%) were women. The median age of all participants was 57 years (interquartile range 49 to 68; range 40 to 85), and the mean body mass index (BMI) was 25.6 kg/m².

Figure 1-2 shows the prevalence of SRBDs according to clinically defined categories (mild, moderate, and severe) in the men and women who participated in the HypnoLaus Study. An AHI of five or more events per hour (mild to severe OSA) was recorded in 858 of the 1,024 men in the study. That is 83.8% of the men (95% confidence interval: 81.4–86.0)! In addition, 60.8% of the women had an AHI greater than 5. This study utilized new nasal pressure sensors able to detect small variations in airflow, whereas older studies utilized thermistors, which have decreased sensitivity. Additionally, the HypnoLaus Study employed the more liberal 2012 American Academy of Sleep Medicine (AASM) definition of hypopnea: 3% desaturation. However, neither the flow sensors nor the AASM scoring criterion fully explained these results. Participants in this study were otherwise healthy adults; they were between 40 and 85 years old without obesity (BMI 25.6). And yet out of the 2,121 participants, 72% of them had an AHI greater than 5. Additional findings of this study indicated that an AHI greater than 20.6 events per hour was independently associated with the presence of hypertension, diabetes, metabolic syndrome, and depression.¹⁰

FIG 1-2 Prevalence of SRBDs and sleep apnea syndrome, according to age and sex, as reported by the HypnoLaus Study in 2015. (a) A mild SRBD was defined as between 5 and 14 events per hour, while severe SRBD was defined as at least 30 events per hour. SRBD categories differed by age (P < .0001 in men and in women). (b) Mild sleep apnea syndrome was defined as between 5 and 14 events per hour and an Epworth score greater than 10, moderate sleep apnea syndrome was defined as between 15 and 19 events per hour and an Epworth score greater than 10, and severe sleep apnea syndrome was defined as at least 30 events per hour and an Epworth score greater than 10. Categories of sleep apnea syndrome differed by age (P < .0001 in men and P < .001 in women).

The HypnoLaus study is not the only study to present proof that the incidence of OSA in the general population has been underestimated. In 2010, a study¹⁴ from São Paulo, Brazil, of 1,042 participants (aged 20 to 80 years) found that 46.6% of men and 30.5% of women had an AHI greater than 5. This São Paulo study also utilized the new airflow sensors to measure nasal pressure and showed that 32.8% of participants had OSA syndrome. It should be noted that the nasal sensors utilized in these studies are currently the standard technique utilized in all modern clinical sleep laboratories.

Sadly, children are not immune to airway issues. It has been estimated that 10% of all children suffer from some form of SRBD. A recent study that looked at SRBDs in children seeking orthodontic treatment found that “approximately 7% of adolescent orthodontic patients may be at significant risk for some form of sleep-disordered breathing.”¹⁵ Most of these patients exhibit pronounced snoring or wheezing during sleep. These children may exhibit craniofacial insufficiency, lymphatic hypertrophy in the form of enlarged tonsils or adenoids, narrow arches, and vaulted palates. Some, but not all, are obese. Growth hormones are primarily released during sleep, and therefore disrupted sleep may inhibit normal growth. Patients with childhood OSA frequently present with symptoms of bruxism, mouth breathing, tongue thrusting, and bedwetting and may be failing to thrive. These patients frequently have an existing diagnosis of attention deficit hyperactivity disorder (ADHD), which is a mental disorder characterized by problems paying attention, excessive activity, or difficulty controlling inappropriate behavior. Children with airway issues often exhibit chronic fatigue, which displays as hyperactivity and frequently causes problems in school. Therapy for children with OSA can include adenotonsillectomy, CPAP, myofunctional appliance therapy, and maxillary expansion orthodontic therapy.¹⁶

Given the results of the epidemiologic studies on the prevalence of SRBDs, we can conservatively conclude that 25% or more of your current dental patients have OSA. It has been estimated that only 15% of patients who suffer from OSA have been diagnosed; therefore, OSA is a significant, underdiagnosed, and undertreated chronic disease in the United States. Now is the time for dentists to join our physician colleagues and tackle this devastating disease.

OSA IS A MEDICAL DISEASE

OSA has been determined to be a medical disease by the AASM. It is currently the position of the AASM and the American Medical Association (AMA) that a board-certified sleep physician is the only medical professional qualified to order an overnight sleep test and diagnose SRBDs. Therefore, a dentist must coordinate with a sleep physician to provide oral appliance therapy (OAT), as all diagnoses and treatment planning for SRBD/OSA is provided by a sleep physician. The sleep physician controls the treatment of OSA and determines when OAT is appropriate for a patient. Because OSA is a medical condition, OAT is filed on the patient’s medical insurance or Medicare. There are no dental codes available for benefiting OAT for OSA. This presents a major opportunity to provide OAT and not utilize your patient’s dental insurance benefits.

