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Sleep disordered breathing and dentistry: Waking up to reality
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Sleep disordered breathing and dentistry: Waking up to reality Sanjivan Kandasamy Sleep Disordered Breathing (SDB), especially obstructive sleep apnea (OSA) is increasingly recognized today as having health implications for individuals who are suffering from this condition, and especially those who remain undiagnosed and may not be receiving the necessary treatment. OSA has gained significant attention by the dental and orthodontic communities due to its prevalence, its short and long term mental and systemic health consequences, and its manifestation within the vicinity of the dentofacial region. It would appear that many dental professionals, including orthodontists, have taken not only significant responsibility in diagnosing and managing OSA by themselves but also have availed themselves of the financial benefits of this new found means of income and practice growth. The goal of this paper is to examine the various controversies surrounding this issue by reviewing the related literature, and discuss what should be the actual role of our specialty in the diagnosis and management of sleep apnea in clinical practice. (Semin Orthod 2019; &:1–8) © 2019 Published by Elsevier Inc.
Introduction What is sleep disordered breathing? leep disordered breathing (SDB) is defined as a disorder characterized by a combination of some or all of the following: primary snoring, hypoventilation, upper airway resistance syndrome (URAS) involving prolonged partial upper airway obstruction, obstructive sleep apnea (OSA) involving repetitive episodes of complete upper airway obstruction, and central sleep apnea (CSA). All of these disorders essentially disrupt normal ventilation, oxygenation, and sleep quality.1,2 This paper primarily focuses on OSA and its relevance to the dental profession. The prevalence of OSA in the general adult population is approximately 13% of men and 6%
S
Dental School, The University of Western Australia; Private practice, Midland, WA 6056, Australia; Centre for Advanced Dental Education, Saint Louis University, Saint Louis, MO, USA. Correspondence author at: West Australian Orthodontics, Suite 9A, 401 Great Eastern Highway, Midland, WA 6056, Australia. E-mail: [email protected] © 2019 Published by Elsevier Inc. 1073-8746/12/1801-$30.00/0 https://doi.org/10.1053/j.sodo.2019.09.001
of women5 with the general pediatric population ranging in prevalence from 1.2% to 5.7%,2 making this a disease that is likely to be encountered by most clinicians in the dental profession.
Pathophysiology and consequences The consequence of the interruption of normal sleep and breathing patterns due to OSA is the reduction in oxygen levels which has been shown to trigger a cascade of events causing oxidative stress, metabolic alterations, damage to the vascular endothelium, and resultant inflammation. It is this systemic inflammatory response that has been linked to an increased risk of insulin resistance, abnormal lipid profiles, and other metabolic abnormalities.2,4 OSA in the pediatric population has also been shown to lead to cognitive and social impairment, behavioral and mood disturbances, impaired growth, and obesity; It also has been reported to cause cardiovascular complications, primarily starting as increased blood pressure.2 OSA when left untreated in children may progress into adulthood, increasing the risk of diabetes, coronary artery disease, congestive heart failure, myocardial infarction, hypertension, cardiac arrhythmia, stroke, and sudden cardiac death.5,6
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Risk factors
Evolution
The main risk factors that have been shown to predispose a pediatric population to OSA are adenotonsillar hypertrophy, allergies and asthma, obesity, and craniofacial abnormalities.2,3,7,8 Adenotonsillar hypertrophy has been shown to be the primary cause of OSA in children2 and this is also reflective of the period where lymphoid tissues undergo significant hypertrophy,9 around the ages of eight to ten years. It is a common finding for children with OSA to exhibit enlargement after this age.10 Adeno-tonsillectomy is the primary and most effective treatment for this issue11; however, persistence of OSA after surgery has been attributed to the fact that those patients may have pre-existing craniofacial characteristics contributing to the reduced size of the upper airway.8 In both children and adults, obesity has been shown to be an independent and key risk factor in OSA, the prevalence of which is estimated to be as high as 45% in obese subjects.12 Indeed, a 10% reduction in body mass has been shown to result in an improvement in the number of OSA events by 25%.14,13 In general, for both children and adults, OSA occurs as a complex interplay between anatomic and non-anatomic factors. Anatomic factors refer to underlying predisposing craniofacial structural abnormalities and obesity, while nonanatomic factors include phenomena such as pharyngeal dilator muscle function, pharyngeal critical closing pressures, arousal thresholds, respiratory drives and nocturnal rostral fluid shifts.14,15 The presence of an underlying craniofacial abnormality may serve as a significant predisposing factor in individuals who exhibit varying levels of adenotonsillar hypertrophy, allergies, asthma and obesity. Given the prevalence of OSA, its short and long term mental and systemic health consequences, and its manifestation within the vicinity of the dentofacial region, OSA has gained significant attention by the orthodontic profession. The simple fact that air has to pass through the dentofacial region to get to the lungs has prompted many within the dental profession to take significant responsibility in diagnosing and managing OSA by themselves, while also taking advantage of the financial benefits of this new found means of income and practice growth.
