JIOH on LinkedIn JIOH on Facebook
  • Users Online: 286
  • Home
  • Print this page
  • Email this page
Home About us Editorial board Ahead of print Current issue Search Archives Submit article Instructions Subscribe Contacts Login 

 Table of Contents  
Year : 2020  |  Volume : 12  |  Issue : 1  |  Page : 8-14

Obstructive sleep apnea and its relation with temporomandibular disorders: A narrative review

1 School of Dental Sciences, Universiti Sains Malaysia, Kelantan, Malaysia
2 Department of Oral Diagnostic and Surgical Sciences, School of Dentistry, International Medical University (IMU), Kuala Lumpur, Malaysia
3 Department of Oral and Craniofacial Health Sciences, College of Dental Medicine, University of Sharjah, Sharjah, UAE

Date of Submission15-Sep-2019
Date of Decision05-Nov-2019
Date of Acceptance05-Nov-2019
Date of Web Publication25-Feb-2020

Correspondence Address:
Dr. Zuryati Ab Ghani
School of Dental Sciences, Universiti Sains Malaysia, KotaBharu, Kubang Kerian 16150, Kelantan.
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jioh.jioh_246_19

Rights and Permissions

Sleep-disordered breathing (SDB) is a broad terminology that denotes a group of disorders. Conditions associated with SDB include obstructive sleep apnea (OSA), central sleep apnea, and upper airway resistance syndrome. Although OSA is most common in the general population, the reported prevalence shows a wide range of differences due to inconsistent study methodology. The pathophysiology of OSA has been described by active and passive theories. Polysomnography is considered as the gold standard and the most accurate tool for the diagnosis of OSA. Definitive diagnosis and determination of the severity of the OSA are instrumental before the commencement of the treatment. Patients with OSA are at increased risk of various endocrinal and metabolic disorders. OSA and temporomandibular disorders (TMD) have shown a clear relationship due to the highly prevalent rate of OSA in individuals with TMD. It may be concluded that concomitant TMD and sleep bruxism may be present in patients with OSA. Furthermore, the use of oral appliances in the treatment of OSA in mandibular advancement may cause TMD. The aim of this article was to review current knowledge on OSA and the association between TMD and OSA. This review also emphasizes that concomitant TMD in OSA is an object worthy of future study.

Keywords: Bruxism, Obstructive Sleep Apnea, Temporomandibular Disorders

How to cite this article:
Zwiri AM, Ab Ghani Z, Husein A, Suan Phaik K, Kassim NK, Zainal SA, Samsudin AR. Obstructive sleep apnea and its relation with temporomandibular disorders: A narrative review. J Int Oral Health 2020;12:8-14

How to cite this URL:
Zwiri AM, Ab Ghani Z, Husein A, Suan Phaik K, Kassim NK, Zainal SA, Samsudin AR. Obstructive sleep apnea and its relation with temporomandibular disorders: A narrative review. J Int Oral Health [serial online] 2020 [cited 2023 Feb 6];12:8-14. Available from:

  Introduction Top

Sleep-disordered breathing (SDB) is a broad terminology that denotes a group of disorders. Several clinical conditions, which cause abnormal respiration during sleep, have been identified during the last few decades. Conditions associated with SDB include obstructive sleep apnea (OSA), central sleep apnea (CSA), and upper airway resistance syndrome (UARS).

Partial or complete obstruction of the upper airway occurs repeatedly during sleep in OSA. Partial or complete obstruction of the airway during hypopnea or apnea results in the partial or complete collapse of the airway. This results in a decrease or a lack of ventilation.[1] Hypopnea and apnea are known as respiratory events. These respiratory events cause serious clinical complications. Disturbances of blood gases causing hypoxemia and hypercapnia are the major consequences of respiratory events. Compensatory mechanisms that include activation of the diaphragm and muscles of the upper airway, increase the neural ventilator drive through chemoreceptor activity that resolves the gas disturbances and reestablishes the airflow.[2] However, this mechanism does not work in many patients with OSA. The airway remains occluded until the patient awakes and tries to breathe normally, which reopens the airway restoring the normal breathing.[3] Continuous occlusion, the collapse of the airway, awakening, reestablishment of the respiration result in fragmented sleep. Consequently, the sleep pattern is altered in most patients with OSA due to excessive anticipation. In comparison to normal individuals, these patients have poor-quality sleep as they spend significantly increased time in two lighter stages (stage I and II) of sleep and decreased time in the restorative slow-wave sleep.[4],[5],[6] Reduced or absent rapid eye movement (REM) sleep has also been observed in some patients with apnea, whereas in some patients, REM sleep remained normal. Longer respiratory events and greater levels of blood deoxygenation have been observed in some patients with REM sleep. Contrary to it, in some patients, no change was observed in the duration and severity of the respiratory events during REM sleep.[3] Excessive daytime sleepiness, snoring, and witnessed breathing events are the most common symptoms of OSA.[7] The daytime sleeping is observable easily, whereas the snoring and witnessed breathing events occur only when the patient is sleeping and become difficult to identify. Bed partners of these apneic individuals used to witness respiratory events and snoring. On the advice of bed partners, these patients consult the clinics.[8] In addition to daytime sleep, patients with OSA also experience several neurocognitive abnormalities due to fragmented sleep and disturbed blood gases.[9],[10] In CSA, patients do not experience obstruction of airway or continued respiratory effort after breathing cessation during sleep as compared to OSA. Patients with UARS present with similar symptoms of OSA. However, they do not present with obstructive apnea or hypopnea. Features of OSA in patients with UARS may be reported using polysomnographic investigations by observing repeated arousals.[5] Treatment of OSA with oral appliance such as mandibular advancement devices (MADs) may be associated with the development of symptoms of temporomandibular disorders (TMD).[3]

