reading

Professor of Oral Medicine and Canada Research Chair in Pain, Sleep and Trauma
Dean, Faculty of Dental Medicine
University of Montreal

Sleep and Biological Rhythm Center and Department of Surgery
Montreal Sacré-Coeur Hospital
Montreal, Quebec, Canada

Professor of Respiratory Medicine
Head, Discipline of Sleep Medicine
University of Sydney

Director, Centre for Sleep Health and Research
Royal North Shore Hospital
Sydney, New South Wales, Australia

Associate Professor of Psychiatry and Behavioral Sciences
Director, Behavioral Sleep Medicine Program
Johns Hopkins University School of Medicine
Baltimore, Maryland

1. Sleep disorders. 2. Dentistry. I. Lavigne, Gilles J. II. Cistulli, Peter A. III. Smith, Michael T. (Michael Timothy), 1967-

Quintessence Publishing Co, Inc
4350 Chandler Drive
Hanover Park, IL 60133
www.quintpub.com

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: Bryn Goates
Cover and internal design: Gina Ruffolo
Production: Patrick Penney

1 The Nature of Sleep
Gilles J. Lavigne, Charles M. Morin, Maria Clotilde Carra

3 Classification of Sleep Disorders
Gilles J. Lavigne, Raphael C. Heinzer, Peter A. Cistulli, Michael T. Smith

4 Sleep-Related Breathing Disorders
Andrew S. L. Chan, Richard W. W. Lee, Peter A. Cistulli

5 Pathophysiology of Obstructive Sleep Apnea
Andrew S. L. Chan, Richard W. W. Lee, Gilles J. Lavigne, Peter A. Cistulli

6 Long-term Consequences of Obstructive Sleep Apnea
Craig L. Phillips, Keith Wong

7 Clinical Approach to Diagnosis of Obstructive Sleep Apnea
Richard W. W. Lee, Andrew S. L. Chan, Peter A. Cistulli

8 Upper Airway Imaging in Obstructive Sleep Apnea
François-Louis Comyn, Richard J. Schwab

9 An Overview of Obstructive Sleep Apnea Treatment
Peter R. Buchanan, Ronald R. Grunstein

11 Dentofacial Orthopedics
M. Ali Darendeliler, Lam L. Cheng, Paola Pirelli, Peter A. Cistulli

12 Definitions, Epidemiology, and Etiology of Sleep Bruxism
Frank Lobbezoo, Ghizlane Aarab, Jacques van der Zaag

14 Clinical Approach to Diagnosis of Sleep Bruxism
Kiyoshi Koyano, Yoshihiro Tsukiyama

15 Pathophysiology of Sleep Bruxism
Gilles J. Lavigne, Henri Tuomilehto, Guido Macaluso

18 Pathophysiologic Conceptualizations of Chronic Pain
Claudia M. Campbell, Robert R. Edwards

19 Mechanisms of Sleep Loss–Pain Interactions
Monika Haack, Jennifer Scott-Sutherland, Navil Sethna, Janet M. Mullington

20 Clinical Implications of Sleep Loss–Pain Interactions
Monika Haack, Jennifer Scott-Sutherland, Navil Sethna, Janet M. Mullington

21 Association of Orofacial Pain Conditions and Sleep Disturbance
Peter Svensson, Lene Baad-Hansen, Taro Arima

22 Impact of Common Temporomandibular Disorder Comorbidities on Sleep Quality and Orofacial Pain
Luis F. Buenaver, Edward G. Grace

23 Pharmacologic Management of Sleep-Pain Interactions
Brian E. Cairns, Parisa Gazerani

24 Nonpharmacologic Management of Insomnia and Pain
Nicole K. Y. Tang, Michael T. Smith

To our students and research associates
who have contributed to the progress in dental sleep medicine

Healthy sleep is vital for mental and physical well-being, and yet our understanding of the mechanisms that link sleep processes and brain and body function is relatively new. Until the discovery of rapid eye movement (REM) sleep in the 1950s, sleep was considered a passive state without particular import in the medical context. Today we understand that sleep is an active process that subserves many functions of the brain and body. In 1989, publication of the first book on sleep medicine (The Principles and Practice of Sleep Medicine, edited by Kryger et al) heralded sleep as a specialty in its own right. In a similar way, this new textbook heralds another phase in the development of clinical sleep practice for dental practitioners.

