JADA Continuing Education
Obstructive sleep apnea
Diagnosis, medical management and dental implications
KELLY R. MAGLIOCCA, D.D.S. and
JOSEPH I. HELMAN, D.M.D.
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ABSTRACT
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Background. Patients with undiagnosed obstructive sleep apnea (OSA) represent a major public health problem, and studies suggest that the incidence of OSA may be even higher than estimated.
Types of Studies Reviewed. The authors reviewed current literature describing comorbidities of patients with OSA.
Results. Sleep medicine is a relatively new field. Dental practitioners may lack educational exposure and, as a result, feel uncomfortable asking their patients sleep-related questions. While patients with well-controlled OSA present few difficulties for routine dental treatment, it is imperative that health care professionals understand the comorbidities associated with OSA and that untreated OSA may contribute to increased morbidity and mortality.
Clinical Implications. Dental professionals have a unique doctor-patient relationship that affords them a role in recognizing sleep disorders by exploring the history of patients who are sleepy.
Key Words: Obstructive sleep apnea; sleep-disorderaffected breathing; dentistry; adults
Obstructive sleep apnea (OSA) is a disturbance in normal sleep patterns; when combined with daytime symptoms, this condition is termed obstructive sleep apnea syndrome. Evidence continues to accumulate in regard to the risk and possible development of comorbid disease in connection with untreated OSA such as systemic hypertension,13 depression,4 stroke,5,6 angina7 and cardiac dysrhythmias.8 Untreated OSA also is associated with motor vehicle accidents,9 poor work performance, occupational accidents and reduced quality of life.10,11 This constellation of issues affects patients on personal, social and, often, professional levels. Public awareness of OSA as a disease is the result of many newspaper articles, Internet sources and television features about snoring and sleep-disorderaffected breathing. Patients understand that dentists have a role in the management of OSA. They may express concerns regarding the effect of OSA on the delivery of dental care1215 and seek reliable information about OSA.
It is imperative that health care professionals understand the comorbidities associated with obstructive sleep apnea.
We conducted a literature review to increase awareness of OSA as a disease that has both medical and dental implications among oral health care practitioners. A secondary goal was to increase interdisciplinary understanding and communication about patients involved in OSA treatment.
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EPIDEMIOLOGY
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OSA occurs in 2 to 4 percent of the adult population between the ages of 30 to 60 years,16 though evidence suggests that many more patients remain undiagnosed.17 While sleep apnea does affect children,18 the etiology, clinical presentation and treatment differ. Therefore, we limited our discussion to adult OSA. In addition to age-related differences, there may be genetic,19 sex20 and ethnic differences.21
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PATHOPHYSIOLOGY
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The etiology of OSA is a complex interplay between neural, hormonal, muscular and structural anatomical factors.22,23 Normal sleep can be divided into two categories: nonrapid eye movement (non-REM), which is characterized by four stages, and rapid eye movement (REM) or paradoxical sleep, which is best characterized by muscle atonia. During the sleep state, a person cycles through the different stages, each associated with a "depth of sleep" for a characteristic period. OSA is characterized by partial or complete obstructive collapse of the upper airway during non-REM or REM sleep. In some cases, both partial and complete collapse are present. During REM sleep, the muscles that form or lie adjacent to the airway are most hypotonic, which may predispose the patient to repeated pathological airway events. Airway luminal narrowing diminishes the ability to freely exchange air, resulting in blood oxygen desaturation to a variable nadir, for a variable length of time. Partial or complete obstruction results in brief awakenings from sleep or a transition to a lighter stage of sleep. Respiratory events, which deplete certain stages of non-REM and REM sleep, contribute to sleep fragmentation and unrefreshing sleep.
The gold standard for diagnosing obstructive sleep apnea involves having the patient complete an overnight sleep study conducted in a laboratory.
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SIGNS AND SYMPTOMS
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Box 1
lists the signs and symptoms commonly associated with OSA. Demographic correlates such as having a positive family history for OSA, being middle-aged or belonging to the male sex also may raise suspicion among practitioners for undiagnosed sleep-disorderaffected breathing in a patient describing many of these symptoms. However, even sleep experts agree that without confirmatory laboratory data, the patients history and clinical assessment do not provide sufficient evidence to diagnose OSA.24 This underscores the need for dentists to refer patients for diagnostic testing to further investigate the nature of the problem.
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DIAGNOSIS
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The gold standard for diagnosing OSA involves having the patient complete polysomnography (an overnight sleep study) conducted in a laboratory. The polysomnogram records parameters including electroencephalography (brain waves), electro-oculography (eye movement), electrocardiography, electromyography (chin and leg movement), sleep positioning, respiratory activity and oxygen saturations.25 Apnea is defined as the cessation of airflowa complete obstruction for at least 10 secondswith a concomitant 2 to 4 percent drop in arterial oxygen saturation.26 The definition of hypopnea is more variable, but it commonly is thought of as a reduction in airflow of at least 30 to 50 percent with a drop in oxygen saturation. The apnea-hypopnea index (AHI) is the average number of apneas and hypopneas per hour of sleep. OSA severity is classified on the basis of the patients AHI score, into three categories: mild (AHI score between 5 and 15), moderate (AHI score between 15 and 30) and severe (AHI score greater than 30).26 Not all studies, however, adhere to the numerical parameters of this classification. Other factors that also influence the severity of OSA include oxygen desaturation, quality of life and the level of daytime sleepiness.