The relationship between OSA and TMD seems to be controversial and unclear. Several studies have suggested that SDB can occur concomitantly with OSA. It has been suggested that TMD be taken into consideration when using oral appliance therapy for the treatment of OSA.[4],[5],[6],[7] With this information in mind, the aim of this review article was to review current knowledge on OSA and the association between TMD and OSA. This review also emphasizes that concomitant TMD in OSA is an object worthy of future study.

  Epidemiology of Obstructive Sleep Apnea Top

Although OSA is most common in the general population, the reported prevalence shows a wide range of differences due to inconsistent study methodology. A study reported that 9%–38% of the adult population has OSA.[11] American Heart Association and the American College of Cardiology have reported that 82% of men and 93% of women with clinically proven OSA are not properly diagnosed.[12] It has also been reported that males, the elderly people, and individuals with a high body mass index (BMI) have a greater prevalence of OSA.[11] It has to be noted that increase in the averages for the BMI in the general population results in increased incidence of OSA. Among other factors, the distribution of body fat, especially in the trunk and neck, predisposes men to OSA. Sex hormones neurologically control the upper respiratory airway ventilation and functions of muscles, which also contribute to the high prevalence of OSA in males.[13]

  Pathophysiology of Obstructive Sleep Apnea Top

The pathophysiology of OSA has been described by active and passive theories. It has been reported that lateral pharyngeal walls and velopharynx close spasmodically at the end of expiration.[14] During inspiration, the muscle contraction persists and remains contracted without returning to relaxed status until the arousal from sleep. Contrary to it, no muscular activity was observed during airway closure using electromyography. This leads to the proposal of the passive theory.[15] The passive theory states that active neuromuscular contraction of the pharyngeal muscles is not required for the closure of the airway. Alternatively, the backward falling off the tongue along with impaired or full loss of dilation of pharyngeal muscles causes the airway obstruction during sleep.[16] As OSA is multifactorial, both theories can be partly assumed to be true. In humans, ventilation, speech, and phonation shall be constantly maintained simultaneously. In addition to that, larynx shall allow the passage of alimentation through the esophagus without effecting or blocking the airway.[17] During sleep, OSA occurs cyclically. Despite respiratory efforts, the pharyngeal airway collapses, which results in repetitive arousal in patients with OSA. Complete or partial airway obstruction due to pharyngeal narrowing or decreased muscles tonicity repose the tongue against the posterior side of the pharyngeal wall.[18] The decreased airflow results in the increased ventilation efforts leading to an episode of arousal that reestablishes the muscle tone and opening of the airway.[19] This process of obstructed airflow, arousal, and reestablishment of the normal breathing occurs many times during sleep, which causes insufficient REM sleep, hypoxemia, and fragmented sleep. Recurrent episodes of these events lead to psychological and physiological complications.[20] Snoring, gasping, awakening during the night, observable apnea, and nocturnal urination are the most consistent features of OSA.[20] Predisposing anatomic factors of OSA include increased BMI, obesity, nasal septum deviation, nasal congestion, reduced volume of the nasopharynx, and craniofacial abnormalities.[21],[22]

Anatomically, the airway may also be reduced due to soft palate elongation, macroglossia, adenoid hypertrophy, and/or enlarged tonsils. Other clinical conditions such as mandibular retrognathia, augmented lower face vertical dimension, maxillary retrognathia, and inferior position of the hyoid bone have shown strong association with OSA.[1],[23],[24] Decreased muscle tone in the pharyngeal muscle is a natural phenomenon during sleep. Other comorbidities that cause OSA can lead to pharyngeal collapse and termination of the respiration.[25]