This history of sleep medicine is quite unique, with some of the earliest scientific research being reported as early as the late 1800s. The most significant developments occurred in the 1950s, which saw sleep medicine move into the clinical practice of medicine, and then eventually dentistry. Interestingly, it was only in 1996 that the American Medical Association (AMA) recognized sleep medicine as a subspecialty in medicine. The involvement of dentistry in the field of sleep medicine officially occurred in 1991 through the establishment of the so-called Sleep Disorders Dental Society, now known as the American Academy of Dental Sleep Medicine (AADSM).16 Given its more recent beginnings in comparison to other medical health fields and specialties, the area of sleep medicine and dentistry is considered young and has been growing rapidly. Although this rapid growth served to help us better understand, diagnose, and manage sleep patients, it has also led some in the dental profession to diagnose and manage sleep patients without much in the way of direction, structure, supervision, and most importantly sound evidence. At the same time, companies have used this opportunity not only to promote and develop their products, but also to serve as authorities for the dissemination of sleep continuing education (CE). In their CE courses, these companies encourage the use of their products and appliances, aided by strategically groomed key opinion leaders using biased, agenda-based, and financially driven so-called ‘evidence’. Dental practitioners are being lured and convinced that by riding the so called ‘sleep wave’ they will be able to establish a new revenue stream within their practices. While this approach is nothing new when it comes to various controversial topics in dentistry over many decades, what makes this unique is that dentists are now getting involved in the practice of a clinical science which includes many issues that go beyond their scope of training and practice. With all the above factors combined, it is not surprising to see controversial ideas, philosophies, and various techniques/treatments leading not to only a confused dental profession, but also and most importantly over-diagnosed, over-serviced and poorly managed sleep patients. In view of this growing controversy, the Board of Trustees of the American Association of
ARTICLE IN PRESS Sleep disordered breathing and dentistry: Waking up to reality
Orthodontists (AAO), in November 2017, tasked a panel of medical and dental experts in sleep medicine to create a document designed to guide practicing orthodontists on the role of the specialty in the management of obstructive sleep apnea.5 The so-called white paper was released in March 2019.5 This 53-page document is the first major step taken by the orthodontic specialty to provide some guidelines and structure for clinicians who want to know more about sleep apnea and, in the process, provide better treatment to their patients. Another paper by Kandasamy and Goonewardene in 201417 deals with sleep disordered breathing and its potential relationships with Class II malocclusion which further supplements the AAO white paper. The purpose of the present paper is to update the AAO’s white paper in order to candidly discuss the practical and evidence-based reality of the management of sleep apnea in clinical dental practice.
Radiographs Individuals with OSA generally present with maxillary and mandibular retrognathism, reduced upper airway space, increased mandibular plane and a low hyoid position.18 21 It is believed that the retro-positioned maxilla and/or especially the mandible results in a more posterior tongue position, thereby leading to a reduction in pharyngeal airway space and a resultant decrease in airflow during sleep. In long faces, the mandible is again positioned downward and backwards, also resulting in a reduction in pharyngeal airway space. Having these predisposing craniofacial characteristics, however, does not necessarily mean that these individuals have or will develop OSA.22 Most studies have attempted to use radiographs, such as lateral cephalograms and/or cone beam computed tomography (CBCT) scans to assess skeletal position and the size of the posterior airway space; however, no clear-cut causeand-effect relationships between those imaging findings and OSA have been established, given that there are many other factors that influence the development of OSA. Radiographs are usually taken in an upright position with teeth in maximum intercuspation as opposed to a supine, side or prone position, with or without the head turned and with teeth usually apart as is the usual situation during sleep.
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Lateral cephalograms also only provide a crude antero-posterior two-dimensional means to assess the three-dimensional (3D) spatial relationship of the airway and skeletal position. Even with a 3D image such as a CBCT scan (as opposed to using a dynamic computed tomography scan that involves significant radiation and which is beyond the common scope of the dental practice), this is still only one image of a single time point in the dynamic functional breathing cycle of one individual within their own unique skeletal and soft tissue framework.23 Taking into consideration the 3D functional dynamics of breathing, referring to or formulating average values or thresholds of airway volume or skeletal positions from such imaging techniques is not possible. Radiographs are also unable to assess the tone or compliance or collapsibility of the peri-pharyngeal soft tissues (i.e., lateral pharyngeal walls, tongue and soft palate). Radiographs also fail to take into consideration factors such as obesity, the relative distribution of fat in the cervical region, and how individuals function with their own unique airway apparatus which greatly influence their risk of pharyngeal airway collapse during sleep. This is one of the reasons why OSA cannot be diagnosed simply by combining a questionnaire, a clinical examination, and a lateral cephalogram or CBCT scan. Any suspicion of SDB following a screening examination is usually confirmed with overnight polysomnography, the gold standard in the diagnosis of SDB.4 However, companies have a financial interest in the promotion of taking radiographs with their equipment to diagnose OSA and have invested significant time and money to uncover and emphasize any type of association. This potential conflict of interest has caused the misguided many within our specialty to believe, embrace and radiate their patients unnecessarily in an attempt to diagnose OSA.