In his historical account of sleep medicine, Bill Dement points out that sleep apnea was overlooked by pulmonologists and otolaryngologists because they did not consider sleep. It was equally true that those doing research in human sleep (mostly neurologists and psychiatrists) also missed sleep apnea because they did not consider breathing. The great irony about the emergence of dental sleep medicine is that generations of dentists have looked in the mouths of countless individuals with sleep-disordered breathing without knowing of the disorder. Given that the dentist is often the first and only health care practitioner to look in the oral cavity, a good knowledge of sleep apnea should be part of the profession’s knowledge base. From a broader perspective, these examples underscore the importance of a multidisciplinary approach; very few centers bring physician, surgeon, and dentist together to develop a management plan.

This book provides a compact introduction to sleep disorders. Appropriately, many chapters focus on sleep-disordered breathing because the dentist has a potentially major role in both its recognition and treatment. While continuous positive airway pressure (CPAP) remains the first-line therapy for sleep apnea, there is an important role for mandibular advancement appliances, which require adequate fitting by a well-informed dentist to be effective.

In addition, we should identify children who are at risk of developing sleep apnea. Approximately 10% of children who snore most nights are likely future apnea patients. Management plans designed to promote the growth of the upper airway and to prevent obesity provide a possibility for real prevention. This will happen only if the dental profession engages actively in the area.

The editors and contributors of this book are to be congratulated on putting together the first comprehensive text on dental sleep medicine.

Colin E Sullivan, AO, MB BS, PhD, FRACP, FTSE, FAA
Professor of Respiratory Medicine
Department of Medicine
University of Sydney
Sydney, New South Wales, Australia

The science and clinical implications of sleep medicine should resonate strongly with the dental profession. Not only does the physiologic and behavioral state of our own and indeed our patients’ sleep experiences involve a significant part of daily life, but dental sleep medicine is a rapidly evolving area of health care. A number of recognized sleep-related disorders have relevance to dental practice, and consequently, the availability of a book devoted to this subject has long been overdue. The book editors and authors collectively have impeccable academic credentials and clinical experience, and they have produced a lucid and apposite synthesis of the many topics that bear on sleep medicine and its particular applicability to dental practice.

The book is organized into four sections that deal first with general aspects of sleep and sleep disorders, then specifically sleep breathing disorders, sleep bruxism and other sleep-related movement disorders, and finally sleep–orofacial pain interactions. The inclusion of an exhaustive range of pertinent topics has ensured a perceptive and balanced approach to the subject. Unlike so many multi-authored texts on equally complex and fascinating health-related subjects, this one provides a mix of science, common sense, and pragmatism, particularly in the review of the management of sleep-related disorders.

We believe that this will prove to be a seminal text for the dental profession. It could very well turn out to be the catalyst required for the subject of dental sleep medicine to be included as an integral part of dental school curricula. The editors are to be commended for breaking new ground and ushering in an era of better understanding of a subject that has been relatively neglected in dental education and practice. Traditional and exclusive preoccupations with teeth, masticatory function, and related disorders—staples of dental education and texts—can now be broadened to include an awareness of our bodies’ more extensive physiology and behavior.

George A. Zarb, BChD, DDS, MS, MS, FRCD(C)
Professor Emeritus
Department of Prosthodontics
Faculty of Dentistry
University of Toronto
Toronto, Ontario, Canada

Barry J. Sessle, MDS, PhD, DSc(hc), FRSC, FCAHS
Professor and Canada Research Chair in Craniofacial Pain and Sensorimotor Function
Faculties of Dentistry and Medicine
University of Toronto
Toronto, Ontario, Canada

The last 50 years have seen remarkable advances in the study of circadian biology and the neurophysiology of sleep. The genes that regulate these biologic rhythms have been isolated, and interactions between sleep and almost all other body systems (eg, respiratory, cardiovascular, endocrine, and neurologic) have become a focus for research. These scientific advances have emanated from diverse clinical disciplines, including internal medicine, pulmonology, neurology, otorhinolaryngology, pediatric medicine, psychiatry, psychology, and nursing. The range in specialties reflects the interdisciplinary nature of sleep and its disorders, and many critical contributions have also come from the field of dentistry. Currently, approximately 100 distinct clinical sleep disorders have been recognized. Certain disorders, including sleep apnea, sleep bruxism, and chronic pain, have a direct bearing on the practice of dentistry, which makes a working understanding of sleep biology (somnology) and sleep pathology (sleep medicine) a useful and necessary addition to the knowledge base of dental practitioners.