  Investigations and Diagnostics in Obstructive Sleep Apnea Top

Various diagnostic strategies may be used for the diagnosis of patients with sleep apnea. These modalities include comprehensive clinical and medical history and laboratory investigations. History is obtained using questionnaires. Questionnaires include queries of sleeping attitudes (during night or day), snoring, or other symptoms of OSA. Two most commonly used questionnaires are STOP-Bang Questionnaire and the Berlin Questionnaire.[26],[27] Identification of patients with suspected OSA can be carried out easily using any of these two questionnaires. Once identified, these patients require a definite diagnosis. Evidence-based recommendations and diagnostic strategies were developed by the American Academy of Sleep Medicine for OSA.[7] Diagnostic and treatment strategies were recommended after reviewing the available literature. Diagnostic strategies include collection of data using sleep-oriented questionnaire, sleeping history, and clinical and physical examination. Tests using polysomnography (PSG) and portable monitors are also the diagnostic tools for OSA. The severity of the sleep disorder is determined by the evaluation of these data. Proper treatment is only possible by knowing the severity of the OSA. Plain cephalometric radiography used for the evaluation of skeletal and soft tissue abnormalities is one of the most common and inexpensive diagnostic tools. However, it is to be kept in mind that this method provides two-dimensional details, whereas the pharyngeal area is three-dimensional structure. This is one of the major disadvantages of plain cephalometric radiography. Advantages include identification of soft tissue abnormalities including tongue size and retro-glossal space. The relationship between maxillofacial complex and cranial base can be assessed using lateral cephalometric method.

PSG is considered as the gold standard and the most accurate tool for the diagnosis of OSA.[28],[29] Functions of the respiratory system, cardiovascular system, eye movement, and muscle activity are easily monitored using PSG. Snoring, apnea, hypopnea, and frequency are determined by this method in patients with OSA. More cost and inconvenience are two major disadvantages of PSG. Reliable, inexpensive, and readily available diagnostic methods at home are required for the diagnosis of highly prevalent OSA. Computed tomography (CT) scan, magnetic resonance imagining (MRI) and endoscopy are used to direct surgical and non-surgical treatment. However, these methods can only be used when the patient is awake, which provides little clinical information about airway obstruction during sleep.[17]

  Treatment of Obstructive Sleep Apnea Top

Definitive diagnosis and determination of the severity of the OSA are instrumental before the commencement of the treatment. Change in the lifestyle is always considered the first step in the treatment of OSA. Obesity, tonsillar hypertrophy, and facial deformities are corrected being the predisposing factors of OSA. Alcoholism and the use of sedatives are circumvented by the patients with OSA.[17]

Once diagnosed, the treatment strategies including surgical and nonsurgical methods are followed to minimize or eradicate the sign and symptoms of OSA. Weight loss in case of obesity, medications, use of oral appliances, and continuous positive airway pressure (CPAP) devices are used as nonsurgical methods for treating OSA. The reduction of BMI in the case of obese patients with OSA is the first-line treatment. It is to be noted that obesity is one of the major predisposing factors of OSA,[30] and reduction in body fat reduces the severity of the OSA. Reduced pharyngeal muscle tonicity, airway resistance, and pharyngeal surface tension are the major contributory factors in OSA. Medications that increase pharyngeal dilation, reduce resistance in the airway, and improve pharyngeal surface tension are used in the treatment of OSA. Among others, nasal congestion is also a predisposing factor of OSA. However, the use of fluticasone nasal spray to decrease nasal congestion has not shown any promising results in improving the daytime sleep or correction of apnea–hypopnea index.[30] Improvement of the inspiration using medications can also be used as a treatment strategy.[31] It has been reported that testosterone level remains low in patients with OSA. In addition to other treatment modalities, testosterone replacement therapy may be used is male patients with OSA.[32],[33] Modafinil and armodafinil are central nervous system stimulants that have shown assistance in residual daytime fatigue in patients with OSA using CPAP therapy.[34] Noncandidatures of surgical procedures and intolerant CPAP therapy patients with OSA can be treated with oxygen therapy.[35] Although as aforementioned, some medications may be used in the treatment of OSA, data advising the use of medications as a primary treatment tool for OSA are scanty.[2]

Continuous positive airway pressure

CPAP is used as a first-line treatment option in patients with OSA.[36] Positive pressure is generated by a blower present in the equipment. It works as a pneumatic splint and prevents the cyclical collapse of the upper airway during sleep. The airway is kept open (“splint effect”) by increased intraluminal upper airway pressure in addition to the pressure of the soft tissue airway structures. This helps in improving oxygenation, increases lung volume, and enhances the ventilation drive.[37],[38] Although CPAP is considered as the gold standard treatment option for the patients with OSA,[39] a major drawback is the interface, that is, mask and inadequate adherence of the equipment.[37]

Oral appliances for treatment of obstructive sleep apnea

OSA can be treated using oral appliances. These appliances move the mandible interiorly. The interior movement of the mandible as a treatment option is successful only in patients with mild to moderate OSA. Tongue, hyoid bone, and the muscles associated are simultaneously advanced by repositioning the mandible that enhances the patency of the airway. Inexpensive oral appliances with decreased noise and increased patient comfort make these devices a best treatment option.[40] However, some disadvantages are also associated with the use of oral appliance use, including temporomandibular joint (TMJ) discomfort, movement of tooth, and downward mandibular rotation.[41] A large number of oral appliances are in use and their count is still growing. These appliances can be divided into three types: mandibular advancement appliances (MAA), tongue retaining devices (TRD), and soft palate lifters (SPL). Of all these types, MAA are commonly used. SPL are not used nowadays. TRD are also used infrequently and are only used in patients with dental complications.