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MEDICAL AND SURGICAL MANAGEMENT
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The sleep medicine team defines possible treatment options for adult patients with OSA based on the severity of the sleep disorder, patients preference, the patients overall health, and the experience and preferences of the team members. Positional therapy involves nocturnal aids (for example, having patients sew a tennis ball into the back of their pajama tops) to prevent patients from sleeping in a supine position. Sleeping in the lateral position may be effective, as it will displace the tongue from the posterior airway such that it is less likely to be a source of obstruction.27 Behavioral modifications are guidelines designed to limit behaviors known to disrupt sleep such as consuming alcohol in the evening. Alcohol often is used before bedtime for its perceived sedative effect. However, alcohol actually may further relax the muscles of the airway, making the airway more prone to obstruction at susceptible sites.28 Weight loss is recommended when applicable; however, not all patients with OSA are obese.29,30 It is not known how much weight loss is required to eliminate OSA, and both the patients sex and weight distribution may contribute to his or her OSA in an unpredictable manner.31,32 Finally, the rate of recidivism is high, and patients who lose weight often regain it.33
Sullivan and colleagues34 reported on the use of nasal continuous positive airway pressure (CPAP) for the treatment of OSA. The concept of nasal CPAP is to maintain upper airway patency during sleep by way of a pneumatic stent. This treatment can be administered via nasal mask, oral mask or other variations. Because of its effectiveness, CPAP is the first-line treatment and the primary form of therapy for OSA, though its success is limited by the patients level of compliance. Roughly 20 to 30 percent of patients experience problems while using CPAP, and the device is ineffective if it is not used regularly.35 Patients list nasal dryness, facial ulcerations at the mask interface and claustrophobia as reasons for CPAP intolerance.
Treatment using an oral appliance has been shown to be effective in subsets of patients with OSA.36 Many commercial devices offer treatment for snoring; however, a device designed to treat OSA should be fabricated by a dentist familiar with device design, maintenance and therapeutic efficacy and who has an association with and referral from a sleep team. A multitude of oral appliances for OSA are available, but not all patients will find the same appliance effective.13 Patient compliance with oral appliances appears to be adequate,37 but not all studies agree.38 Difficulty with the device owing to temporary or persistent occlusal, temporomandibular joint or individual tooth discomfort13 or a perceived lack of efficacy may cause compliance issues.38 The patient should undergo nocturnal polysomnography with the oral appliance in place to document its effectiveness.36
The main surgical treatments offered for OSA often target the anatomical areas of the posterior airway where collapse is suspected to occur. Treatment is designed to enlarge the posterior airway space, reduce airway collapsibility and, ideally, stabilize the airway for the long term. Surgery has the advantage of correcting any craniofacial abnormalities that may have caused the OSA and of removing the variable of patient compliance with the long-term treatment. As with the nonsurgical treatment modalities, polysomnograph testing after surgery is essential for judging the efficacy of a procedure. Uvu-lopalatopharyngoplasty may be performed alone or in conjunction with a genial advancement, hyoid suspension or both.39 While these procedures may be warranted in select cases of OSA, they are not useful as first-line therapy in moderate or severe cases of multilevel airway obstruction.40 Maxillomandibular advancement (MMA) surgery, which is based on traditional orthognathic surgery techniques, has been proven effective in retrospective studies for a range of OSA disease.4143 Dentists may encounter patients who even have a permanent tracheotomy in place for treatment of OSA. These patients likely have multiple medical comorbidities and severe OSA.44 Although a tracheotomy is effective, it often is a last resort, owing to the associated social stigma and potential complications.45,46
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OROFACIAL FINDINGS
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Patients with sleep apnea have a wide range of physical attributes. The most common orofacial characteristics encountered include a retrognathic mandible, narrow palate, large neck circumference, long soft palate (which leads to dentists being unable to visualize the entire length of the uvula when the patients mouth is open wide), tonsillar hypertrophy, nasal septal deviation and relative macroglossia. The population with OSA is a heterogeneous group, and patients with OSA may not have all of these physical features.
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DENTAL IMPLICATIONS
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Some patients may not be forthcoming about non-compliance with OSA treatment, perhaps believing that disclosures regarding treatment, or lack thereof, are not relevant to dental care. Also, dentists may not ask patients about their compliance with OSA treatment in follow-up questioning, a failure perhaps stemming from a lack of familiarity with treatment options or with the significance of the untreated disease. The following is a compelling argument for dentists to ensure that they discuss treatment and compliance concerns with patients who have OSA.
The medical history dialogue is essential in assessing whether a patient can tolerate the physical stress of dental treatment.47 In patients with untreated or undiagnosed OSA, hypertension can be difficult to control,23 and some investigators have reported exacerbations of epilepsy48 and increased severity of asthma.49 There is evidence to suggest that effective OSA treatment may improve asthma and blood pressure control in some patients.23,50,51 The presence of hypertension and cardiac dys-rthymias23 may raise concern regarding the appropriate use of vasoconstrictor agents during dental treatment. There is no scientific consensus in the literature regarding the use of local anesthetic agents that contain epinephrine in patients with pre-existing medical conditions such as hypertension,52 stroke, dysrhythmias53 or concurrent use of certain medications such as beta-blockers and tricyclic anti-depressants. Nonetheless, idiosyncratic drug reactions52 are well-documented, and it seems wise to adopt a prudent approach.