Extraction The debate on premolar extractions in orthodontics has been around for over 100 years. The majority of the debate historically has centered around whether premolar teeth extractions cause temporomandibular joint disorders, flat faces and lips, and dark buccal corridors, and now it also is being used to explain reduced airway spaces.24
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The belief is that following the extraction of four premolar teeth, the retraction of the upper and lower anterior teeth will encroach the oral space for the tongue, forcing it posteriorly and resulting in a reduction in the oropharyngeal (OP) airway space, thereby predisposing or causing OSA. Although one might argue that intuitively this line of thinking may initially sound logical and thus appealing, it soon loses its intellectual impact when we ask how this presumed reduced space affects the tongue and the OP space when patients sleep on their side, front or back. Indeed, it would seem that gravity would have a greater effect on the tongue than the position of the incisors. When one takes into consideration the underlying issues pertaining to OSA and factors such as pharyngeal dilator muscle function, pharyngeal critical closing pressures, arousal thresholds, and respiratory drives, how could incisor retraction and space closure (in which buccal segments also come forward) have any real influence any of these underlying aetiologic factors? Thus, it is not surprising that well-conducted CBCT studies have found that four premolar teeth extraction followed by incisor retraction did not affect the oropharyngeal volume in comparison to a non-extraction control group.25,26 Larsen and associates in 2015 examined the medical and dental records of 5584 patients to assess the relationship between OSA and premolar teeth extractions. Half of the patients had four premolar teeth missing presumably as a result of orthodontic treatment and the other half did not. The presence or absence of OSA was confirmed by polysomnography. The prevalence of OSA in the extraction versus non-extraction groups was 9.56% and 10.71%, respectively. The small difference was statistically non-significant.27 In summary, based on the current available studies, morphological changes produced by orthodontic treatment such as incisor retraction within the anterior maxilla following premolar teeth extractions have no effect on the oropharyngeal airway space.25 27
other studies have shown relapse to pre-expansion values in many cases.31 33 The variation observed in the findings of these studies are primarily due to the lack of long-term follow-up, the use of small heterogeneous samples with no controls, and differences in the amount of expansion in each subject. In addition, the observed, large individual variability may have exaggerated the effects of expansion on the airway. More recently, studies have shown a significant improvement in apnea-hypopnea index scores in children with sleep apnea following rapid maxillary expansion.34,35 As a result, the authors advocate rapid maxillary expansion before adenotonsillectomy in children as this may reduce the need for the adenotonsillectomy following expansion in a large proportion of cases. According to the inclusion criteria, it would appear that in those studies maxillary expansion might have been carried out in many cases without the presence of a posterior crossbite. Instead, the expansion was prescribed due to the presence of a high palatal vault and narrow maxillary arch related to the contraction of the upper jaw at its base.34,35 Many clinicians have interpreted the results of these studies as a reason to advocate early maxillary expansion as some kind of medical prophylaxis or so-called “vaccination” for preventing the development of OSA in the future. If there is no posterior crossbite, lower arch dental expansion will be required to establish a harmonious transverse relationship. Unlike in the maxilla there is no patent midline mandibular suture, so any expansion in the lower arch is purely dentoalveolar tipping. This effect has been shown to be limiting and unstable in the long term.36 43 Unfortunately, advocating maxillary expansion on the sole basis of addressing airway issues or OSA when there is no obvious posterior crossbite is neither evidence-based nor justified. This approach would lead to significant bite opening, posterior scissors bite, and unfavorable dentoalveolar compensations.
Expansion A narrow maxilla has been suggested as a predisposing craniofacial morphological risk factor for OSA. Studies have shown an improvement in airway dimension and reduction in nasal resistance following maxillary expansion.28 30 However,
Scope of practice, competency, and informed consent Specialist and general dental practitioners generally are aware of their ability or limitations, what they have been trained to do and what is
ARTICLE IN PRESS Sleep disordered breathing and dentistry: Waking up to reality
expected of them in terms of standards of care and treatment outcomes. Presumably, they are also aware of the professional, ethical, and legal ramifications of failing to deliver at one or more of these levels. When it comes to malpractice complaints, it appears that most complaints are due to performance issues related to failure to attain adequate informed consent and to provide appropriate and timely treatment. Other complaints include issues regarding fees and false and misleading advertising creating unreasonable expectations.44 47 These complaints occur during the routine practice of what dental practitioners are trained to do routinely. Let us assume that the majority of clinicians are striving to ‘do the right thing’ routinely. Even with the best intentions, things do not always go according to expectations due to events that in some instances are unforeseeable and sometimes beyond the control of the clinician. So what happens when a clinician ventures beyond their scope of practice, understanding, or training in the diagnosis and management of sleep patients? Sleep disordered breathing, respiratory physiology, and medicine and/or dental sleep medicine are not routinely taught in undergraduate and post graduate dental and specialist dental programs. Untutored knowledge obtained from key-opinion leaders and companies often is not enough for clinicians to carry out treatment on patients with sleep disordered breathing. What is the value of an informed consent when the patient has not been made aware of the clinician’s probable lack of understanding, training and skill to diagnose and render care to a reasonable standard and manage any complications that arise in a sleep patient? If something goes wrong, will this be covered by their dental professional indemnity insurers? Should the patient be referred to another practitioner, specialist, or physician with sufficient training and ability to improve the prospects of a successful outcome and minimize risks? The standard of care generally refers to the care and skill of reputable members of the same profession practicing under similar circumstances. What is the standard of care when it comes to the sleep patient in dental practice? Firstly, it is not the same standard of care as in the practice of a respiratory physician, as some dental sleep medicine “experts” might like us to believe. If it were, then these dental practitioners would need to be held to the same standards of peer review,
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continuing education, malpractice premiums, patient complications, and overall medical management as respiratory physicians. When complications arise in the management of a sleep patient, such as cardiovascular or diabetic issues, for example, who is responsible? Certainly not a dentist or an orthodontist. These medical conditions are certainly by no means analogous to dental complications that occur in dental practice, such as a fractured endodontic file or a restoration overhang causing a food trap and gingival inflammation. It is important for dental practitioners to realize that no matter how exciting, intellectually stimulating, practice enhancing, or financially lucrative it is to ‘flirt’ with sleep medicine, this is one field that is genuinely beyond the scope of a dental practitioner. At best, if a dental practitioner is to be involved in the multidisciplinary care of a sleep patient, it is always carried out under the overall medical supervision of the patient’s primary care physician.
Practical reality To briefly summarize the findings from the AAO’s 53-page white paper, Orthodontists are strongly recommended to screen their patients for signs and symptoms of OSA using various recommended questionnaires along with a thorough clinical examination; Orthodontists are advised to refer to the appropriate medical specialists for further evaluation and a definitive diagnosis; If interested and appropriately trained, orthodontists can participate in the treatment of OSA with oral appliance therapy as well as monitor and manage their side effects. Orthodontists are to participate in the interdisciplinary care of an OSA patient in order to achieve the best outcome for the patient; The AAO may consider developing a separate health history form for OSA or include it in the current health forms; Screening should consider recording the patients’ height, weight and neck size and as well as calculating patients’ body-mass index; and The AAO might also consider whether the definition of orthodontics needs modification relative to OSA.