  Biomarkers Associated with Obstructive Sleep Apnea Top

The determination of serum and urinary proteins has shown promising results in the diagnosis of OSA.[42] However, it may be worth noting that no simple, single, and useful set of biomarkers is available, which can be carried out routinely in clinical practice. Further research is needed in this field.[43] At this initial stage of discovering and validating the specific set of biomarkers to diagnose OSA in children and adults, data suggest the use of these biomarkers. Data show that biomarkers are useful enough to diagnose OSA in children and adult patients although there is no available recommended specific set of markers at this initial stage of research.[44] Blood analysis has been carried out in most of the studies. Interleukin-6 (IL-6), tissue necrosis factor α, and C-reactive proteins have been explored in the diagnosis of OSA in adults. To discriminate patients with and without OSA, IL-6 and IL-10 have shown encouraging results as a set of biomarkers.[44] Literature reports a clear correlation of IL-6 with psychosocial stress.[45],[46] IL-18 has also been suggested as a marker of the stress response.[47]

  Obstructive Sleep Apnea and Hormones and Vitamin D Top

Patients with OSA are at increased risk of various endocrinal and metabolic disorders. These disorders may lead to serious clinical complications including reduced life expectancy. It is pivotal to understand and recognize the interaction of upper airway dysfunction and its endocrinal complications.[48] A transient increase in cortisol level has been observed in hypoxia and nocturnal awakening.[49] Studies have reported the sleep-promoting properties of melatonin as well.[50] In patients with OSA, nocturnal plasma levels of melatonin have been investigated using PSG during diagnosis and one day after CPAP therapy in a study by Hernández et al.[51] Abnormal section of melatonin was found in patients with OSA with absent nocturnal melatonin peak before and after therapy. The pathogenesis of OSA is multifactorial and complex. The upper airway skeletal muscles are instrumental in the pathogenesis of OSA.[1] A study conducted to find the seasonal effects on the prevalence of OSA has shown an increased incidence of OSA in more severe clinical complications in winter.[52] This seasonal variation may be linked to decreased vitamin D levels in winter in patients with OSA.[53] Reduced 25-hydroxyvitamin D (25[OH] D) levels decrease the functional capability of the musculoskeletal system.[54]

  Obstructive Sleep Apnea and Temporomandibular Disorder Relationship Top

TMD are a group of musculoskeletal and neuromuscular clinical conditions involving the temporomandibular junctions (TMJs), masticatory muscles, and all other associated tissues.[55] As the clinical manifestations are associated with various sites, TMD can be classified into TMJ articular disorders, masticatory muscles disorders, and inflammatory disorders.[56] OSA and TMD disorders have shown a clear relationship due to the highly prevalent rate of OSA in individuals with TMD.[57] Other studies have also established the increased frequency of TMD in patients with OSA.[58] It has been evident that some patients using MADs developed TMD. Care should be taken during clinical examination for the presence of signs and symptoms in patients with TMD.[56] A study conducted in adults free on baseline TMD, developed TMD later in almost 73% of the cases. It suggests that the resistance in inspiration leading to OSA also decreases the sensitivity and impairment of baroreceptors, which results in TMD. Most of the present cases with OSA also show bruxism that can trigger TMD.[59]

Association of TMD or orofacial pain and SDB has been evaluated and correlated.[60],[61] A patient experiencing TMJ pain also shows other signs and symptoms. These signs and symptoms include soreness of muscles and/or joints, bruxism, reduced or altered movement, facial pain, tooth chipping, and tooth movement. Detailed clinical examination, radiographic studies, a careful review of the medical history of the patient needed to prevent the consulting dentist from being biased considering these symptoms to be of dental or oral origin.[62] Once the diagnosis of TMD, bruxism, or muscular spasms is made; treatment protocols are suggested. Treatment options include the use of oral appliances, medications, and exercises.[62] To find the relationship between oral appliances and TMD, patients attending the sleep clinic with sleep disorders were recommended the use of oral appliances. It was found that after treatment, nearly 52% of patients with OSA had TMD. This concluded that TMD was associated with high prevalence of pain after the use of oral appliances. To manage and reduce the pain, supportive medication should be used.[63] Misinterpretation of SDB considering it as TMD can be made due to the similar signs and symptoms. When misdiagnosed, dental treatment can worsen, these clinical manifestations increase the risk of untreated and progressive SDB in addition to the presenting clinical presentation.[62] A study reported that in 100 diagnosed cases of OSA, 2% of the patients also had clear signs and symptoms of TMD.[64] Cunali et al.[58] applied the research diagnostic criteria for TMD on mild to moderate patients with OSA and found that 52% of the patients had TMD.