Sleep disorders decrease the quality of sleep by breaking its continuity, ie, they trigger a physiologic response that tends to push a sleeping person to a sublevel of wakefulness. Although the sleeping individual is unaware, his or her brain and autonomic nervous system are under a state of transient arousal. It is normal to observe brief arousals during sleep, but when these are too frequent or too long, they can cause mood alterations, memory problems, and performance deficits in healthy subjects after only a few days. Disordered breathing during sleep may cause serious alteration to patients’ daytime vigilance, resulting in an increased risk of transport- or work-related accidents. In the long term, sleep apnea is known to be a serious and potentially modifiable factor for cardiovascular disease, including heart failure and stroke. The intrusion of snoring and tooth-grinding sounds are also a major cause of sleep disruption for the patient’s bed partner and can be a source of marital conflict.

Orofacial pain may be associated with delayed sleep onset and disturbed sleep continuity; hence, it is a major cause of insomnia that may predispose patients to mood alteration and depression. Poor sleep is known to impair pain processing and can directly contribute to pain augmentation. Therefore, the prevention and management of sleep disorders should become a routine component of the treatment plan for chronic orofacial pain–related conditions.

Sleep medicine is often an overlooked part of public health. In many countries, access to sleep medicine constitutes a major public health challenge. In countries where therapy is available, treating sleep disturbances either as primary disorders or as comorbidities with other medical, psychiatric, or dental conditions is a significant opportunity to improve and prevent medical and psychiatric morbidity. It may also minimize the substantial financial burden related to the direct and indirect consequences of disturbed sleep. In Australia, for example, the overall cost of sleep disorders in 2004 was estimated to be US $7.5 billion with indirect costs of $808 million in related motor vehicle accidents.

The dentist plays an important role in sleep medicine by examining patients during their annual or biannual dental checkup for the risk of sleep-disordered breathing. Patients reporting snoring, sleepiness, and morning headaches in the presence of obesity, large tonsils, and/or dental malformation (eg, retrognathia, deep palate, large tongue) need to be guided by dentists to see their otorhinolaryngologist, respiratory-pulmonologist, or physician, as well as a sleep medicine expert. To manage the sound and tooth damage or pain generated by bruxism, oral appliances can be used, but the dentist needs to understand when such an appliance is indicated and the risks associated with its use. In cases where surgery is indicated, maxillofacial surgeons or otorhinolaryngologists collaborate closely with dentists to provide treatment.

When patients complain of morning headaches and temporomandibular disorders (TMDs), the exclusion of breathing disorders is a critical decision that is usually made in collaboration with the sleep medicine specialist, pulmonologist, neurologist, psychiatrist, and internal medicine physician. Dentists should refer patients who experience sleep bruxism in combination with a TMD for polysomnographic evaluation when they also complain of significant insomnia or poor sleep, even if they do not meet the traditional risk factors for sleep apnea. An increasing body of data suggests that both sleep bruxism and TMDs, which often occur in females of normal weight, are associated with increased risk for sleep disorder breathing.

Dentists caring for patients with chronic orofacial pain conditions (such as TMDs) also need to understand basic sleep hygiene principles and to know when to refer patients with chronic or intractable insomnia for behavioral sleep medicine evaluation. Behavioral treatments for chronic insomnia are considered first-line interventions over pharmacologic treatment options. A subset of chronic orofacial pain patients presents with a complex psychologic overlay that contributes to their ongoing pain and disability, a combination that can be managed by sleep psychologists working in conjunction with the interdisciplinary team.

The key aim of Sleep Medicine for Dentists is to provide a rapid source of practical information to students, practicing dentists, and scientists. Section I introduces dental sleep medicine, while sections II to IV provide an overview of how to understand, recognize, and manage sleep disorders such as sleep apnea, sleep bruxism, and orofacial pain, which often interfere with or intrude into sleep and are critically important to the practice of dentistry.

Dental sleep medicine is a rapidly evolving field of preventive medicine. However, there remains a shortage of well-trained dental sleep medicine specialists. Those learning more about this field will discover an exciting interdisciplinary arena that is rife with opportunities to develop new dental interventions to treat complex clinical situations and improve the health and well-being of the estimated 20% of the population suffering from sleep disorders.