General dentists may or may not be involved with obstructive sleep apnea therapy for their patients, but they should be aware of the potential occlusal changes that can result from therapy.
Based on the diagnosis of OSA and the presence of existing comorbidities, the dentist should assess the patients ability to tolerate the psychological stress of dental treatment.47 Patients may be intolerant of CPAP because they have claustrophobia.54 This may affect how the professional staff applies sterile draping, if used during surgical procedures. Patients with OSA also may be depressed.55 Cautionary advice for treating dental patients who are depressed has been published.56 There is a risk of developing caries owing to xerostomia in connection with many antidepressant medications.57 Furthermore, depression may affect compliance with medication58 and oral hygiene.57
Dentists may need to modify treatment to ensure that patients safely tolerate treatment.47 Reflecting a mucoperiosteal flap to accomplish surgical extractions or other procedures may preclude the patient from using CPAP for one to two evenings to avoid the possible risk of developing subcutaneous emphysema.59 If a patient requests dental treatment with adjunctive intravenous sedation, the dentist must stress that a subset of the OSA population are known to have a hazardous airway60 and that airway obstruction in patients with OSA after the administration of sedating drugs has been documented.6164 The dental practitioner may be the first to recognize a patients sleep-disorderaffected breathing by witnessing repeated apneic events in patients undergoing sedation.64 Also, patients with OSA may have an impaired swallowing reflex.65 Gastroesophageal reflux disease (GERD) is associated with OSA, which increases the patients risk of experiencing aspiration and subsequent chemical pneumonitis. Additionally, discomfort due to GERD can mimic chest pain during a dental appointment. In the case of a patient with serious cardiac disease associated with OSA, a complaint of chest pain is an obvious source of stress in the dental office.
In addition to the patients medical history, the dentists clinical examination findings influence treatment planning. As we noted previously, patients may be taking medication with xerostomic effects, and certain types of CPAP delivery may add to the patients complaints of xerostomia.66 While the incidence of caries has not been reviewed in the OSA population, it would seem prudent to educate patients with xerostomia about avoiding cariogenic foods and beverages. Dentists should prescribe artificial saliva products and fluoride applications for patients with xerostomia. Patients using CPAP also may have dorsal nasal excoriation or a rash that precludes the use of nitrous oxide sedation secondary to nasal hood discomfort.
General dentists may or may not be involved with OSA therapy for their patients, but they should be aware of the potential occlusal changes that can result from therapy. Researchers have reported occlusal changes in patients using oral appliances for mandibular advancement, including development of posterior open bite, altered inclination of incisors and decreased anterior open bite.6771 In many of these cases, the patient did not notice or appear to be troubled by the changes.68,70 Robertson and colleagues67 suggested keeping the patients bite opening to a minimum when fabricating an appliance to reduce the impact on the occlusion. Dentists must communicate with the practitioners who fabricate oral appliances about these abnormalities, as a consensus has not been reached on whether intervention is required. Rose and colleagues69 recommend mandatory regular dental visits when an oral appliance is used as a treatment modality.
MMA surgery for OSA likely will have an effect on occlusion for a multitude of reasons, including skeletal relapse. Before engaging in corrective restorative or prosthodontic measures, dentists and oral and maxillofacial surgeons must communicate to determine the present stage of the patients OSA treatment. It is possible that further surgical correction of the facial bones is planned and that the occlusal relation will change once again. Furthermore, patients undergoing MMA surgery spend a considerable amount of time with their jaws "wired shut" (that is, maxillomandibular fixation). Temporizing or restoring large areas of caries and presurgical prophylaxis and extraction of hopeless teeth would benefit the patient and prevent interruptions in postsurgical maxillomandibular fixation.
While occasional fatigue on the part of a patient may be normal, his or her routinely falling asleep while unattended in the dental chair is not.
Calcified atheromas are likely to appear more often on panoramic radiographs of patients with sleep apnea than on those of age-matched controls.72 Promptly referring a patient with calcified atheromas for a vascular evaluation is warranted.73 Dentists often discuss smoking cessation with patients, usually with regard to risk reduction of oral cancer, but smoking also is known to adversely affect the mucosa of the upper airway in patients with OSA.74 Smoke is an airway irritant and results in mucosal edema, which likely contributes to an increase in mucosal edema and secretions.74
Patients with untreated OSA may develop neurocognitive deficiencies75,76 that can have implications for dental professionals during the informed-consent process. Dentists may need to put forth additional effort to ensure that patients understand the risks, benefits and alternatives to treatment. Ideally, dentists should document the exchange thoroughly.
Finally, patients with OSA tend to have more motor vehicle accidents9; in fact, sleepiness has been likened to alcohol use. Advising patients to refrain from driving while sleepy or suggesting an escort or alternate driver is a sensible strategy when patients appear overtly sleepy.
