Predicting and preventing sleep-disordered breathing.
By Regina Patrick, RPSGT
An estimated 12 to 18 million Americans are affected by sleep-disordered breathing (SDB),1 which involves interruptions in the rhythmicity of respiration or impaired ventilation in the lungs during sleep. SDB can induce frequent arousals from sleep. Some consequences of the arousals can be excessive daytime sleepiness, impaired cognition, decreased attention span, and inattentiveness. Some well-known risk factors for SDB are obesity, age, and male gender. However, less familiar risk factors for SDB such as craniofacial structure, infant feeding method, maternal smoking, and enlarged tonsils or adenoids may be missed by clinicians and allow a person with SDB to remain undiagnosed.
SDB is a feature of several respiratory disorders such as central sleep apnea, Cheyne-Stokes respiration, hypoventilation, and obstructive sleep apnea (OSA). OSA is the most common SDB disorder and most widely studied. It affects about 20% of adults in the United States, and scientists believe that about 90% of people who have OSA may be undiagnosed.2
Scientists use various factors to predict a person’s risk of having OSA, based on their demographics, symptoms, and body-mass index. Using these factors, scientists can correctly identify 76% to 96% of patients who have OSA and 13% to 54% of patients who do not have OSA.3 However, because of the great disparity in each of these ranges, scientists continue efforts to improve identifying people who may have OSA.
In keeping with the goal of improving predictability, Lee3 and associates recently measured the predictive value of face width, eye width, cervicomental angle, and mandibular length. Photographs of 180 sleep study patients with suspected OSA were taken before they underwent the sleep study.
Based on the sleep study, OSA was present in 114 patients. Using a mathematical formula that incorporated face width, eye width, cervicomental angle, and mandibular length (as measured from the photographs), Lee correctly identified 76.1% of patients who did or did not have OSA. He furthermore found that three of the four factors—eye width, face width, and mandibular length—could each be predictive of a person’s having OSA. Lee suggests that eye width is predictive of OSA since the width of one’s eyes is correlated with the dimensions of the cranial base. (Alterations in the dimensions of the cranial base, such as having a narrow maxilla, can play a role in SDB.)
Other researchers have focused on various dentofacial features for predicting SDB in children. For example, Tsuda4 and colleagues examined 173 pediatric orthodontic patients who ranged in age from 8 to nearly 13 years old. The children’s parents filled out the OSA-18 questionnaire, which assesses SDB risk in children; it consists of 18 questions concerning sleep disturbance, physical symptoms, emotional symptoms, daytime functioning, and caregiver concerns about a child. A total score of 60 or greater on the OSA-18 questionnaire indicates that a child may have SDB.
Based on just the total score, only two children were at risk of having SDB. However, on looking at parental responses to individual questions, Tsuda found that the risk may have been greater—20% of the children had loud snoring, mouth breathing, difficulty awakening, and rhinorrhea—symptoms that can indicate SDB in a child. Tsuda additionally found that younger children (8 to 10 years old) with a high total score on the OSA-18 questionnaire tended to have retroclined upper incisors, whereas older children (11 to 13 years old) with a high total score on the OSA-18 questionnaire tended to have a high palatal arch. Based on these findings, Tsuda suggests that dentists and orthodontists should examine children for a high palatal arch and retroclined incisors and should question parents about the presence of loud snoring, mouth breathing, difficulty awakening, and rhinorrhea in their child.
IS EARLY PREVENTION ACHIEVABLE?
The size of the maxilla may be a predictive factor for SDB—many people with OSA have a small maxilla. When the maxilla is smaller than normal, the tongue and other soft tissues take up more room in the oropharynx. This can set the stage for SDB by impeding airflow.5
A small maxilla in a child can result in midface hypoplasia and increase a child’s risk of having SDB. One treatment for severe midface hypoplasia involves surgically separating the maxilla from the skull, advancing it into a more correct position, and maintaining it in this position with the use of screws, pins, and bone grafts. An alternative treatment also involves surgically separating the maxilla from the skull, but rather than immediately placing it in the desired position, it is incrementally moved forward a small distance (approximately 1 mm [1/25 inch]) each day. This incremental advancement (a process called distraction osteogenesis) is repeated for a period of several weeks until the maxilla is in the desired position. A distractor device, which is typically an external halo-like device, and a dental splint are used throughout the distraction process; these then hold the maxilla in its new position as the bone completes the healing process.
Bannink6 and colleagues recently investigated the impact of midface advancement on OSA symptoms in 11 children with midface hypoplasia and moderate to severe OSA. All had been treated with oxygen therapy, tracheostomy, a nasopharyngeal tube, or continuous positive airway pressure (CPAP) for their OSA. Four months after midface advancement, six of the children had discontinued oxygen or CPAP therapy, or no longer needed a tracheostomy or nasopharyngeal tube. At least 2 years later, five of the six remained free of these respiratory treatments. On noting that OSA symptoms did not resolve in all or most of the children after surgery, Bannink suggests that the degree of presurgical upper airway obstruction may be correlated with the degree of postsurgical improvement. Other studies6 have similarly demonstrated that midface advancement does not successfully resolve OSA in all children with midface hypoplasia.