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Orthodontics is not short on controversial topics. Despite sound evidence-based data available these controversies often continue to exist for many decades. OSA is the new controversy, but it appears that this new controversy exhibits a similar theme to the others. We would like to believe that those who have embraced diagnosing and managing OSA in clinical dental and orthodontic practice are innovators and pioneers aiming to break new ground in patient care, gaining enough experience and understanding to ultimately disseminate this knowledge to the rest of the profession. Is this the case? Perhaps for the minority. Unfortunately, even with sound evidence-based information available, many clinicians continue to persist with their experiencebased view, ideas and philosophies. Today the sleep movement appears to be primarily financially motivated with interested parties including orthodontic and dental companies and associated clinicians keen on finding another avenue to generate an income and market their business. Is there any harm in being a sleep centered or airway friendly orthodontist? Perhaps not. But let’s put it another way; what do you think a malocclusion centered sleep physician’s agenda is? What would this sleep physician be trying to sell or marketing his/her practice as being different to others? There is certainly a business angle to this sleep movement. There is no doubt as orthodontists, amongst other things orthodontics related we are in the business of straightening teeth. But when does the needs of the business surpass the needs and best interests of the patient? More importantly, is it ethical to subtly mask the needs of the business as concern for the welfare and long-term systemic health of the patient when it comes to proposing orthodontic treatment as a means for reducing the risk of or curing OSA in patients? No. As stomatological doctors, we all understand that the risks of leaving OSA untreated in the long term may increase the risk of diabetes, coronary artery disease, congestive heart failure, hypertension, cardiac arrhythmia, myocardial infarction, stroke and sudden cardiac death. But does knowing these risks mean that every time a patient sits in the dental chair we have an obligation to concentrate on finding OSA problems and proceed to preventing or fixing them? Can we justify doing that by thinking that if so-called sleep curing
orthodontic treatment is not carried out now or early or ever our patients will be at risk one day of developing amongst other diseases, myocardial infarctions, strokes and sudden cardiac deaths? Is there enough evidence now to have an excuse to market and promote non-extraction treatments with various appliances, administer expansion that is otherwise unnecessary, and take unnecessary radiographs and measurements to diagnose OSA, all under the proviso of preventing or curing OSA patients from eventually developing amongst other diseases myocardial infarctions, strokes and sudden cardiac death? Based on what we know currently, it would be fair to ask just how does the medical significance of OSA really fit in to the day to day practice of orthodontics? What happened to all those patients who were not properly screened for OSA by their orthodontist in the last 100 years? Have significant numbers of them developed amongst other OSA related diseases, myocardial infarctions, strokes, and sudden cardiac deaths? Are they coughing and gasping for air in bed while struggling to get a good night’s sleep because at some point in the past their orthodontist failed them by not detecting the signs and symptoms of OSA and administering the appropriate care? No data exists to answer those questions. I understand that as orthodontists, it is recommended that we screen for signs and symptoms of OSA. But what if we do not? Are we responsible for all the ensuing consequences? Is this burden our responsibility to shoulder? Where is the patient’s family doctor during all this? He is probably too busy screening for malocclusions and temporomandibular disorders. When do we stop being orthodontists and start playing doctor? If we are to take responsibility for screening OSA, why then has there been such little emphasis on screening and managing real world issues such obesity for example? Obesity increases the risks of developing a multitude of diseases including OSA. Where is the white paper on orthodontics and obesity? Where do we draw the line? Do we need to also start taking vital signs, urine samples, mouth swabs and carrying out pap smears and blood tests as well? The reason for this is simple. There is little or no financial benefit in promoting or marketing an orthodontic business as so-called obesity centered or aware.
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Conclusion When it comes to OSA in clinical orthodontic practice, orthodontists may choose to play a role in the screening process of OSA. They may also take further interest and training to get involved in the diagnosis and management of OSA patients with either oral appliances or orthognathic surgery as part of a multidisciplinary approach to the overall care of these patients. What orthodontists choose to do is up to each individual clinician; but to market and promote non-extraction treatments with various appliances, vaccinate patients with expansion, and take unnecessary radiographs and measurements to diagnose OSA under the proviso that they are essentially preventing or curing OSA patients, however, is simply unethical. To expect orthodontists to shoulder the responsibility of detecting airway issues in patients today or in the future is clearly unreasonable, although there is no doubt that the least we could do is aim to screen for any obvious airway issues if present. To expect any more at this stage is unsubstantiated by the available evidence. Orthodontics used to be considered a “thinking man’s specialty.” Has this specialty evolved from being primarily concerned with craniofacial growth and development, biomechanics, occlusion and facial and dental aesthetics, to one that now includes OSA in order to augment the economics of clinical practice first, followed by evidence-based patient care as a second or even third level of professional responsibility?