Some cohort and case-control studies have also shown a high probability of the association between OSA and TMD.[65] A large case-control study showed that almost 10% of the adult patients with TMD had OSA.[66] It was reported that most adult patients with TMD were also having OSA when compared to age- and sex-matched controls.[26] Patients with masticatory myofascial pain were found to sleep more in daytime.[67] A randomized, double-blind, and placebo-controlled study was conducted by advising oral appliances in addition to exercise to preclude the incidence of TMD. To one group, jaw exercise was advised to reduce or prevent the occurrence of TMD pain, whereas the placebo group was kept on neck exercise. Both groups showed no difference in the occurrence of TMD except one case in the placebo group developed arthralgia. It was then concluded that jaw exercise has very little effect to prevent TMD. Further studies on a large sample size were recommended to find the effectiveness of exercise in TMD.[68] Sleep bruxism (SB) is a stereotyped movement disorder that occurs due to rhythmic masticatory muscle activity. It is usually associated with tooth grinding and tooth clenching.[69] An international group of experts reviewed bruxism and SDB. In 2013, they adopted and published an online updated definition for the classification of sleep disorders. Two distinct cardinal clinical features of bruxism were recognized, which include sleep (designated as SB) and awakening (designated as awake bruxism). They defined SB as a repetitive jaw muscle movement in which grinding or clenching of teeth and invigoration and pushing of the mandible occurs.[69],[70],[71] Sleep position was reported as a common factor between SB and OSA. In 50%–58% of the sleeping time in both conditions, the patient’s position was supine. The most effective treatment protocol in the management of SB and OSA is the maintenance of the airway by CPAP.[71]

  Conclusion Top

The concomitant TMD and SB may be present in patients with OSA. Furthermore, it is evident that the use of oral appliances in the treatment of OSA in mandibular advancement may cause TMD. Detailed clinical history, physical examination, and presentation of the associated conditions should be observed for the better management of patients with OSA. Physical and psychological treatment approaches should be used for these patients.