Gilles J. Lavigne, DMD, MSc, PhD, FRCD(C)
Charles M. Morin, PhD
Maria Clotilde Carra, DMD

In the animal kingdom, sleep is a universal and imperative biologic process to maintain and restore health. Sleep is defined as a physiologic and behavioral state characterized by partial isolation from the environment. A baby’s cry, the vibration of an earthquake, or a sudden pain intrusion will all interrupt sleep continuity; a sleeping brain maintains a sentinel function to awaken the organism for protection purposes.

The duration of sleep usually is 6 to 9 hours in adults. Although most adults sleep an average of 7.5 hours, some are short sleepers and some are long sleepers (ie, less than 5.5 hours and more than 9.0 hours, respectively). Good sleep quality is usually associated with a sense of having slept continuously through the night and feeling refreshed and alert on awakening in the morning. The perception of sleep quality is subjective, however, and varies widely among individuals. Some individuals perceive their sleep as satisfying most of the time, and some consistently report being poor sleepers (eg, having difficulties in initiating or maintaining sleep, feeling unrefreshed when they awaken, and having nightmares). However, sleep recording systems indicate that, in general, poor sleepers tend to underestimate the length of time they sleep (as do some good sleepers).

It is essential for dentists entering the field of dental sleep medicine to recognize sleep disorders, such as insomnia, respiratory or movement disorders (eg, snoring, obstructive sleep apnea, bruxism, gastroesophageal reflux), and pain interference. The direct and indirect costs of sleep disorders in Australia were estimated at US $7.5 billion for 2004.¹ The diagnosis, prevention, and management of sleep disorders are currently domains of high impact in public health (eg, prevention of breathing disorders from childhood, management of daytime sleepiness to decrease the risk of transportation accidents, and the relationship of hypertension and sleep apnea). An understanding of the nature of sleep is essential to the dentist’s role in management of such problems. The neurobiology of sleep is described in chapter 2, and a classification of the various sleep disorders relevant to dentistry is presented in chapter 3.

Like the management of pain, the diagnosis and management of sleep disorders are interdisciplinary. Dentists can achieve advances in sleep disorder management through collaboration with physicians (including pulmonologists, psychiatrists, neurologists, and surgeons), psychologists, respiratory therapists, and physical therapists.

Sleep entails several functions, including physical recovery, biochemical refreshment (eg, synaptic function), memory consolidation, and emotional regulation²^–⁶ (Box 1-1). Lack of sleep is also known as sleep deprivation, that is, insufficient sleep resulting from short sleep duration or loss of a sleep segment because of environmental factors (eg, noise) or a contributing medical condition (eg, pain or diabetes). An experiment in young individuals comparing the consequences of sleep deprivation (4 hours of sleep over 3 to 4 days) to the effects of the subjects’ usual 8 hours of sleep showed that sleep deprivation triggers mood alteration, sociability dysfunction, and complaints of bodily pain.⁷ A persistent reduction in sleep duration can cause physical and mental health problems because of the cumulative effect of lack of sleep on several physiologic functions.

Box 1-1 Functions of sleep

Fatigue reversal

• Sleep allows the individual to recover and reenergize.

Biochemical refreshment

• Sleep promotes synaptic efficiency, protein synthesis, neurogenesis, metabolic (eg, glycogen) restoration, growth (secretion of growth hormone peaks during sleep), etc.

Immune function

• Reset or protection.

Memory

• Daytime learning needs sleep for memory consolidation.

• Sleep seems to facilitate encoding of new information.

Psychologic well-being

• Dreams occur in all sleep stages. REM dreams are more vivid.

• Lack of sleep presents a risk of mood alteration to depression.

Moreover, both too-short and too-long sleep durations have been associated with higher risks of diseases and mortality. However, the complicated interactions among lifestyle, mortality risk, and sleep duration remain to be understood.⁸ In fact, there is some evidence to support the relationship between sleep duration (too little or too much) and the risk of cardiovascular diseases (such as myocardial infarction and atherosclerosis), diabetes, obesity, depression, and even cancer.⁷^–¹⁰ Although these risk estimates are modest, they have been reproduced in too many studies to reject the putative effect of cumulative sleep debt on health maintenance. Higher risks of myocardial infarction have been found in women who are short sleepers as well as women who are long sleepers.⁹ Elevated risks of cardiovascular problems and atherosclerosis also have been reported in people who sleep too much during the day.¹⁰

Because dentists are health professionals who, in some countries, see more than 50% of the population each year for annual dental checkups, they are in an excellent position to convey the message of the importance of good sleep habits for overall health.