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syndrome: 12-month follow-up. Sleep Med. 2007;8(2): 128–134. Pirelli P, Saponara M, Guilleminault C. Rapidmaxiallary expansion before and after adenotonsillectomy in children with obstructive sleep apnea. Somnologie. 2012;16:125–132. Sinclair P, Little R. Maturation of untreated normal occlusion. Am J Orthod. 1983;83(2):114–123. Bishara SE, Jakobsen JR, Treder J, Nowak A. Arch width changes from 6 weeks to 45 years of age. Am J Orthod Dentofac Orthop. 1997;111(4):401–409. Little RM, Riedel RA, Artun J. An evaluation of changes in mandibular anterior alignment from 10 to 20 years of postretention. Am J Orthod Dentofac Orthop. 1988;93(5):423–428. Little RM. Stability and relapse: early treatment of arch length deficiency. Am J Orthod Dentofac Orthop. 2002;121 (6):578–581. Lagravere MO, Heo G, Major PW, Flores-Mir C. Metaanalysis of immediate changes with rapid maxillary expansion treatment. J Am Dent Assoc. 2006;137(1):44–53. Lagravere MO, Major PW, Flores-Mir C. Long-term dental arch changes after rapid maxillary expansion treatment: a systematic review. Angle Orthod. 2005:155–161. Schiffman PH, Tuncay OC. Maxillary expansion: a meta analysis. Clin Orthod Res. 2001;4(2):86–96. Little R, Reidel R. Postretention evaluation of stability and relapse: mandibular arches with generalized spacing. Am J Orthod Dentofacial Orthop. 1989;95(1):37–41. Thomas LA, Tibble H, Too LS, Hopcraft MS, Bismark MM. Complaints about dental practitioners: an analysis of 6 years of complaints about dentists, dental prosthetists, oral health therapists, dental therapists and dental hygienists in Australia. Aust Dent J. 2018;63(3):285–293. Dym H. Risk management in the dental office. Dent Clin N Am. 2012;56(1):113–120. Lok V, Kruger E, Tennant M. Patient complaints in dentistry: a Western Australian retrospective analysis 1996 2004. Asia Pac J Health Manage. 2007;2:34. Jerrold L. Informed consent and orthodontics. Am J Orthod Dentofac Orthop. 1988;93(3):251–258.
Sleep disordered breathing and dentistry: Waking up to reality Sanjivan Kandasamy Sleep Disordered Breathing (SDB), especially obstructive sleep apnea (OSA) is increasingly recognized today as having health implications for individuals who are suffering from this condition, and especially those who remain undiagnosed and may not be receiving the necessary treatment. OSA has gained significant attention by the dental and orthodontic communities due to its prevalence, its short and long term mental and systemic health consequences, and its manifestation within the vicinity of the dentofacial region. It would appear that many dental professionals, including orthodontists, have taken not only significant responsibility in diagnosing and managing OSA by themselves but also have availed themselves of the financial benefits of this new found means of income and practice growth. The goal of this paper is to examine the various controversies surrounding this issue by reviewing the related literature, and discuss what should be the actual role of our specialty in the diagnosis and management of sleep apnea in clinical practice. (Semin Orthod 2019; &:1–8) © 2019 Published by Elsevier Inc.
Introduction What is sleep disordered breathing? leep disordered breathing (SDB) is defined as a disorder characterized by a combination of some or all of the following: primary snoring, hypoventilation, upper airway resistance syndrome (URAS) involving prolonged partial upper airway obstruction, obstructive sleep apnea (OSA) involving repetitive episodes of complete upper airway obstruction, and central sleep apnea (CSA). All of these disorders essentially disrupt normal ventilation, oxygenation, and sleep quality.1,2 This paper primarily focuses on OSA and its relevance to the dental profession. The prevalence of OSA in the general adult population is approximately 13% of men and 6%
S
Dental School, The University of Western Australia; Private practice, Midland, WA 6056, Australia; Centre for Advanced Dental Education, Saint Louis University, Saint Louis, MO, USA. Correspondence author at: West Australian Orthodontics, Suite 9A, 401 Great Eastern Highway, Midland, WA 6056, Australia. E-mail: [email protected] © 2019 Published by Elsevier Inc. 1073-8746/12/1801-$30.00/0 https://doi.org/10.1053/j.sodo.2019.09.001
of women5 with the general pediatric population ranging in prevalence from 1.2% to 5.7%,2 making this a disease that is likely to be encountered by most clinicians in the dental profession.
Pathophysiology and consequences The consequence of the interruption of normal sleep and breathing patterns due to OSA is the reduction in oxygen levels which has been shown to trigger a cascade of events causing oxidative stress, metabolic alterations, damage to the vascular endothelium, and resultant inflammation. It is this systemic inflammatory response that has been linked to an increased risk of insulin resistance, abnormal lipid profiles, and other metabolic abnormalities.2,4 OSA in the pediatric population has also been shown to lead to cognitive and social impairment, behavioral and mood disturbances, impaired growth, and obesity; It also has been reported to cause cardiovascular complications, primarily starting as increased blood pressure.2 OSA when left untreated in children may progress into adulthood, increasing the risk of diabetes, coronary artery disease, congestive heart failure, myocardial infarction, hypertension, cardiac arrhythmia, stroke, and sudden cardiac death.5,6
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Risk factors
Evolution
The main risk factors that have been shown to predispose a pediatric population to OSA are adenotonsillar hypertrophy, allergies and asthma, obesity, and craniofacial abnormalities.2,3,7,8 Adenotonsillar hypertrophy has been shown to be the primary cause of OSA in children2 and this is also reflective of the period where lymphoid tissues undergo significant hypertrophy,9 around the ages of eight to ten years. It is a common finding for children with OSA to exhibit enlargement after this age.10 Adeno-tonsillectomy is the primary and most effective treatment for this issue11; however, persistence of OSA after surgery has been attributed to the fact that those patients may have pre-existing craniofacial characteristics contributing to the reduced size of the upper airway.8 In both children and adults, obesity has been shown to be an independent and key risk factor in OSA, the prevalence of which is estimated to be as high as 45% in obese subjects.12 Indeed, a 10% reduction in body mass has been shown to result in an improvement in the number of OSA events by 25%.14,13 In general, for both children and adults, OSA occurs as a complex interplay between anatomic and non-anatomic factors. Anatomic factors refer to underlying predisposing craniofacial structural abnormalities and obesity, while nonanatomic factors include phenomena such as pharyngeal dilator muscle function, pharyngeal critical closing pressures, arousal thresholds, respiratory drives and nocturnal rostral fluid shifts.14,15 The presence of an underlying craniofacial abnormality may serve as a significant predisposing factor in individuals who exhibit varying levels of adenotonsillar hypertrophy, allergies, asthma and obesity. Given the prevalence of OSA, its short and long term mental and systemic health consequences, and its manifestation within the vicinity of the dentofacial region, OSA has gained significant attention by the orthodontic profession. The simple fact that air has to pass through the dentofacial region to get to the lungs has prompted many within the dental profession to take significant responsibility in diagnosing and managing OSA by themselves, while also taking advantage of the financial benefits of this new found means of income and practice growth.