Many dentists are now partnering with our colleagues in sleep medicine to provide therapy for SRBD patients. SRBDs directly or indirectly affect many biologic systems within the human body; therefore, numerous medical disciplines are involved in the treatment of OSA comorbid conditions. This fact has allowed dentists to develop an extensive physician-based referral practice. Dentists trained in DSM can be a vital member of a multidisciplinary team of health care professionals working together to control this deadly disease.

WHY DO WE HAVE OSA?

OSA is primarily classified as an anatomical problem. The physical characteristics that contribute to the human ability of complex vocalization also places us at risk for OSA. Humans have a flexible upper airway and a suspended mandible that enables speech. This evolutionary advantage places humans at risk for upper airway collapse, which occurs superior to the thyroid cartilage and inferior to the hard palate. During sleep, muscle tone decreases, which can allow inspiratory pressure to collapse the airway in susceptible individuals. The mandible and hyoid bones are suspended, allowing the tongue, soft palate, uvula, and epiglottis to collapse into the airway during sleep, creating a complete or partial obstruction. Furthermore, as modern man has evolved, the human cranium has progressively increased in size and capacity; however, the craniofacial respiratory complex (CFRC) has progressively become smaller. As a result of the smaller oral cavity, the tongue has been progressively displaced posteriorly into the airway. This problem is exacerbated during sleep. The collapsible nature of the upper airway coupled with a narrow maxilla, small mandible, and displaced tongue has placed humans at great risk for airway obstruction.

In addition to the anatomical component of OSA, Western civilization has adopted a fast-food, microwave style of living. The resulting lack of proper diet has resulted in rampant obesity in the United States. OSA is closely linked to obesity and diabetes. These diseases are almost inseparable and have long-term health consequences. According to the Centers for Disease Control and Prevention, approximately 65% of Americans are now overweight or obese. In many states, 35% of the population is obese, with the percentages rising each year. It is estimated that 70% of OSA sufferers are obese.¹⁷ As patients become larger, fat deposits in the base of the tongue and the lateral walls of the airway enlarge as well. Therefore, obesity greatly contributes to or exacerbates OSA.

Additionally, OSA appears to have some roots in the Western practice of bottle-feeding and use of pacifiers and sippy cups. Nonproductive suckling may result in CFRC collapse and increased dental crowding in children, exacerbating childhood sleep disorders.¹⁸ The interaction of a smaller orofacial complex, increased BMI, an aging population base, and decreased levels of exercise have resulted in an explosion of OSA in the United States.

Risk factors

There are several risk factors for OSA:

●Family history of OSA

●Male sex (for adults): male/female (M/F) ratio of 3:1

●Menopausal state in women: Hormone replacement therapy decreases the risk for OSA in postmenopausal patients

●Age: OSA risk increases with age but plateaus after middle age (50 to 55 years of age)

●Obesity or excessive body weight:

›70% of patients with OSA are overweight or obese

›The prevalence of OSA increases in direct proportion to total weight

›The association between BMI and OSA is weaker in the Asian population

›A 10% increase in weight is associated with a sixfold increase in risk for OSA

›Central obesity found within the waist and hips results in more risk for OSA than general obesity

›The risk for OSA is greater if the patient’s waist is greater than 40 inches for men and 36 inches for women

›Obesity increases the risk for OSA by decreasing pharyngeal diameter due to fat deposition; decreasing lung volumes resulting in the loss of caudal traction on the upper airway, which increases the risk for oxygen desaturation; and reducing upper airway muscle tone and neuromuscular control

›OSA may predispose patients to worsening obesity due to modification in leptin, ghrelin, and orexin levels

›Sleep deprivation may increase a patient’s appetite and caloric intake

›OSA may predispose patients to insulin resistance and diabetes mellitus

›OSA may result in daytime somnolence and diminished physical activity

●Snoring

●Craniofacial insufficiency and oropharyngeal anatomical factors:

›Increased neck size (greater than 17 inches in men and 16 inches in women)

›Brachycephaly

›Nasal narrowing and congestion

›Macroglossia (enlarged tongue)

›Elongated soft palate and enlarged uvula (high Mallampati score)

›Narrow dental arches and loss of teeth (edentulous)