By using a different type of oral device, Villa7 and colleagues recently demonstrated greater success in improving SDB in children. The device, an endo-oral rapid maxillary expander (RME), uses distraction osteogenesis to broaden the maxilla laterally, rather than lengthening it anteriorly. The RME fits into the mouth and has an expansion screw fixed to the second molars in the upper jaw. In this position, the screws apply pressure to the midpalatal suture, thereby incrementally pushing the left and right side of the maxilla away from each other and inducing new bone growth (ie, distraction osteogenesis). As a result, the upper jaw is widened.
The Villa study involved 14 children, all of whom had OSA, a high palatal arch, and enlarged tonsils. The children did not undergo tonsillectomy. They were treated by an RME, which was removed after 12 months. Before treatment, 86% of the children had apneas; at 6 months, this percentage had fallen to 21%; and at 12 months, it had further fallen to 14%. In patients with mildly enlarged tonsils, the apnea-hypopnea index (AHI) fell by 82% (from 5.6 events/hour to 1 event/hour). In patients with severely enlarged tonsils, the AHI fell by 63% (from 6.2 events/hour to 2.3 events/hour). Villa proposes that the enlarged oropharyngeal space, created by widening the maxilla, may have decreased the ability of the tonsils to occlude the airway and contribute to SDB.
Villa additionally noted that 13 of the 14 children were mouth breathers before RME treatment, but only two children remained mouth breathers after treatment. Mouth breathing can occur when there is insufficient air passing through the nasal cavity. In mouth breathing, the jaw is lowered and positioned backward; this pushes the tongue backward into the oropharynx. With the mouth and tongue in this position, airflow through the oropharynx is restricted, which can contribute to SDB. Villa believes the decrease in the patients’ mouth breathing may have resulted from the widened maxilla. Widening the maxilla also widens the nasal passage, which decreases airway resistance in the nasal cavity and increases airflow through the nasopharynx (ie, the portion of the pharynx that lies above the soft palate). This allowed the patients to breathe through their nose rather than the mouth during sleep.
In a different study, Villa8 and colleagues investigated the efficacy of an oral jaw-positioning device in treating OSA in children. The device is an acrylic resin bite plate that fits over the teeth and moves the jaw forward, thereby opening the oropharynx, increasing airflow, and reducing OSA. Fourteen children were treated with the oral appliance. The treatment successfully reduced OSA in nine of them, based on a drop of 50% or more in the AHI after treatment. Villa concluded that the jaw positioning device can effectively treat OSA in children.
Factors that can impede airflow through the nasopharynx and play a role in SDB are enlarged tonsils, enlarged turbinates, a deviated septum, enlarged adenoids, polyps, and the inspiratory collapse of the alar rim. In children, enlarged adenoids and tonsils are the most common cause of OSA and mouth breathing. Surgically removing these tissues resolves 80% of symptoms in most children with OSA.9 (However, there is some conflict concerning whether enlarged tonsils or adenoids play a role in apnea—about 98% of children with enlarged tonsils do not have OSA or other SDB disorder.)9 In adults, turbinectomy, rhinoplasty, removal of polyps, as well as adenotonsillectomy may be used to improve airflow through the nasopharynx and reduce SDB symptoms.
ORIGINS OF OSA IN INFANCY
The origins of SDB may be inadvertently established during infancy. Many parents feed their infants using a bottle or give their infants pacifiers, unaware that these objects may result in a high palatal arch. Since the bones of an infant are very malleable, the hard palate can be easily pushed upward because of the forces exerted on it by the upward thrusts of an infant’s tongue against the hard plastic nipple of a bottle or pacifier.
A high palatal arch has two consequences that promote SDB. First, it elevates the floor of the nasal cavity. This narrows the nasal passage, thereby increasing airway resistance in the nasal cavity and decreasing airflow to the oropharynx. Second, a high palatal arch may result in small choanae. These two openings in the back of the nasal cavity allow air to flow from the nasopharynx into the oropharynx. Small choanae reduce the amount of air that can flow into the oropharynx. With reduced airflow to the oropharynx, soft tissues during inspirations can more easily be drawn into and block the airway. These factors may explain the increased prevalence of SDB noted in children who have been bottle-fed or have used pacifiers.10,11
Pre- and post-natal nicotine exposure may contribute to the higher prevalence of OSA and central sleep apnea noted in infants of mothers who smoke.12,13 Some research14 indicates that prolonged overstimulation of nicotinic receptors in brainstem structures controlling respiration may decrease the normal respiratory response to hypoxia and inhibit the inspiratory drive. This diminished response in infants of smoking mothers could play a role in OSA and central sleep apnea episodes during sleep. It may also play a role in sudden infant death syndrome, which is thought to occur because apnea-induced hypoxia does not trigger the infant to arouse to breathe, resulting in the infant’s death.