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IDENTIFICATION OF AT-RISK PATIENTS AND MAKING APPROPRIATE REFERRALS
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While occasional fatigue on the part of a patient may be normal, his or her routinely falling asleep while unattended in the dental chair is not. A small percentage of patients with OSA have symptomatic hypothyroidism74 as a codiagnosis. Another small percentage of patients has been discovered to have a tumor mass representing the obstructing tissue.
The prevalence of OSA may be higher than estimated.17 When OSA is left untreated, regardless of the reason, the potential for mortality increases.77,78 Adding sleep-related questions (Box 2
) to the written or oral medical history and consideration of both orofacial and physical findings may result in the detection of a sleep disorder.15,24,79 The direct costs of sleep apnea include increased health care use,80,81 and indirect costs may include reduced work performance.82 All of these issues make OSA an important public health concern.
No review of OSA is complete without a discussion of obesity. At least two reviews that define the relevance of obesity to dentistry are available.83,84 Obesity is intimately associated with OSA85; the majority of obese patients have some degree of OSA, and the majority of patients with OSA are obese.64,86
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MEDICAL HISTORY AND CONSIDERATIONS
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Contemporary weight loss medications may interfere with dental treatment. Sibutramine is a medicinal strategy used in weight loss therapy that is associated with xerostomia and has sympath-omimetic properties. A small increase in blood pressure and heart rate can occur in patients who use this drug.8789
Obesity is associated with eccentric hypertrophy of the heart, which causes cardiac diastolic dysfunction, with potential systolic dysfunction.90 Dysfunction may lead to dysrhythmias, congestive heart failure and even sudden death.91,92 Type 2 diabetes mellitus (DM) is strongly correlated with obesity in all ethnic groups.93 Weight gain precedes the onset of DM,94,95 and weight loss is associated with a decreased risk of developing OSA96 and type 2 DM.97 Postoperative non-steroidal anti-inflammatory drug (NSAID) therapy may not be advisable in patients with nephropathy, which typically is associated with hypertension98 and DM.99 The presence of congestive heart failure also compounds the risks associated with the use of NSAIDs.100,101
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CHALLENGES IN DENTAL TREATMENT
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Obese patients often are exposed to public disapproval because of their habitus. This stigma is seen in education and employment, and multiple studies document its presence in health care.102,103 By incorporating obesity education into dental school curriculum and continuing education courses, dental professionals acquire important information regarding the health risks of obesity. The conventional dental chair may not accommodate a corpulent patient, which can present an awkward scenario for the patient and the practitioner. The standard adult blood pressure cuff is inadequate for obese patients, and using a standard cuff on a large arm will result in a false elevation of blood pressure.104 The presence of oropharyngeal soft tissue redundancy, including excess tongue volume, reduces dentists visualization and places patients at increased risk of inadvertently aspirating foreign debris, crowns, extracted teeth and restorative material. Redundant oral tissues also make it difficult for dentists to locate landmarks for regional local anesthetic blocks, and a thick neck poses a challenge in performing an accurate head and neck examination.
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OFFICE EMERGENCIES
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One study noted that people with obesity reported shortness of breath and chest discomfort more often than did control subjects from the average population.105 While the alteration in respiratory mechanics and lung volumes play a role,106 dentists should not exclude the possibility that a more acute medical emergency could be present, such as atypical angina, myocardial infarction or pulmonary embolism. Should a medical emergency arise, difficulty or inability to establish intravenous access has been well-documented in the obese population.107,108 Intramuscular injections in obese patients thighs or buttocks rarely are intramuscular but more often are into fat, which has a relatively poor blood supply, leading to unpredictable effects. Finally, dose instructions for many drugs are weight-based. Prescribing medications for obese patients may be difficult since dosages based on pharmacokinetics obtained in people of average weight could induce errors when treating obese patients.108,109
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CONCLUSIONS
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Patients with well-controlled OSA present few difficulties for routine dental treatment. However, patients with untreated or undiagnosed OSA can present the dental practitioner with multiple issues and challenges. Dentists have a unique doctor-patient relationship and, by posing a few additional questions in the patient interview, can have a role in recognizing sleep disorders. Dentists should refer patients who are sleepy, stentorian snorers who have had witnessed apneas to their primary care physician for a full sleep-related medical history and a comprehensive evaluation. The primary care physician then may work in concert with accredited sleep-disorder programs to rule out environmental, medical, pharmacological, psychological and behavioral causes for sleep-disorderaffected breathing. Finally, Box 3
offers several reputable Internet resources for patients or clinicians seeking more information on sleep disorders.
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FOOTNOTES
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Dr. Magliocca is an adjunct assistant professor, Department of Oral and Maxillofacial Surgery, University of Michigan, 1011 N. University Drive, Ann Arbor, Mich. 48109, e-mail "cottrk{at}hotmail.com". Address reprint requests to Dr. Magliocca.
Dr. Helman is the chairman, Department of Oral and Maxillofacial Surgery, University of Michigan, Ann Arbor.
The authors thank Dr. Sam Zwetchkenbaum and Dr. Flavia Consens for their thoughtful review of this manuscript.