This history of sleep medicine is quite unique, with some of the earliest scientific research being reported as early as the late 1800s. The most significant developments occurred in the 1950s, which saw sleep medicine move into the clinical practice of medicine, and then eventually dentistry. Interestingly, it was only in 1996 that the American Medical Association (AMA) recognized sleep medicine as a subspecialty in medicine. The involvement of dentistry in the field of sleep medicine officially occurred in 1991 through the establishment of the so-called Sleep Disorders Dental Society, now known as the American Academy of Dental Sleep Medicine (AADSM).16 Given its more recent beginnings in comparison to other medical health fields and specialties, the area of sleep medicine and dentistry is considered young and has been growing rapidly. Although this rapid growth served to help us better understand, diagnose, and manage sleep patients, it has also led some in the dental profession to diagnose and manage sleep patients without much in the way of direction, structure, supervision, and most importantly sound evidence. At the same time, companies have used this opportunity not only to promote and develop their products, but also to serve as authorities for the dissemination of sleep continuing education (CE). In their CE courses, these companies encourage the use of their products and appliances, aided by strategically groomed key opinion leaders using biased, agenda-based, and financially driven so-called ‘evidence’. Dental practitioners are being lured and convinced that by riding the so called ‘sleep wave’ they will be able to establish a new revenue stream within their practices. While this approach is nothing new when it comes to various controversial topics in dentistry over many decades, what makes this unique is that dentists are now getting involved in the practice of a clinical science which includes many issues that go beyond their scope of training and practice. With all the above factors combined, it is not surprising to see controversial ideas, philosophies, and various techniques/treatments leading not to only a confused dental profession, but also and most importantly over-diagnosed, over-serviced and poorly managed sleep patients. In view of this growing controversy, the Board of Trustees of the American Association of
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Orthodontists (AAO), in November 2017, tasked a panel of medical and dental experts in sleep medicine to create a document designed to guide practicing orthodontists on the role of the specialty in the management of obstructive sleep apnea.5 The so-called white paper was released in March 2019.5 This 53-page document is the first major step taken by the orthodontic specialty to provide some guidelines and structure for clinicians who want to know more about sleep apnea and, in the process, provide better treatment to their patients. Another paper by Kandasamy and Goonewardene in 201417 deals with sleep disordered breathing and its potential relationships with Class II malocclusion which further supplements the AAO white paper. The purpose of the present paper is to update the AAO’s white paper in order to candidly discuss the practical and evidence-based reality of the management of sleep apnea in clinical dental practice.
Radiographs Individuals with OSA generally present with maxillary and mandibular retrognathism, reduced upper airway space, increased mandibular plane and a low hyoid position.18 21 It is believed that the retro-positioned maxilla and/or especially the mandible results in a more posterior tongue position, thereby leading to a reduction in pharyngeal airway space and a resultant decrease in airflow during sleep. In long faces, the mandible is again positioned downward and backwards, also resulting in a reduction in pharyngeal airway space. Having these predisposing craniofacial characteristics, however, does not necessarily mean that these individuals have or will develop OSA.22 Most studies have attempted to use radiographs, such as lateral cephalograms and/or cone beam computed tomography (CBCT) scans to assess skeletal position and the size of the posterior airway space; however, no clear-cut causeand-effect relationships between those imaging findings and OSA have been established, given that there are many other factors that influence the development of OSA. Radiographs are usually taken in an upright position with teeth in maximum intercuspation as opposed to a supine, side or prone position, with or without the head turned and with teeth usually apart as is the usual situation during sleep.
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Lateral cephalograms also only provide a crude antero-posterior two-dimensional means to assess the three-dimensional (3D) spatial relationship of the airway and skeletal position. Even with a 3D image such as a CBCT scan (as opposed to using a dynamic computed tomography scan that involves significant radiation and which is beyond the common scope of the dental practice), this is still only one image of a single time point in the dynamic functional breathing cycle of one individual within their own unique skeletal and soft tissue framework.23 Taking into consideration the 3D functional dynamics of breathing, referring to or formulating average values or thresholds of airway volume or skeletal positions from such imaging techniques is not possible. Radiographs are also unable to assess the tone or compliance or collapsibility of the peri-pharyngeal soft tissues (i.e., lateral pharyngeal walls, tongue and soft palate). Radiographs also fail to take into consideration factors such as obesity, the relative distribution of fat in the cervical region, and how individuals function with their own unique airway apparatus which greatly influence their risk of pharyngeal airway collapse during sleep. This is one of the reasons why OSA cannot be diagnosed simply by combining a questionnaire, a clinical examination, and a lateral cephalogram or CBCT scan. Any suspicion of SDB following a screening examination is usually confirmed with overnight polysomnography, the gold standard in the diagnosis of SDB.4 However, companies have a financial interest in the promotion of taking radiographs with their equipment to diagnose OSA and have invested significant time and money to uncover and emphasize any type of association. This potential conflict of interest has caused the misguided many within our specialty to believe, embrace and radiate their patients unnecessarily in an attempt to diagnose OSA.