An adult’s 24-hour cycle is divided into 16 hours of wakefulness and 8 hours of sleep. Synchronization and equilibrium between the sleep-wake cycle and feeding behaviors are essential for survival. Mismatches in the synchronization of the feeding cue and metabolic activity are associated with eating disorders.¹¹ Poor sleep can cause health problems, as already discussed, and can increase the risk of transportation- and work-related accidents and even death (see section II).¹

The propensity to sleep is directly dependent on the duration of the prior wakefulness episode. As the duration of wakefulness increases, sleep pressure accumulates and builds to a critical point, when sleep onset is reached. As this sleep pressure increases, an alerting circadian signal helps the person to remain awake throughout the day. The ongoing 24-hour circadian rhythm therefore runs parallel to the homeostasis process, also known as process S (Fig 1-1). The S process corresponds to the sleep pressure that individuals accumulate during the wakefulness period before being able to fall asleep. With increasing sleep pressure, sleep is proportionally longer and deeper in the following recovery period.

9780867155448_lavigne_0018_001

Fig 1-1 Normal cycle for circadian rhythm (process C) (black arrow) and process S (black line/dashed arrow) over about 24 hours. During wakefulness periods, the increase in sleep pressure (dotted line), parallels the increase in fatigue (gray arrow) and results in sleep (dashed and dotted gray line) at a given time over a 24-hour circadian cycle.

Changes in the frequency of slow-wave sleep waves can be estimated by a mathematic transformation of brain wave electrical signals or by quantitative spectral analysis of the electroencephalographic (EEG) activity. Rising or rebound of slow-wave EEG activity in the first hours of sleep is a marker of sleep debt.¹² In contrast, a reduction in slow-wave activity is observed in patients with chronic pain.¹³ However, the cause-and-effect association of these biologic signals with reports of fatigue and poor sleep is unknown. During the day, the effects of energy expenditure are accumulated, which may be connected to the feeling of tiredness.

Two times in the 24-hour cycle are characterized by a strong sleep pressure, 4 PM and 4 AM, +/-1 to 2 hours (see Fig 1-1). At a certain point, sleep pressure is so powerful that an individual will fall asleep regardless of the method or strategies used to remain awake.

Humans tend to alternate between a period of wakefulness lasting approximately 16 hours and a continuous block of 8 hours of sleep (see Fig 1-1). Most mammals sleep around a 24-hour cycle that is driven by clock genes that control the circadian rhythm (process C). Light helps humans synchronize their rhythm with the cycles of the sun and moon by sending a retinal signal (melanopsin) to the hypothalamic suprachiasmatic nucleus. The suprachiasmatic nucleus is a network of brain cells and genes that acts as a pacemaker to control the circadian timing function.¹⁴

The investigation of sleep-wake process C uses biologic markers to assess a given individual’s rhythm. A slight drop (hundredths of a degree centigrade) in body temperature and a rise in salivary and blood melatonin and growth hormone release—peaking in the first hours of sleep, around midnight in the 24-hour cycle—are key indications of the acrophase (high peak) of the process C. Interestingly, corticotropins (adrenocorticotropic hormone and cortisol) reach a nadir (lowest level) during the first hour of sleep. They then reach an acrophase in the second half of the¹¹^,¹⁵ The process C can also be studied using temperature recordings in relation to hormone release and polygraphy to measure brain, muscle, and heart activities.

Under the 24-hour process C of sleep and wakefulness, sleep onset and maintenance are governed by an ultradian cycle of three to five periods in which the brain, muscles, and autonomic cardiac and respiratory activities fluctuate (Figs 1-2 and 1-3). These cycles consist of rapid eye movement (REM) sleep (active stage) and non-REM sleep (light and deep stages). The REM stage is known as paradoxical sleep in Europe.

9780867155448_lavigne_0019_001

Fig 1-2 One non-REM-to-REM cycle of consecutive sleep stages. This cycle is repeated every 70 to 110 minutes for a total of three to five non-REM-to-REM cycles per sleep period.

9780867155448_lavigne_0020_001

Fig 1-3 Consecutive waves of non-REM-to-REM (solid horizontal boxes) sleep cycles (I to IV). During the first third of the night, slow-wave sleep (stages 3 and 4) is dominant. During the last third of the night, the REM stage is longer. (MT) movement time; (WT) wake time. (Adapted from Lavigne et al¹⁶ with permission.)