The authors would like to acknowledge the Universiti Sains Malaysia (USM) Fellowship awarded to Dr Abdalwhab M A Zwiri.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Dempsey JA, Veasey SC, Morgan BJ, O’Donnell CP. Pathophysiology of sleep apnea. Physiol Rev 2010;90:47-112.  Back to cited text no. 1
Osman AM, Carter SG, Carberry JC, Eckert DJ. Obstructive sleep apnea: Current perspectives. Nat Sci Sleep 2018;10:21-34.  Back to cited text no. 2
Spicuzza L, Caruso D, Di Maria G. Obstructive sleep apnoea syndrome and its management. Ther Adv Chronic Dis 2015;6:273-85.  Back to cited text no. 3
Kim DS, Lee CL, Ahn YM. Sleep problems in children and adolescents at pediatric clinics. Korean J Pediatr 2017;60:158-65.  Back to cited text no. 4
Berry RB, Budhiraja R, Gottlieb DJ, Gozal D, Iber C, Kapur VK, et al; American Academy of Sleep Medicine. Rules for scoring respiratory events in sleep: Update of the 2007 AASM manual for the scoring of sleep and associated events. Deliberations of the sleep apnea definitions task force of the American Academy of Sleep Medicine. J Clin Sleep Med 2012;8:597-619.  Back to cited text no. 5
Lévy P, Kohler M, McNicholas WT, Barbé F, McEvoy RD, Somers VK, et al. Obstructive sleep apnoea syndrome. Nat Rev Dis Primers 2015;1:15015.  Back to cited text no. 6
Epstein LJ, Kristo D, Strollo PJ Jr, Friedman N, Malhotra A, Patil SP, et al; Adult Obstructive Sleep Apnea Task Force of the American Academy of Sleep Medicine. Clinical guideline for the evaluation, management and long-term care of obstructive sleep apnea in adults. J Clin Sleep Med 2009;5:263-76.  Back to cited text no. 7
Esmaeel HM, Mohammadien HA, Saleh AE, Mohamed FH. Prepolysomnography evaluation can predict obstructive sleep apnea and is correlated to its severity. Egypt J Bronchol 2019;13:556-62.  Back to cited text no. 8
  [Full text]  
Saper CB, Fuller PM. Wake-sleep circuitry: An overview. Curr Opin Neurobiol 2017;44:186-92.  Back to cited text no. 9
Lee W, Nagubadi S, Kryger MH, Mokhlesi B. Epidemiology of obstructive sleep apnea: A population-based perspective. Expert Rev Respir Med 2008;2:349-64.  Back to cited text no. 10
Senaratna CV, Perret JL, Lodge CJ, Lowe AJ, Campbell BE, Matheson MC, et al. Prevalence of obstructive sleep apnea in the general population: A systematic review. Sleep Med Rev 2017;34:70-81.  Back to cited text no. 11
Witkowski A, Prejbisz A, Florczak E, Kądziela J, Śliwiński P, Bieleń P, et al. Effects of renal sympathetic denervation on blood pressure, sleep apnea course, and glycemic control in patients with resistant hypertension and sleep apnea. Hypertension 2011;58:559-65.  Back to cited text no. 12
Mallampalli MP, Carter CL. Exploring sex and gender differences in sleep health: A society for women’s health research report. J Womens Health (Larchmt) 2014;23:553-62.  Back to cited text no. 13
Edwards BA, Eckert DJ, Jordan AS. Obstructive sleep apnoea pathogenesis from mild to severe: Is it all the same? Respirology 2017;22:33-42.  Back to cited text no. 14
Younes M. Fifty years of physiology in obstructive sleep apnea. Am J Respir Crit Care Med 2017;196:954-7.  Back to cited text no. 15
McLaren AT, Bin-Hasan S, Narang I. Diagnosis, management and pathophysiology of central sleep apnea in children. Paediatr Respir Rev 2019;30:49-57.  Back to cited text no. 16
Rasmusson L, Bidarian A, Sennerby L, Scott G. Pathophysiology and treatment options in obstructive sleep apnoea: A review of the literature. Int J Clin Med 2012;3:473-84.  Back to cited text no. 17
Veys B, Pottel L, Mollemans W, Abeloos J, Swennen G, Neyt N. Three-dimensional volumetric changes in the upper airway after maxillomandibular advancement in obstructive sleep apnoea patients and the impact on quality of life. Int J Oral Maxillofac Surg 2017;46:1525-32.  Back to cited text no. 18
Jordan AS, O’Donoghue FJ, Cori JM, Trinder J. Physiology of arousal in obstructive sleep apnea and potential impacts for sedative treatment. Am J Respir Crit Care Med 2017;196:814-21.  Back to cited text no. 19
Wenner JB, Cheema R, Ayas NT. Clinical manifestations and consequences of obstructive sleep apnea. J Cardiopulm Rehabil Prev 2009;29:76-83.  Back to cited text no. 20
Stubbs B, Vancampfort D, Veronese N, Solmi M, Gaughran F, Manu P, et al. The prevalence and predictors of obstructive sleep apnea in major depressive disorder, bipolar disorder and schizophrenia: A systematic review and meta-analysis. J Affect Disord 2016;197:259-67.  Back to cited text no. 21
Surtees ADR, Oliver C, Jones CA, Evans DL, Richards C. Sleep duration and sleep quality in people with and without intellectual disability: A meta-analysis. Sleep Med Rev 2018;40:135-50.  Back to cited text no. 22
Hourfar J, Kinzinger GS, Feifel H, Vehr VM, Lisson JA. Effects of combined orthodontic-orthognathic treatment for class II and III correction on posterior airway space: Comparison of mono- and bignathic osteotomies. J Orofac Orthop 2017;78:455-65.  Back to cited text no. 23