›Enlarged tonsils and adenoids, especially in children

›Bruxism

›Occlusal wear

›Lingual and palatal tori

›Scalloped tongue

›Vaulted palate or narrow lateral pharyngeal wall distance (generally the lateral upper airway dimension is more important than the anteroposterior dimension in the predictive risk of OSA)

›Midface hypoplasia, retrognathia, micrognathia, or mandibular hypoplasia

›Caudal displacement of the hyoid bone

●Race: African Americans, Asians and Pacific Islanders, and Hispanics have a greater risk than Caucasians

●Smoking and alcohol use

●Medications: Use of muscle relaxants, sedatives, anesthetics, and opioid analgesics increases AHI and the risk for OSA⁷

THE PHYSICAL AND MONETARY COST OF UNTREATED AND UNDIAGNOSED OSA

During sleep, people should be quiescent. The parasympathetic nervous system should be in control, and blood pressure and heart rates should be at their lowest. Sleep should be a time of physical and mental repair. However, patients with OSA experience repeated sympathetic spikes throughout the night. Hypoxia (absence of oxygen supply) results in a sympathetic response and the resultant release of cortisol, which initiates a cascade of physiologic events known as the fight or flight response. This contributes to sleep disruption (fragmentation) and daytime sleepiness. The carotid bodies are a small cluster of chemoreceptors and supporting cells located near the bifurcation of the carotid arteries. The carotid bodies detect changes in the oxygen/ carbon dioxide (O₂/CO₂) composition of arterial blood. A decrease in the partial pressure of oxygen (PaO₂) and increase in partial pressure of carbon dioxide (PaCO₂) activates the sympathetic nervous system, which causes the patient’s heart rate to elevate, blood pressure to increase, and respiratory effort to increase. The effect of these sympathetic episodes is an increase in chronic disease and shortened life expectancy in untreated OSA patients.

Consequences of untreated OSA include the following⁷:

●Increased mortality (particularly among young and middle-aged adults)

●Decreased SaO₂ and PaO₂, increased PaCO₂ during sleep

●Increased systemic and pulmonary artery pressure: Increased left ventricular and right ventricular output and increased pulmonary ventricular resistance

●Neurocognitive and psychiatric effects:

›Depression and anxiety

›Decreased quality of life

›Decreased alertness and vigilance (likely the result of sleep fragmentation and hypoxemia)

›Impairment of neurocognitive performance (executive function, learning, and memory)

●Sleep fragmentation/disturbance (increased arousals result in EDS and/or insomnia; the severity of EDS correlates better with the degree of sleep fragmentation and not very well with the patient’s AHI)

●Cardiovascular effects:

›Systemic hypertension (independent of obesity): Due to an increase in sympathetic nervous system activity, there is an increase in systolic and diastolic blood pressure, which does not fall during sleep (nondipping)

›The prevalence of OSA increases in drug-resistant hypertension:

●Each additional apnea event per hour of sleep increases the odds of hypertension by about 1%

●Each 10% decrease in nocturnal SaO₂ increases the odds of hypertension by 13%

›Pulmonary hypertension (prevalence of 20% to 70% of OSA patients)

›PAP therapy has been shown to improve OSA-related pulmonary hypertension

›Coronary artery disease (nocturnal angina)

›Sudden cardiac death (typically occurs between 12 and 6 am)

›Congestive heart failure: There is an increased prevalence in patients with OSA due to compromised heart function with both systolic and diastolic dysfunction

›Cardiac arrhythmias: Sinus arrhythmias are most common, and there is an increase in atrial fibrillation; apneic events result in a severe disruption to heart homeostasis

›Cerebrovascular disease: There is an increased risk of stroke in persons with OSA, an increased risk of mortality, and an increased risk of OSA following a stroke

›OSA is associated with an increase in carotid artery intima-media thickness (marker for atherosclerosis)

●Metabolic dysfunction:

›Insulin resistance and altered glucose metabolism

›Increased risk of type 2 diabetes

›Increased serum level of leptin and ghrelin

›Metabolic syndrome (obesity, hypertension, insulin resistance, and dyslipidemia):

●Two-thirds of children with OSA have metabolic syndrome

●One in four children with metabolic syndrome has OSA

●Miscellaneous consequences:

›Increased health care utilization

›Erectile dysfunction

›GERD

›Negative intrathoracic pressure

OSA, combined with societal pressures on sleep, has given birth to a generation of individuals who are dangerously sleepy.¹² Less than 15% of those suffering from OSA have been diagnosed, and of the 8 million patients who have been diagnosed, less than 50% are compliant with CPAP therapy. The economic costs of unmanaged moderate to severe OSA in the United States is estimated to be as much as $165 billion annually.¹² This figure is skewed as it does not include the millions of patients suffering from UARS who are frequently very sleepy and prone to accidents. For clarity, UARS is resistance to breathing during sleep that causes an arousal but does not fit the definition of OSA.