That an estimated 90% of people may have undiagnosed OSA suggests that clinicians are unaware of risk factors for this SDB disorder, and therefore are not having patients assessed. Some consequences of untreated OSA or other SDB disorder can be an increased risk of cardiovascular problems such as hypertension and stroke; an increased risk of physical harm due to sleepiness or inattentiveness (eg, car accidents); and a reduced treatment response in certain diseases (eg, poorly controlled hypertension despite treatment).
Patients—especially children—may not present with the more common risk factors for SDB (eg, obesity, a thick neck, and loud snoring), but present with less familiar risk factors such as a small maxilla, a high palatal arch, rhinorrhea, and mouth breathing. Increased eye width (the distance between the inner corners of the eyes),15 retroclined incisors, enlarged turbinates, collapse of the alar rim, and small choanae may also be risk factors for SDB, although they have not been extensively investigated for this.
Physicians, dentists, and orthodontists can play an important role in preventing SDB and reducing the consequences of untreated SDB by examining patients for these less familiar risk factors; by routinely using questionnaires (eg, the OSA-18 questionnaire) to screen for SDB in patients; by asking parents about their use of pacifiers and bottles for their infant; and by asking parents (especially mothers) about nicotine use around their infant or child.
Regina Patrick, RPSGT, is a contributing writer for Sleep Review.
- National Heart, Lung, and Blood Institute Communications Office. Sleep apnea linked to increased risk of death. August 1, 2008. public.nhlbi.nih.gov/newsroom/home/GetPressRelease.aspx?id=2580. Accessed August 6, 2010.
- Finkel KJ, Searleman AC, Tymkew H, et al. Prevalence of undiagnosed obstructive sleep apnea among adult surgical patients in an academic medical center. Sleep Med. 2009;10(7):753–758.
- Lee RW, Petocz P, Prvan T, Chan AS, Grunstein RR, Cistulli PA. Prediction of obstructive sleep apnea with craniofacial photographic analysis. Sleep. 2009;32(1):46–52.
- Tsuda H, Fastlicht S, Almeida FR, Lowe AA. The correlation between craniofacial morphology and sleep-disordered breathing in children in an undergraduate orthodontic clinic. Sleep Breath. April 13, 2010. Epub ahead of print. www.springerlink.com/content/1731h1gt18n78540/.
- Tsuiki S, Isono S, Ishikawa T, Yamashiro Y, Tatsumi K, Nishino T. Anatomical balance of the upper airway and obstructive sleep apnea. Anesthesiology. 2008;108(6):1009–1015.
- Bannink N, Nout E, Wolvius EB, Hoeve HL, Hoosten KF, Mathijssen IM. Obstructive sleep apnea in children with syndromic craniosynostosis: long-term respiratory outcome of midface advancement. Int J Oral Maxillofac Surg. 2010;39(2):115–121.
- Villa MP, Malagola C, Pagani J, et al. Rapid maxillary expansion in children with obstructive sleep apnea syndrome: 12 month follow-up. Sleep Med. 2007;8:128–134.
- Villa MP, Bernkopf E, Pagani J, Broia V, Montesano M, Ronchetti R. Randomized controlled study of an oral jaw-positioning appliance for the treatment of obstructive sleep apnea in children with malocclusion. Am J Crit Care Med. 2002;165:123–127.
- Zhang X-W, Li Y, Zhou F, Guo CK, Huang ZT. Comparison of polygraphic parameters in children with adenotonsillar hypertrophy with vs without obstructive sleep apnea. Arch Otolaryngol Head Neck Surg. 2007;133:122–126.
- Palmer B. Breast-feeding: reducing the risk for obstructive sleep apnea. Breast-feeding Abstracts. 1999;18(3):19–20. www.brianpalmerdds.com/bfing_reduces.htm. Accessed August 12, 2010.
- Hultcrantz E, Löfstrand-Tideström B, Ahlquist-Rastad J. The epidemiology of sleep related breathing disorder in children. Int J Pediatr Otorhinolaryngol. 1995;32 Suppl:S63-S66.
- Sawnani H, Jackson T, Murphy T, Beckerman R, Simakajornboon N. The effect of maternal smoking on respiratory and arousal patterns in preterm infants during sleep. Am J Resp Crit Care Med. 2004;169:733–738.
- Toubas PL, Duke JC, McCaffree MA, Mattice CD, Bendell D, Orr WC. Effects of maternal smoking and caffeine habits on infantile apnea: a retrospective study. Pediatrics. 1986;78(1):159–163.
- Cohen G, Han ZY, Grailhe R, et al. beta 2 nicotinic acetylcholine receptor subunit modulates protective responses to stress: a receptor basis for sleep-disordered breathing after nicotine exposure. Proc Natl Acad Sciences USA. 2002;99(20):13272–13277.
- Lee RW, Chan AS, Grunstein RR, Cistulli PA. Craniofacial phenotyping in obstructive sleep apnea—a novel quantitative photographic approach. Sleep. 2009;32(1):37–45.