Izu SC, Itamoto CH, Pradella-Hallinan M, Pizarro GU, Tufik S, Pignatari S, et al. Obstructive sleep apnea syndrome (OSAS) in mouth breathing children. Braz J Otorhinolaryngol 2010;76:552-6.  Back to cited text no. 24
Van de Heyning PH, Badr MS, Baskin JZ, Cramer Bornemann MA, De Backer WA, Dotan Y, et al. Implanted upper airway stimulation device for obstructive sleep apnea. Laryngoscope 2012;122:1626-33.  Back to cited text no. 25
Abrishami A, Khajehdehi A, Chung F. A systematic review of screening questionnaires for obstructive sleep apnea. Can J Anaesth 2010;57:423-38.  Back to cited text no. 26
Enciso R, Clark GT. Comparing the Berlin and the ARES questionnaire to identify patients with obstructive sleep apnea in a dental setting. Sleep Breath 2011;15:83-9.  Back to cited text no. 27
Shigeta Y. Diagnosis and treatment for obstructive sleep apnea: Fundamental and clinical knowledge in obstructive sleep apnea. J Prosthodont Res 2015;59:161-71.  Back to cited text no. 28
Mannarino MR, Di Filippo F, Pirro M. Obstructive sleep apnea syndrome. Eur J Intern Med 2012;23:586-93.  Back to cited text no. 29
El-Anwar MW, Amer HS, Askar SM, Elsobki A, Awad A. Could nasal surgery affect multilevel surgery results for obstructive sleep apnea? J Craniofac Surg 2018;29:1897-9.  Back to cited text no. 30
Hedner J, Zou D. Drug therapy in obstructive sleep apnea. Sleep Med Clin 2018;13:203-17.  Back to cited text no. 31
Burschtin O, Wang J. Testosterone deficiency and sleep apnea. Sleep Med Clin 2016;11:525-9.  Back to cited text no. 32
Burschtin O, Wang J. Testosterone deficiency and sleep apnea. Urol Clin North Am 2016;43:233-7.  Back to cited text no. 33
Nakai T, Matsuo A, Takata Y, Usui Y, Kitamura K, Chikazu D. Role of dental sleep medicine in management of patients with obstructive sleep apnea disorders using a team approach. Acta Odontol Scand 2018;76:605-11.  Back to cited text no. 34
Mehta V, Vasu TS, Phillips B, Chung F. Obstructive sleep apnea and oxygen therapy: A systematic review of the literature and meta-analysis. J Clin Sleep Med 2013;9:271-9.  Back to cited text no. 35
McNicholas WT, Bonsignore MR, Lévy P, Ryan S. Mild obstructive sleep apnoea: Clinical relevance and approaches to management. Lancet Respir Med 2016;4:826-34.  Back to cited text no. 36
Guzman MA, Sgambati FP, Pho H, Arias RS, Hawks EM, Wolfe EM, et al. The efficacy of low-level continuous positive airway pressure for the treatment of snoring. J Clin Sleep Med 2017;13:703-11.  Back to cited text no. 37
Mendelson M, Bailly S, Marillier M, Flore P, Borel JC, Vivodtzev I, et al. Obstructive sleep apnea syndrome, objectively measured physical activity and exercise training interventions: A systematic review and meta-analysis. Front Neurol 2018;9:73.  Back to cited text no. 38
Liu T, Li W, Zhou H, Wang Z. Verifying the relative efficacy between continuous positive airway pressure therapy and its alternatives for obstructive sleep apnea: A network meta-analysis. Front Neurol 2017;8:289.  Back to cited text no. 39
Hamoda MM, Kohzuka Y, Almeida FR. Oral appliances for the management of OSA: An updated review of the literature. Chest 2018;153:544-53.  Back to cited text no. 40
Nazarali N, Altalibi M, Nazarali S, Major MP, Flores-Mir C, Major PW. Mandibular advancement appliances for the treatment of paediatric obstructive sleep apnea: A systematic review. Eur J Orthod 2015;37:618-26.  Back to cited text no. 41
Gozal D. Serum, urine, and breath-related biomarkers in the diagnosis of obstructive sleep apnea in children: Is it for real? Curr Opin Pulm Med 2012;18:561-7.  Back to cited text no. 42
Fleming WE, Holty JE, Bogan RK, Hwang D, Ferouz-Colborn AS, Budhiraja R, et al. Use of blood biomarkers to screen for obstructive sleep apnea. Nat Sci Sleep 2018;10:159-67.  Back to cited text no. 43
Canto GD, Pachêco-Pereira C, Aydinoz S, Major PW, Flores-Mir C, Gozal D. Biomarkers associated with obstructive sleep apnea: A scoping review. Sleep Med Rev 2015;23:28-45.  Back to cited text no. 44
Del Giudice M, Gangestad SW. Rethinking IL-6 and CRP: Why they are more than inflammatory biomarkers, and why it matters. Brain Behav Immun 2018;70:61-75.  Back to cited text no. 45
Prasad B. Determinants of sleepiness in obstructive sleep apnea. Sleep 2018;41:199.  Back to cited text no. 46
La Fratta I, Tatangelo R, Campagna G, Rizzuto A, Franceschelli S, Ferrone A, et al. The plasmatic and salivary levels of IL-1β, IL-18 and IL-6 are associated to emotional difference during stress in young male. Sci Rep 2018;8:3031.  Back to cited text no. 47
Ruchała M, Bromińska B, Cyrańska-Chyrek E, Kuźnar-Kamińska B, Kostrzewska M, Batura-Gabryel H. Obstructive sleep apnea and hormones—A novel insight. Arch Med Sci 2017;13:875-84.  Back to cited text no. 48