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REFERENCES
|
|---|
- Richert A, Ansarin K, Baran AS. Sleep apnea and hypertension: pathophysiologic mechanisms. Semin Nephrol 2002;22(1):717.[Medline]
- Wolk R, Shamsuzzaman AS, Somers VK. Obesity, sleep apnea, and hypertension. Hypertension 2003;42:106774.[Abstract/Free Full Text]
- Nieto FJ, Young TB, Lind BK, et al. Association of sleep-disordered breathing, sleep apnea, and hypertension in a large community-based study. Sleep Heart Health Study. JAMA 2000;283:182936.[Abstract/Free Full Text]
- Baran AS, Richert AC. Obstructive sleep apnea and depression. CNS Spectr 2003;8(2):12834.[Medline]
- Poza JJ, Martinez A, Emparanza JI, Lopez de Munain A, Marti Masso JF. Sleep apnea syndrome and cerebral infarction (in Spanish). Neurologia 2000;15(1):37.[Medline]
- Palomaki H. Snoring and the risk of ischemic brain infarction. Stroke 1991;22:10215.[Abstract/Free Full Text]
- Loui WS, Blackshear JL, Fredrickson PA, Kaplan J. Obstructive sleep apnea manifesting as suspected angina: report of three cases. Mayo Clinic Proc 1994;69:2448.[Medline]
- Gula LJ, Krahn AD, Skanes AC, Yee R, Klein GJ. Clinical relevance of arrhythmias during sleep: guidance for clinicians. Heart 2004;90:34752.[Free Full Text]
- Horne JA, Reyner LA. Sleep related vehicle accidents. BMJ 1995;310:5657.[Abstract/Free Full Text]
- Goncalves MA, Paiva T, Ramos E, Guilleminault C. Obstructive sleep apnea syndrome, sleepiness, and quality of life. Chest 2004;125:20916.[Medline]
- Lacasse Y, Bureau MP, Series F. A new standardised and self-administered quality of life questionnaire specific to obstructive sleep apnoea. Thorax 2004;59:4949.[Abstract/Free Full Text]
- Friedlander AH, Friedlander IK, Pogrel MA. Dentistrys role in the diagnosis and co-management of patients with sleep apnoea/hypopnoea syndrome. Br Dent J 2000;189(2):7680.[Medline]
- Veis RW. Snoring and obstructive sleep apnea from a dental perspective. J Calif Dent Assoc 1998;26:55765.[Medline]
- Brousseau M, Manzini C, Thie N, Lavigne G. Understanding and managing the interaction between sleep and pain: an update for the dentist. J Can Dent Assoc 2003;69:43742.[Medline]
- Bailey DR, Attanasio R. Dentistrys role in the management of sleep disorders: recognition and management. Dent Clin North Am 2001;45:61930.[Medline]
- Young T, Palta M, Dempsey J, Skatrud J, Weber S, Badr S. The occurrence of sleep disordered breathing among middle aged adults. N Engl J Med 1993;328:12305.[Abstract/Free Full Text]
- Kapur V, Strohl KP, Redline S, Iber C, OConnor G, Nieto J. Underdiagnosis of sleep apnea syndrome in U.S. communities. Sleep Breath 2002;6(2):4954.[Medline]
- Messner AH. Treating pediatric patients with obstructive sleep disorders: an update. Otolaryngol Clin North Am 2003;36:51930.[Medline]
- Pillar G, Lavie P. Assessment of the role of inheritance in sleep apnea syndrome. Am J Respir Crit Care Med 1995;151(3 pt 1):68891.[Abstract]
- Kapsimalis F, Kryger MH. Gender and obstructive sleep apnea syndrome, part 2: mechanisms. Sleep 2002;25:499506.[Medline]
- Profant J, Ancoli-Israel S, Dimsdale JE. Are there ethnic differences in sleep architecture. Am J Hum Biol 2002;14:3216.[Medline]
- Shamsuzzaman AS, Gersh BJ, Somers VK. Obstructive sleep apnea: implications for cardiac and vascular disease. JAMA 2003;290:190614.[Abstract/Free Full Text]
- Sharabi Y, Dagan Y, Grossman E. Sleep apnea as a risk factor for hypertension. Curr Opin Nephrol Hypertens 2004;13:35964.[Medline]
- Schlosshan D, Elliott MW. Sleep, part 3: clinical presentation and diagnosis of the obstructive sleep apnoea hypopnoea syndrome. Thorax 2004;59:34752.[Abstract/Free Full Text]
- Polysomnography Task Force, American Sleep Disorders Association Standards of Practice Committee. Practice parameters for the indications for polysomnography and related procedures. Sleep 1997;20:40622.[Medline]
- Flemons WW, Buysse D. Redline S, et al. Sleep-related breathing disorders in adults: recommendations for syndrome definition and measurement techniques in clinical researchthe report of an American Academy of Sleep Medicine task force. Sleep 1999;22:66789.[Medline]
- Penzel T, Moller M, Becker HF, Knaack L, Peter JH. Effect of sleep position and sleep stage on the collapsibility of the upper airways in patients with sleep apnea. Sleep 2001;24(1):905.[Medline]
- Scrima L, Broudy M, Nay KN, Cohn MA. Increased severity of obstructive sleep apnea after bedtime alcohol ingestion: diagnostic potential and proposed mechanism of action. Sleep 1982;5:31828.[Medline]
- Vorona R, Ware J. History and epidemiology of sleep-related breathing disorders. Oral Maxillofac Surg Clin 2002;14:27383.