In humans, a clear decline in electrical brain and muscle activities as well as heart rhythm is observed from wakefulness to sleep onset. This decline is associated with a synchronization of brain waves toward stage 1 sleep. Stage 1 is a transitional period between wakefulness and sleep. Stage 2 sleep then begins, accounting for about 50% to 60% of total sleep duration. Stage 2 sleep is characterized by two EEG signals, K-complexes (brief, high-amplitude brain waves) and spindles (rapid, springlike EEG waves), both of which are described as sleep-promoting and sleep-preserving factors. Sleep stages 1 and 2 are categorized as light sleep.

Next, sleep enters a quiet period known as deep sleep, or stages 3 and 4. These stages are characterized by slow, high-amplitude brain wave activities. Stages 3 and 4 are usually scored together and are characterized by a dominance of slow-wave activity (delta sleep = 0.5 to 4.5 Hz). This sleep period is associated with a so-called sleep recovery process.

Finally, sleep enters an ascension period and rapidly turns into either light sleep or REM sleep. REM sleep is associated with a reduction in the tone of postural muscles (which is poorly described as “atonia” in literature but is in fact hypotonia because muscle tone is never zero) and a rise in heart rate and brain activity to levels that frequently surpass the rates observed during wakefulness. Humans can dream in all stages of sleep, but REM dreams may involve intensely vivid imagery with fantastic and creative content. During REM sleep, the body is typically in a paralyzed-like state (muscle hypotonia). Otherwise, dreams with intense emotional content and motor activity might cause body movements that could injure individuals and their sleep partners.

An understanding of the presence of ultradian sleep cycles is relevant because certain pathologic events occur during sleep, including the following sleep disorders:

• Most periodic body movements (leg or arm) and jaw movements, such as sleep bruxism, are observed in stage 2 sleep and with less frequency in REM sleep.

• Sleep-related breathing events, such as apnea and hypopnea (cessation or reduction of breathing), are observed in stage 2 and REM sleep.

• Acted dreams with risk of body injury, diagnosed as the sleep movement disorder REM behavior disorder, occur during REM sleep (see chapter 3).

When a polygraphic sleep record of a sleeping patient (collected either at home with an ambulatory system or in a sleep laboratory) is assessed, the scoring of sleep fragmentation is a key element in assessing sleep quality. Poor sleep quality, as reported subjectively by the patient, is associated with frequent arousals, with or without body movements, frequent stage shifts (from a deeper to a lighter sleep stage), respiratory disturbances, and higher muscle tone. All these signs of sleep fragmentation interrupt the continuity of sleep and alter the sleep architecture.

Sleep efficiency is another important variable to evaluate through sleep recordings. A standard index of sleep impairment, sleep efficiency is defined as the amount of time asleep divided by the amount of time spent in bed, expressed as a percentage. Sleep efficiency greater than 90% is an indicator of good sleep.

The ultradian cycle of sleep, described previously, includes another repetitive activity: sleep-related arousals. During non-REM sleep, arousals are recurrent (6 to 14 times per hour of sleep), involving brief (3 to 10 seconds) awakenings associated with increased brain, muscle, and heart activities (tachycardia, or rapid heart rate) in the absence of the return of consciousness.¹⁷^–¹⁹ In the presence of sleep movements, breathing disorders, or chronic pain, these arousals are more frequent. Sleep arousals can be viewed as the body’s attempt to prepare the sleeping individual (who is in a low-vigilance state) to react to a potential risk, ie, a fight-or-flight state.

Sleep arousals are concomitant with or precede most periodic limb movements and sleep bruxism (described in section III). In contrast, sleep apnea and hypopnea (described in section II) are respiratory distress–like events that trigger sleep arousals. An index of motor events (leg or oromotor), respiratory disturbances, and frequency of shifts in sleep stage can be calculated to assess the presence of periodic limb movements, bruxism, snoring, and sleep-related apnea and hypopnea (see chapter 3 and sections II to IV for more information).

In addition to these methods to assess sleep fragmentation, the cyclic alternating pattern (CAP) can be used to evaluate the instability of sleep. CAP is an infraslow oscillation, with a periodicity of 20 to 40 seconds, between the sleep maintenance system and the arousal pressure involved in the dynamic organization of non-REM sleep and the activation of motor events. CAP is the estimate of the dominance of active phasic arousal periods, that is, the rise in heart rate, muscle tone, and EEG activities (phase A), over more stable and quiet sleep periods (phase B).¹⁹^–²¹ The active phase is subclassified as A1, a period that promotes sleep onset and maintenance; A2, a transition phase; and A3, the final phase, or the arousal window, involving a marked increase in muscle tone and cardiorespiratory rate. Most sleep bruxism events are scored in phase A3 (see chapter 15).