Extraction The debate on premolar extractions in orthodontics has been around for over 100 years. The majority of the debate historically has centered around whether premolar teeth extractions cause temporomandibular joint disorders, flat faces and lips, and dark buccal corridors, and now it also is being used to explain reduced airway spaces.24
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The belief is that following the extraction of four premolar teeth, the retraction of the upper and lower anterior teeth will encroach the oral space for the tongue, forcing it posteriorly and resulting in a reduction in the oropharyngeal (OP) airway space, thereby predisposing or causing OSA. Although one might argue that intuitively this line of thinking may initially sound logical and thus appealing, it soon loses its intellectual impact when we ask how this presumed reduced space affects the tongue and the OP space when patients sleep on their side, front or back. Indeed, it would seem that gravity would have a greater effect on the tongue than the position of the incisors. When one takes into consideration the underlying issues pertaining to OSA and factors such as pharyngeal dilator muscle function, pharyngeal critical closing pressures, arousal thresholds, and respiratory drives, how could incisor retraction and space closure (in which buccal segments also come forward) have any real influence any of these underlying aetiologic factors? Thus, it is not surprising that well-conducted CBCT studies have found that four premolar teeth extraction followed by incisor retraction did not affect the oropharyngeal volume in comparison to a non-extraction control group.25,26 Larsen and associates in 2015 examined the medical and dental records of 5584 patients to assess the relationship between OSA and premolar teeth extractions. Half of the patients had four premolar teeth missing presumably as a result of orthodontic treatment and the other half did not. The presence or absence of OSA was confirmed by polysomnography. The prevalence of OSA in the extraction versus non-extraction groups was 9.56% and 10.71%, respectively. The small difference was statistically non-significant.27 In summary, based on the current available studies, morphological changes produced by orthodontic treatment such as incisor retraction within the anterior maxilla following premolar teeth extractions have no effect on the oropharyngeal airway space.25 27
other studies have shown relapse to pre-expansion values in many cases.31 33 The variation observed in the findings of these studies are primarily due to the lack of long-term follow-up, the use of small heterogeneous samples with no controls, and differences in the amount of expansion in each subject. In addition, the observed, large individual variability may have exaggerated the effects of expansion on the airway. More recently, studies have shown a significant improvement in apnea-hypopnea index scores in children with sleep apnea following rapid maxillary expansion.34,35 As a result, the authors advocate rapid maxillary expansion before adenotonsillectomy in children as this may reduce the need for the adenotonsillectomy following expansion in a large proportion of cases. According to the inclusion criteria, it would appear that in those studies maxillary expansion might have been carried out in many cases without the presence of a posterior crossbite. Instead, the expansion was prescribed due to the presence of a high palatal vault and narrow maxillary arch related to the contraction of the upper jaw at its base.34,35 Many clinicians have interpreted the results of these studies as a reason to advocate early maxillary expansion as some kind of medical prophylaxis or so-called “vaccination” for preventing the development of OSA in the future. If there is no posterior crossbite, lower arch dental expansion will be required to establish a harmonious transverse relationship. Unlike in the maxilla there is no patent midline mandibular suture, so any expansion in the lower arch is purely dentoalveolar tipping. This effect has been shown to be limiting and unstable in the long term.36 43 Unfortunately, advocating maxillary expansion on the sole basis of addressing airway issues or OSA when there is no obvious posterior crossbite is neither evidence-based nor justified. This approach would lead to significant bite opening, posterior scissors bite, and unfavorable dentoalveolar compensations.
Expansion A narrow maxilla has been suggested as a predisposing craniofacial morphological risk factor for OSA. Studies have shown an improvement in airway dimension and reduction in nasal resistance following maxillary expansion.28 30 However,
Scope of practice, competency, and informed consent Specialist and general dental practitioners generally are aware of their ability or limitations, what they have been trained to do and what is
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expected of them in terms of standards of care and treatment outcomes. Presumably, they are also aware of the professional, ethical, and legal ramifications of failing to deliver at one or more of these levels. When it comes to malpractice complaints, it appears that most complaints are due to performance issues related to failure to attain adequate informed consent and to provide appropriate and timely treatment. Other complaints include issues regarding fees and false and misleading advertising creating unreasonable expectations.44 47 These complaints occur during the routine practice of what dental practitioners are trained to do routinely. Let us assume that the majority of clinicians are striving to ‘do the right thing’ routinely. Even with the best intentions, things do not always go according to expectations due to events that in some instances are unforeseeable and sometimes beyond the control of the clinician. So what happens when a clinician ventures beyond their scope of practice, understanding, or training in the diagnosis and management of sleep patients? Sleep disordered breathing, respiratory physiology, and medicine and/or dental sleep medicine are not routinely taught in undergraduate and post graduate dental and specialist dental programs. Untutored knowledge obtained from key-opinion leaders and companies often is not enough for clinicians to carry out treatment on patients with sleep disordered breathing. What is the value of an informed consent when the patient has not been made aware of the clinician’s probable lack of understanding, training and skill to diagnose and render care to a reasonable standard and manage any complications that arise in a sleep patient? If something goes wrong, will this be covered by their dental professional indemnity insurers? Should the patient be referred to another practitioner, specialist, or physician with sufficient training and ability to improve the prospects of a successful outcome and minimize risks? The standard of care generally refers to the care and skill of reputable members of the same profession practicing under similar circumstances. What is the standard of care when it comes to the sleep patient in dental practice? Firstly, it is not the same standard of care as in the practice of a respiratory physician, as some dental sleep medicine “experts” might like us to believe. If it were, then these dental practitioners would need to be held to the same standards of peer review,
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continuing education, malpractice premiums, patient complications, and overall medical management as respiratory physicians. When complications arise in the management of a sleep patient, such as cardiovascular or diabetic issues, for example, who is responsible? Certainly not a dentist or an orthodontist. These medical conditions are certainly by no means analogous to dental complications that occur in dental practice, such as a fractured endodontic file or a restoration overhang causing a food trap and gingival inflammation. It is important for dental practitioners to realize that no matter how exciting, intellectually stimulating, practice enhancing, or financially lucrative it is to ‘flirt’ with sleep medicine, this is one field that is genuinely beyond the scope of a dental practitioner. At best, if a dental practitioner is to be involved in the multidisciplinary care of a sleep patient, it is always carried out under the overall medical supervision of the patient’s primary care physician.