The Harvard study on sleep-disordered breathing indicates that the average person with uncontrolled moderate to severe OSA personally spends between $4,000 and $6,000 each year as a direct result of untreated OSA. These costs come from job absenteeism, medical costs, sleep aids, lost productivity, and accidents.¹²

Today, automobile and truck accidents attributed to excessive sleepiness are commonplace. A recent poll by the National Sleep Foundation found that 60% of adults admit to driving drowsy within the last year. Drowsy drivers are involved in more than 300,000 accidents each year, which results in over 6,000 deaths. Further, 4.5% of drivers surveyed admit to nodding off or falling asleep while driving over the last month. Collision costs associated with drowsy driving are estimated to be $11.1 billion annually. The 2012 National Sleep Foundation poll found that 37.9% of adults in this country admit to unintentionally falling asleep during the day at least once over the last month.

Individuals with OSA are frequently unaware that they are having difficulty breathing during sleep. OSA is most commonly recognized as a problem by family members or bed partners who observe the individual during obstructive episodes. Individuals who sleep alone may be unaware of the condition because no one is present at night to poke them in the ribs. OSA patients may seek medical care for symptoms of fatigue or daytime sleepiness, but not all patients exhibit EDS. Sadly, patients may have OSA for years or even decades without detection because they frequently become conditioned to the daytime sleepiness and fatigue associated with significant levels of sleep disturbance.

WHY ARE WE SO SLEEPY?

There are many reasons people are sleepy, and not all are related to SRBD. Insomnia is the most common sleep disorder and is frequently comorbid with OSA. Insomnia, also known as sleeplessness, is a sleep disorder where patients have difficulty falling asleep or staying asleep as long as desired. Insomnia typically results in daytime sleepiness, low energy, irritability, and a depressed mood. It may result in an increased risk of motor vehicle accidents and problems focusing and learning. Insomnia can be short term, lasting for days or weeks, or long term, lasting for months or years. Insomnia can occur independently or as a result of another problem. Conditions that frequently produce insomnia include OSA, psychologic stress, chronic pain, heart failure, hyperthyroidism, heartburn, restless leg syndrome, menopause, certain medications, and drugs such as caffeine, nicotine, and alcohol. Insomnia can also be directly associated with jet lag or working a night shift or swing shift. Diagnosis is based on history, sleep habits, and an examination to look for underlying causes. Screening may be done with two questions: (1) Do you experience difficulty sleeping? (2) Do you have difficulty falling or staying asleep?

Americans seem to place a low priority on sleep. Our lifestyles glorify long hours of work and study pursuing prosperity. Americans have bought into the relevant cultural norm that sleep deprivation is an essential element in achieving success. However, when a patient complains of fatigue or EDS, our differential diagnosis must include SRBDs. OSA results in sleep fragmentation and arousals that frequently increase a patient’s daytime sleepiness. An arousal is defined as an abrupt change from sleep to wakefulness, or from a “deeper” stage of non–rapid eye movement (NREM) sleep to a “lighter” stage. Frequently, patients are completely unaware that these arousals are occurring during the night. Sleep fragmentation, by definition, is a series of brief arousals occurring throughout the night, reducing the total amount of time spent in the deeper levels of sleep. When a patient experiences frequent arousals secondary to asphyxiation, excessive sleepiness is the frequent outcome. If a patient has OSA and experiences clinically significant EDS, the term obstructive sleep apnea syndrome (OSAS) is used.¹⁹

EDS is typically determined by the Epworth Sleepiness Scale (ESS). The ESS is widely used in the field of sleep medicine as a subjective measure of a patient’s overall sleepiness. The test consists of a list of eight situations in which you rate your tendency to become sleepy on a scale of 0 (no chance of dozing) to 3 (high chance of dozing). The scale estimates whether you are experiencing excessive sleepiness that possibly requires medical attention.¹⁵ Typically, a patient with OSAS has an AHI greater than 5 and an ESS of at least 10.

Subsequent chapters will discuss screening methods and the utilization of the ESS. However, conscientious dental practitioners should be aware of the various causes of sleep deprivation and the resultant EDS. Screening patient populations for OSA based on levels of sleepiness can be unproductive. Other methods of screening, discussed later, seem to result in better specificity.

DIAGNOSING OSA