People appear to have individual levels of tolerance for sleep fragmentation. These levels may be genetically determined. Nevertheless, recurrent sleep deprivation or fragmentation produces a cumulative sleep debt, which in turn is likely to increase complaints of fatigue, memory and mood dysfunction, and bodily pain. The cause-and-effect relationship remains to be confirmed.

The human sleep-wake pattern changes with biologic maturation and aging. In the first 6 weeks of life, human infants mainly present a specific sleep stage, REM sleep, which occupies about 50% of their sleep time. Around age 6 to 9 months, their wakefulness and nighttime sleep pattern tends to become more synchronized with their parents’ feeding and sleeping schedule.²² Preschool children sleep about 14 hours per 24-hour cycle, and most stop napping somewhere between the ages of 3 and 5 years.

Pre-adolescents are sleep-wake phase advanced. They fall asleep earlier and awaken earlier than middle-aged adults. At the age of 16 years, teenagers tend to sleep about 9 hours per 24 hours (ranging from 6.5 to 9.5 hours). Teenagers tend to be phase delayed. They fall asleep and awaken later than their parents and younger siblings.

Most adults sleep about 6 to 7 hours on work days and more on the weekends. By about the age of 40 years, adults’ sleep starts to become more fragile, and individuals are more aware of being awake for a few seconds to a few minutes a night. In the elderly, the sleep-wake pattern returns to a multiphase pattern typical of young children. Elderly people go to sleep earlier than middle-aged adults and awaken earlier in the morning, taking occasional naps (catnapping) during the day.

The human biologic clock can adapt to sleep deprivation and changes in the sleep-wake schedule within certain limits. For example, some people can adapt better than others to jet lag or sleep deprivation because of night work, but most individuals find such variations difficult.

The relevance of this information for dental clinicians is evident. Treating certain patients early in the morning (teenagers tend to sleep until 11 AM) is not always a rewarding experience. Similarly, treating patients at their usual nap time can be challenging because the patient may experience more discomfort and express more complaints. Moreover, pain sensitivity may increase toward the end of the afternoon and evening.²³^,²⁴ Therefore, it may be advisable to schedule an intervention at a time when the person is more alert, responsive, and cooperative and has a higher pain threshold.

Good-quality sleep allows humans a means of physical recovery, biochemical refreshment, memory consolidation, and emotional regulation. The diagnosis, prevention, and management of disorders that interfere with the quality of sleep are currently domains of high impact in public health. Dentists should work with other health professionals to improve sleep disorder management for their patients. Strategies to improve the efficacy of the sleep-wake process, such as light exposure, exercise, general sleep hygiene, a relaxing situation, and use of medications, are described in the following chapters.

1. Hillman DR, Murphy AS, Pezzullo L. The economic cost of sleep disorders. Sleep 2006;29:299–305.

2. Siegel JM. The REM sleep-memory consolidation hypothesis. Science 2001;294(5544):1058–1063.

3. Siegel JM. The stuff dreams are made of: Anatomical substrates of REM sleep. Nat Neurosci 2006;9:721–722.

5. Saper CB, Cano G, Scammell TE. Homeostatic, circadian, and emotional regulation of sleep. J Comp Neurol 2005;493: 92–98.

6. Tononi G, Cirelli C. Sleep function and synaptic homeostasis. Sleep Med Rev 2006;10:49–62.

7. Haack M, Mullington JM. Sustained sleep restriction reduces emotional and physical well-being. Pain 2005;119:56–64.

8. Hublin C, Partinen M, Koskenvuo M, Kaprio J. Sleep and mortality: A population-based 22-year follow-up study. Sleep 2007;30:1245–1253.

9. Meisinger C, Heier M, Löwel H, Schneider A, Döring A. Sleep duration and sleep complaints and risk of myocardial infarction in middle-aged men and women from the general population: The MONICA/KORA Augsburg cohort study. Sleep 2007;30:1121–1127.

10. Stang A, Dragano N, Poole C, et al. Daily siesta, cardiovascular risk factors, and measures of subclinical atherosclerosis: Results of the Heinz Nixdorf Recall Study. Sleep 2007;30: 1111–1119.