Practical reality To briefly summarize the findings from the AAO’s 53-page white paper, Orthodontists are strongly recommended to screen their patients for signs and symptoms of OSA using various recommended questionnaires along with a thorough clinical examination; Orthodontists are advised to refer to the appropriate medical specialists for further evaluation and a definitive diagnosis; If interested and appropriately trained, orthodontists can participate in the treatment of OSA with oral appliance therapy as well as monitor and manage their side effects. Orthodontists are to participate in the interdisciplinary care of an OSA patient in order to achieve the best outcome for the patient; The AAO may consider developing a separate health history form for OSA or include it in the current health forms; Screening should consider recording the patients’ height, weight and neck size and as well as calculating patients’ body-mass index; and The AAO might also consider whether the definition of orthodontics needs modification relative to OSA.
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Orthodontics is not short on controversial topics. Despite sound evidence-based data available these controversies often continue to exist for many decades. OSA is the new controversy, but it appears that this new controversy exhibits a similar theme to the others. We would like to believe that those who have embraced diagnosing and managing OSA in clinical dental and orthodontic practice are innovators and pioneers aiming to break new ground in patient care, gaining enough experience and understanding to ultimately disseminate this knowledge to the rest of the profession. Is this the case? Perhaps for the minority. Unfortunately, even with sound evidence-based information available, many clinicians continue to persist with their experiencebased view, ideas and philosophies. Today the sleep movement appears to be primarily financially motivated with interested parties including orthodontic and dental companies and associated clinicians keen on finding another avenue to generate an income and market their business. Is there any harm in being a sleep centered or airway friendly orthodontist? Perhaps not. But let’s put it another way; what do you think a malocclusion centered sleep physician’s agenda is? What would this sleep physician be trying to sell or marketing his/her practice as being different to others? There is certainly a business angle to this sleep movement. There is no doubt as orthodontists, amongst other things orthodontics related we are in the business of straightening teeth. But when does the needs of the business surpass the needs and best interests of the patient? More importantly, is it ethical to subtly mask the needs of the business as concern for the welfare and long-term systemic health of the patient when it comes to proposing orthodontic treatment as a means for reducing the risk of or curing OSA in patients? No. As stomatological doctors, we all understand that the risks of leaving OSA untreated in the long term may increase the risk of diabetes, coronary artery disease, congestive heart failure, hypertension, cardiac arrhythmia, myocardial infarction, stroke and sudden cardiac death. But does knowing these risks mean that every time a patient sits in the dental chair we have an obligation to concentrate on finding OSA problems and proceed to preventing or fixing them? Can we justify doing that by thinking that if so-called sleep curing
orthodontic treatment is not carried out now or early or ever our patients will be at risk one day of developing amongst other diseases, myocardial infarctions, strokes and sudden cardiac deaths? Is there enough evidence now to have an excuse to market and promote non-extraction treatments with various appliances, administer expansion that is otherwise unnecessary, and take unnecessary radiographs and measurements to diagnose OSA, all under the proviso of preventing or curing OSA patients from eventually developing amongst other diseases myocardial infarctions, strokes and sudden cardiac death? Based on what we know currently, it would be fair to ask just how does the medical significance of OSA really fit in to the day to day practice of orthodontics? What happened to all those patients who were not properly screened for OSA by their orthodontist in the last 100 years? Have significant numbers of them developed amongst other OSA related diseases, myocardial infarctions, strokes, and sudden cardiac deaths? Are they coughing and gasping for air in bed while struggling to get a good night’s sleep because at some point in the past their orthodontist failed them by not detecting the signs and symptoms of OSA and administering the appropriate care? No data exists to answer those questions. I understand that as orthodontists, it is recommended that we screen for signs and symptoms of OSA. But what if we do not? Are we responsible for all the ensuing consequences? Is this burden our responsibility to shoulder? Where is the patient’s family doctor during all this? He is probably too busy screening for malocclusions and temporomandibular disorders. When do we stop being orthodontists and start playing doctor? If we are to take responsibility for screening OSA, why then has there been such little emphasis on screening and managing real world issues such obesity for example? Obesity increases the risks of developing a multitude of diseases including OSA. Where is the white paper on orthodontics and obesity? Where do we draw the line? Do we need to also start taking vital signs, urine samples, mouth swabs and carrying out pap smears and blood tests as well? The reason for this is simple. There is little or no financial benefit in promoting or marketing an orthodontic business as so-called obesity centered or aware.
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Conclusion When it comes to OSA in clinical orthodontic practice, orthodontists may choose to play a role in the screening process of OSA. They may also take further interest and training to get involved in the diagnosis and management of OSA patients with either oral appliances or orthognathic surgery as part of a multidisciplinary approach to the overall care of these patients. What orthodontists choose to do is up to each individual clinician; but to market and promote non-extraction treatments with various appliances, vaccinate patients with expansion, and take unnecessary radiographs and measurements to diagnose OSA under the proviso that they are essentially preventing or curing OSA patients, however, is simply unethical. To expect orthodontists to shoulder the responsibility of detecting airway issues in patients today or in the future is clearly unreasonable, although there is no doubt that the least we could do is aim to screen for any obvious airway issues if present. To expect any more at this stage is unsubstantiated by the available evidence. Orthodontics used to be considered a “thinking man’s specialty.” Has this specialty evolved from being primarily concerned with craniofacial growth and development, biomechanics, occlusion and facial and dental aesthetics, to one that now includes OSA in order to augment the economics of clinical practice first, followed by evidence-based patient care as a second or even third level of professional responsibility?
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