- Gami AS, Caples SM, Somers VK. Obesity and obstructive sleep apnea. Endocrin Metab Clin North Am 2003;32:86994.[Medline]
- Peppard PE, Young T, Palta M, Dempsey J, Skatrud J. Longitudinal study of moderate weight change and sleep-disordered breathing. JAMA 2000;284:301521.[Abstract/Free Full Text]
- Millman RP, Carlisle CC, McGarvey ST, Eveloff SE, Levinson PD. Body fat distribution and sleep apnea severity in women. Chest 1995;107:3626.[Medline]
- Suratt PM, McTier RF, Findley LJ, Pohl SL, Wilhoit S. Changes in breathing and the pharynx after weight loss in obstructive sleep apnea. Chest 1987;92:6317.[Medline]
- Sullivan CE, Issa FG, Berthon-Jones M, Eves L. Reversal of obstructive sleep apnoea by continuous positive airway pressure applied through the nares. Lancet 1981;1(8225):8625.[Medline]
- Wright J, White J. Continuous positive airways pressure for obstructive sleep apnoea (update appears in Cochrane Database Syst Rev 2002;[2]:CD001106)]. Cochrane Database Syst Rev 2000;(2):CD001106.
- Hoekema A, Stegenga B, De Bont LG. Efficacy and co-morbidity of oral appliances in the treatment of obstructive sleep apnea-hypopnea: a systematic review. Crit Rev Oral Biol Med 2004;15(3): 13755.[Abstract/Free Full Text]
- Randerath WJ, Heise M, Hinz R, Ruehle KH. An individually adjustable oral appliance vs. continuous positive airway pressure in mild-to-moderate obstructive sleep apnea syndrome. Chest 2002; 122:56975.[Medline]
- Neill A, Whyman R, Bannan S, Jeffrey O, Campbell A. Mandibular advancement splint improves indices of obstructive sleep apnoea and snoring but side effects are common. N Z Med J 2002;115: 28992.[Medline]
- Riley RW, Powell NB, Guilleminault C. Obstructive sleep apnea syndrome: a review of 306 consecutively treated surgical patients. Otolaryngol Head Neck Surg 1993;108(2):11725.[Medline]
- Bettega G, Pepin JL, Veale D, Deschaux C, Raphael B, Levy P. Obstructive sleep apnea syndrome: fifty-one consecutive patients treated by maxillofacial surgery. Am J Respir Crit Care Med 2000;162(2 pt 1):6419.[Abstract/Free Full Text]
- Conradt R, Hochban W, Brandenburg U, Heitmann J, Peter JH. Long-term follow-up after surgical treatment of obstructive sleep apnoea by maxillomandibular advancement. Eur Respir J 1997; 10(1):1238.[Abstract]
- Riley RW, Powell NB, Li KK, Troell RJ, Guilleminault C. Surgery and obstructive sleep apnea: long-term clinical outcomes. Otolaryngol Head Neck Surg 2000;122:41521.[Medline]
- Prinsell JR. Maxillomandibular advancement surgery in a site-specific treatment approach for obstructive sleep apnea in 50 consecutive patients. Chest 1999;116:151929.[Medline]
- Thatcher GW, Maisel RH. The long-term evaluation of tra-cheostomy in the management of severe obstructive sleep apnea. Laryngoscope 2003;113:2014.[Medline]
- Myers EN, Carrau RL. Early complications of tracheotomy: incidence and management. Clin Chest Med 1991;12:58995.[Medline]
- Wood DE, Mathisen DJ. Late complications of tracheotomy. Clin Chest Med 1991;12:597609.[Medline]
- Malamed SF, Quinn CL. Sedation: A guide to patient management. 3rd ed. St. Louis: Mosby; 1995:32.