11. Van Carter E. Endocrine physiology. In: Kryger MH, Roth T, Dement WC (eds). Principles and Practice of Sleep Medicine. Philadelphia: Elsevier Saunders, 2005:266–282.

12. Borbély AA, Achermann P. Sleep homeostasis and models of sleep regulation. In: Kryger MH, Roth T, Dement WC (eds). Principles and Practice of Sleep Medicine, ed 4. Philadelphia: Saunders, 2005:405–417.

13. Lavigne GJ, McMillan D, Zucconi M. Pain and sleep. In: Kryger MH, Roth T, Dement WC (eds). Philadelphia: Elsevier Saunders, 2005:1246–1255.

14. Moore RY. Suprachiasmatic nucleus in sleep-wake regulation. Sleep Med 2007;8:S27–S33.

15. Kluge M, Schüssler P, Künzel HE, Dresier M, Yassouridis A, Steiger A. Increased nocturnal secretion of ACTH and cortisol in obsessive compulsive disorder. J Psychiatr Res 2007; 41:928–933.

16. Lavigne GJ, Kato T, Mayer P. Pain and sleep disturbances. In: Sessle BJ, Lavigne GJ, Lund JP, Dubner R (eds). Orofacial Pain: From Basic Science to Clinical Management, ed 2. Chicago: Quintessence, 2008:125–132.

17. EEG arousals: Scoring rules and examples. A preliminary report from the Sleep Disorders Atlas Task Force of the American Sleep Disorders Association. Sleep 1992;15:173–184.

18. Boselli M, Parrino L, Smerieri A, Terzano MG. Effect of age on EEG arousals in normal sleep. Sleep 1998;21:351–357.

19. Parrino L, Zucconi M, Terzano GM. Sleep fragmentation and arousal in the pain patient. In: Lavigne G, Sessle BJ, Choinière M, Soja PJ (eds). Sleep and Pain. Seattle: IASP Press, 2007: 213–234.

20. Terzano MG, Parrino L. Origin and significance of the cyclic alternating pattern (CAP). Sleep Med Rev 2000;4:101–123.

21. Parrino L, Smerieri A, Spaggiari MC, Terzano GM. Cyclic alternating pattern (CAP) and epilepsy during sleep: How a physiological rhythm modulates a pathological event. Clin Neurophysiol 2000;111(suppl 1):S39–S46.

22. Iglowstein I, Jenni OG, Molinari L, Largo RH. Sleep duration from infancy to adolescence: Reference values and generational trends. Pediatrics 2003;111:302–307.

23. Bentley AJ. Pain perception during sleep and circadian influences: The experimental evidence. In: Lavigne G, Sessle BJ, Choinière M, Soja PJ (eds). Sleep and Pain. Seattle: IASP Press, 2007:123–136.

24. Kundermann B, Lautenbacher S. Effects of impaired sleep quality and sleep deprivation on diurnal pain perception. In: Lavigne G, Sessle BJ, Choinière M, Soja PJ (eds). Sleep and Pain. Seattle: IASP Press, 2007:137–152.

Sleep is the state during which the organism restores energy that has been exhausted during daily activity. This resting function, which was known since ancient times, has also been believed to extend to the brain, the structure that is the prime controlling organ of states of vigilance. However, numerous results of recent research have converged to emphasize that, in contrast to this long-held belief, the sleeping brain is the host of numerous and complex activities that are, at least partially, at odds with the cerebral activity during wakefulness.

Humans spend between 23% (older adults) and 67% (infants) of their time in sleep. This state encompasses two major and distinct states: the so-called slow-wave sleep, also known as non–rapid eye movement (non-REM) or quiet sleep, and paradoxical sleep, also known as rapid eye movement (REM) or active sleep (see chapter 1). Although most sleep states can produce dreams, REM dreams are associated with more active and fantastic content.

Sleep can be defined by means of behavioral criteria, such as reduced mobility and responsiveness to external stimuli, closed eyes, characteristic posture, and reversible unconsciousness, as well as electrophysiologic parameters. These parameters, including electrical activity of the brain, muscle activity, and ocular movements, are demonstrated on polygraphic recordings of electroencephalograms (EEGs), electromyograms (EMGs), and electrooculograms (EOGs), respectively.

• Which key structures are responsible for the genesis of sleep and for the switching among various vigilance states?

As will be shown in this chapter, some of these questions have been answered, some are still under debate, and others are unresolved.