- Britton TC, ODonoghue M, Duncan JS, Hirsch NP. Exacerbation of epilepsy by obstructive sleep apnoea. J Neurol Neurosurg Psychiatry 1997;63:808.[Free Full Text]
- Bohadana AB, Hannhart B, Teculescu DB. Nocturnal worsening of asthma and sleep-disordered breathing. J Asthma 2002;39(2):85100.[Medline]
- Chan CS, Woolcock AJ, Sullivan CE. Nocturnal asthma: role of snoring and obstructive sleep apnea. Am Rev Respir Dis 1988; 137:15024.[Medline]
- Guilleminault C, Quera-Salva MA, Powell N, et al. Nocturnal asthma: snoring, small pharynx and nasal CPAP. Eur Respir J 1988;1:9027.[Abstract]
- Bader JD, Bonito AJ, Shugars DA. A systematic review of cardiovascular effects of epinephrine on hypertensive dental patients. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2002;93:64753.[Medline]
- Little JW. The impact on dentistry of recent advances in the management of hypertension. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2000;90:5919.[Medline]
- Edinger JD, Radtke RA. Use of in vivo desensitization to treat a patients claustrophobic response to nasal CPAP. Sleep 1993;16:67880.[Medline]
- Means MK, Lichstein KL, Edinger JD, et al. Changes in depressive symptoms after continuous positive airway pressure treatment for obstructive sleep apnea. Sleep Breath 2003;7(1):3142.[Medline]
- Friedlander AH, Friedlander IK, Gallas M, Velasco E. Late-life depression: its oral health significance. Int Dent J 2003;53:4150.[Medline]
- Friedlander AH, Norman DC. Late-life depression: psy-chopathology, medical interventions, and dental implications. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2002;94:40412.[Medline]
- Wang PS, Bohn RL, Knight E, Glynn RJ, Mogun H, Avorn J. Non-compliance with antihypertensive medications: the impact of depressive symptoms and psychosocial factors. J Gen Intern Med 2002;17:50411.[Medline]
- Kramer NR, Fine MD, McRae RG, Millman RP. Unusual complication of nasal CPAP: subcutaneous emphysema following facial trauma. Sleep 1997;20:8957.[Medline]
- Riley RW, Powell NB, Guilleminault C, Pelayo R, Troell RJ, Li KK. Obstructive sleep apnea surgery: risk management and complications. Otolaryngol Head Neck Surg 1997;117:64852.[Medline]
- Montravers P, Dureuil B, Desmonts JM. Effects of i.v. midazolam on upper airway resistance. Br J Anaesth 1992;68(1):2731.[Abstract/Free Full Text]
- Sharma VK, Galli W, Haber A, et al. Unexpected risks during administration of conscious sedation: previously undiagnosed obstructive sleep apnea. Ann Intern Med 2003;139:7078.[Free Full Text]
- Hillman DR, Loadsman JA, Platt PR, Eastwood PR. Obstructive sleep apnoea and anaesthesia. Sleep Med Rev 2004;8:45971.[Medline]
- Weaver JM. Increased anesthetic risk for patients with obesity and obstructive sleep apnea. Anesth Prog 2004;51:75.[Medline]
- Teramoto S, Sudo E, Matsuse T, et al. Impaired swallowing reflex in patients with obstructive sleep apnea syndrome. Chest 1999; 116(1):1721.[Medline]
- Kalan A, Kenyon GS, Seemungal TA, Wedzicha JA. Adverse effects of nasal continuous positive airway pressure therapy in sleep apnoea syndrome. J Laryngol Otol 1999;113:88892.[Medline]
- Robertson C, Herbison P, Harkness M. Dental and occlusal changes during mandibular advancement splint therapy in sleep disordered patients. Eur J Orthod 2003;25:3716.[Abstract/Free Full Text]
- Rose EC, Schnegelsberg C, Staats R, Jonas IE. Occlusal side effects caused by a mandibular advancement appliance in patients with obstructive sleep apnea. Angle Orthod 2001;71:45260.[Medline]
- Rose EC, Staats R, Virchow C Jr, Jonas IE. Occlusal and skeletal effects of an oral appliance in the treatment of obstructive sleep apnea. Chest 2002;122:8717.[Medline]
- Marklund M, Franklin KA, Persson M. Orthodontic side-effects of mandibular advancement devices during treatment of snoring and sleep apnoea. Eur J Orthod 2001;23(2):13544.[Abstract/Free Full Text]
- Panula K, Keski-Nisula K. Irreversible alteration in occlusion caused by a mandibular advancement appliance: an unexpected complication of sleep apnea treatment. Int J Adult Orthodon Orthognath Surg 2000;15(3):1926.[Medline]
- Friedlander AH, Friedlander IK, Yueh R, Littner MR. The prevalence of carotid atheromas seen on panoramic radiographs of patients with obstructive sleep apnea and their relation to risk factors for atherosclerosis. J Oral Maxillofac Surg 1999;57:51621.[Medline]
- Cohen SN, Friedlander AH, Jolly DA, Date L. Carotid calcification on panoramic radiographs: an important marker for vascular risk. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2002;94:5104.[Medline]
- Moore K, Esther M. Current medical management of sleep-related breathing disorders. Oral Maxillofac Surg Clin 2002; 14:297304.
- Findley LJ, Barth JT, Powers DC, Wilhoit SC, Boyd DG, Suratt PM. Cognitive impairment in patients with obstructive sleep apnea and associated hypoxemia. Chest 1986;90:68690.[Medline]
- Salorio CF, White DA, Piccirillo J, Duntley SP, Uhles ML. Learning, memory, and executive control in individuals with obstructive sleep apnea. J Clin Exp Neuropsychol 2002;24(1):93100.[Medline]
- Coughlin SR, Mawdsley L, Mugarza JA, Calverley PM, Wilding JP. Obstructive sleep apnoea is independently associated with an increased prevalence of metabolic syndrome. Eur Heart J 2004; 25:73541.[Abstract/Free Full Text]
- Partinen M, Jamieson A, Guilleminault C. Long-term outcome for obstructive sleep apnea syndrome patients: mortality. Chest 1988;94:12004.[Medline]
- Prinsell JR. Maxillomandibular advancement surgery for obstructive sleep apnea syndrome. JADA 2002;133:148997.[Abstract/Free Full Text]
- Wittmann V, Rodenstein DO. Health care costs and the sleep apnea syndrome. Sleep Med Rev 2004;8:26979.[Medline]
- Petersen EJ, Reiter ER. Hospital use in the treatment of sleep apnea. Laryngoscope 2004;114:4606.[Medline]
- Ulfberg J, Jonsson R, Edling C. Improvement of subjective work performance among obstructive sleep apnea patients after treatment with continuous positive airway pressure. Psychiatry Clin Neurosci 1999;53:6779.[Medline]
- Kempers KG, Foote JW, DiFlorio-Brennan T. Obesity: prevalence and considerations in oral and maxillofacial surgery. J Oral Maxillofac Surg 2000;58(2):13743.[Medline]
- Marciani RD, Raezer BF, Marciani HL. Obesity and the practice of oral and maxillofacial surgery. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2004;98(1):105.[Medline]
- Carmelli D, Swan GE, Bliwise DL. Relationship of 30-year changes in obesity to sleep-disordered breathing in the Western Collaborative Group Study. Obes Res 2000;8:6327.[Medline]
- Malhotra A, White DP. Obstructive sleep apnoea. Lancet 2002;360:23745.[Medline]
- Bray GA, Tartaglia LA. Medicinal strategies in the treatment of obesity. Nature 2000;404:6727.[Medline]
- Narkiewicz K. Sibutramine and its cardiovascular profile. Int J Obesity Relat Metab Disord 2002;26(supplement 4):S3841.
- Arterburn DE, Crane PK, Veenstra DL. The efficacy and safety of sibutramine for weight loss: a systematic review. Arch Intern Med 2004;164:9941003.[Abstract/Free Full Text]
- Alpert MA, Hashimi MW. Obesity and the heart. Am J Med Sci 1993;306(2):11723.[Medline]
- Schmieder RE, Messerli FH. Obesity hypertension. Med Clin North Am 1987;71:9911001.[Medline]
- Alpert MA. Obesity cardiomyopathy: pathophysiology and evolution of the clinical syndrome. Am J Med Sci 2001;321:22536.[Medline]
- Ramachandran A, Snehalatha C, Viswanathan V, Viswanathan M, Haffner SM. Risk of noninsulin dependent diabetes mellitus conferred by obesity and central adiposity in different ethnic groups: a comparative analysis between Asian Indians, Mexican Americans and Whites. Diabetes Res Clin Pract 1997;36(2):1215.[Medline]
- Willett WC, Dietz WH, Colditz GA. Guidelines for healthy weight. N Engl J Med 1999;341:42734.[Free Full Text]
- van Dam RM, Rimm EB, Willett WC, Stampfer MJ, Hu FB. Dietary patterns and risk for type 2 diabetes mellitus in U.S. men. Ann Intern Med 2002;136:2019.[Abstract/Free Full Text]
- Scheuller M, Weider D. Bariatric surgery for treatment of sleep apnea syndrome in 15 morbidly obese patients: long-term results. Otolaryngol Head Neck Surg 2001;125:299302.[Medline]
- Colditz GA, Willett WC, Rotnitzky A, Manson JE. Weight gain as a risk factor for clinical diabetes mellitus in women. Ann Intern Med 1995;122:4816.[Abstract/Free Full Text]
- Ruoff GE. The impact of nonsteroidal anti-inflammatory drugs on hypertension: alternative analgesics for patients at risk. Clin Ther 1998;20:37687.[Medline]
- Pinter GG, Atkins J. What causes diabetic renal failure? Lancet 1990;335:5901.[Medline]
- Page J, Henry D. Consumption of NSAIDs and the development of congestive heart failure in elderly patients: an underrecognized health problem. Arch Intern Med 2000;160:77784.[Abstract/Free Full Text]
- Brater DC. Anti-inflammatory agents and renal function. Semin Arthritis Rheum 2002;32:(3 supplement 1):3342.[Medline]
- Gortmaker SL, Must A, Perrin JM, Sobol AM, Dietz WH. Social and economic consequences of overweight in adolescence and young adulthood. N Engl J Med 1993;329:100812.[Abstract/Free Full Text]
- Wiese HJ, Wilson JF, Jones RA, Neises M. Obesity stigma reduction in medical students. Int J Obes Relat Metab Disord 1992;16:85968.[Medline]
- Wilson AT, Reilly CS. Anaesthesia and the obese patient. Int J Obes Relat Metab Disord 1993;17(8):42735.[Medline]
- Sin DD, Jones RL, Man SF. Obesity is a risk factor for dyspnea but not for airflow obstruction. Arch Intern Med 2002;162:147781.[Abstract/Free Full Text]
- Jenkins S, Moxham J. The effects of mild obesity on lung function. Respir Med 1991;85:30911.[Medline]
- Mey U, Glasmacher A, Hahn C, et al. Evaluation of an ultrasound-guided technique for central venous access via the internal jugular vein in 493 patients. Support Care Cancer 2003;11(3):14855.[Medline]
- Nasraway SA Jr, Hudson-Jinks TM, Kelleher RM. Multidiscipli-nary care of the obese patient with chronic critical illness after surgery. Crit Care Clin 2002;18:64357.[Medline]
- Cheymol G. Clinical pharmacokinetics of drugs in obesity: an update. Clin Pharmacokinet 1993;25(2):10314.[Medline]
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