Koren D, Dumin M, Gozal D. Role of sleep quality in the metabolic syndrome. Diabetes Metab Syndr Obes 2016;9:281-310.  Back to cited text no. 49
Xu Kun, Hu Cai Hong, Subramanian P. Melatonin and sleep. Biol Rhythm Res 2019;50:490-3.  Back to cited text no. 50
Hernández C, Abreu J, Abreu P, Castro A, Jiménez A. Nocturnal melatonin plasma levels in patients with OSAS: The effect of CPAP. Eur Respir J 2007;30:496-500.  Back to cited text no. 51
Cassol CM, Martinez D, Da Silva FABS, Fischer MK, Lenz MDCS, Bós ÂJG. Is sleep apnea a winter disease?: Meteorologic and sleep laboratory evidence collected over 1 decade. Chest 2012;142:1499-507.  Back to cited text no. 52
Van Schoor NM, Knol DL, Deeg DJ, Peters FP, Heijboer AC, Lips P. Longitudinal changes and seasonal variations in serum 25-hydroxyvitamin D levels in different age groups: Results of the longitudinal aging study Amsterdam. Osteoporos Int 2014;25:1483-91.  Back to cited text no. 53
Bischoff-Ferrari HA, Dietrich T, Orav EJ, Hu FB, Zhang Y, Karlson EW, et al. Higher 25-hydroxyvitamin D concentrations are associated with better lower-extremity function in both active and inactive persons aged > or =60 y. Am J Clin Nutr 2004;80:752-8.  Back to cited text no. 54
Khan M, Nishi SE, Hassan SN, Islam MA, Gan SH. Trigeminal neuralgia, glossopharyngeal neuralgia, and myofascial pain dysfunction syndrome: An update. Pain Res Manag 2017;2017:7438326.  Back to cited text no. 55
Merrill RL. Temporomandibular disorder pain and dental treatment of obstructive sleep apnea. Dent Clin North Am 2012;56:415-31.  Back to cited text no. 56
Olmos SR. Comorbidities of chronic facial pain and obstructive sleep apnea. Curr Opin Pulm Med 2016;22:570-5.  Back to cited text no. 57
Cunali PA, Almeida FR, Santos CD, Valdrighi NY, Nascimento LS, Dal’Fabbro C, et al. Prevalence of temporomandibular disorders in obstructive sleep apnea patients referred for oral appliance therapy. J Orofac Pain 2009;23:339-44.  Back to cited text no. 58
Sanders AE, Essick GK, Fillingim R, Knott C, Ohrbach R, Greenspan JD, et al. Sleep apnea symptoms and risk of temporomandibular disorder: OPPERA cohort. J Dent Res 2013;92:70S-7S.  Back to cited text no. 59
Smith MT, Wickwire EM, Grace EG, Edwards RR, Buenaver LF, Peterson S, et al. Sleep disorders and their association with laboratory pain sensitivity in temporomandibular joint disorder. Sleep 2009;32:779-90.  Back to cited text no. 60
Wickwire E, Bellinger K, Kronfli T, Grace E, Sarlani E, Wang K, et al. (153) Relations between objective sleep data, sleep disorders, and signs and symptoms of temporomandibular joint disorder (TMD). J Pain 2008;9:14.  Back to cited text no. 61
Babiec DF. Temporomandibular pain caused by sleep disorders: A review and case report. Gen Dent 2017;65: 30-3.  Back to cited text no. 62
Ohrbach R, Dworkin SF. The evolution of TMD diagnosis: Past, present, future. J Dent Res 2016;95:1093-101.  Back to cited text no. 63
Randerath WJ, Verbraecken J, Andreas S, Bettega G, Boudewyns A, Hamans E, et al; European Respiratory Society task force on non-CPAP therapies in sleep apnoea. Non-CPAP therapies in obstructive sleep apnoea. Eur Respir J 2011;37:1000-28.  Back to cited text no. 64
Almoznino G, Benoliel R, Sharav Y, Haviv Y. Sleep disorders and chronic craniofacial pain: Characteristics and management possibilities. Sleep Med Rev 2017;33:39-50.  Back to cited text no. 65
Hoffmann RG, Kotchen JM, Kotchen TA, Cowley T, Dasgupta M, Cowley AW Jr. Temporomandibular disorders and associated clinical comorbidities. Clin J Pain 2011;27:268-74.  Back to cited text no. 66
Klasser GD, Almoznino G, Fortuna G. Sleep and orofacial pain. Dent Clin North Am 2018;62:629-56.  Back to cited text no. 67
Ishiyama H, Inukai S, Nishiyama A, Hideshima M, Nakamura S, Tamaoka M, et al. Effect of jaw-opening exercise on prevention of temporomandibular disorders pain associated with oral appliance therapy in obstructive sleep apnea patients: A randomized, double-blind, placebo-controlled trial. J Prosthodont Res 2017;61:259-67.  Back to cited text no. 68
Jokubauskas L, Baltrušaitytė A. Relationship between obstructive sleep apnoea syndrome and sleep bruxism: A systematic review. J Oral Rehabil 2017;44:144-53.  Back to cited text no. 69
Herrero Babiloni A, Lavigne GJ. Sleep bruxism: A “bridge” between dental and sleep medicine. J Clin Sleep Med 2018;14:1281-3.  Back to cited text no. 70
Balasubramaniam R, Klasser GD, Cistulli PA, Lavigne GJ. The link between sleep bruxism, sleep disordered breathing and temporomandibular disorders: An evidence-based review. J Dent Sleep Med 2014;1:27-37.  Back to cited text no. 71

This article has been cited by
1 Temporomandibular disorders: a problem-based approach, 2nd edition
Larry Z. Lockerman
CRANIO®. 2022; 40(5): 468
[Pubmed] | [DOI]


Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

  In this article
Epidemiology of ...
Pathophysiology ...
Investigations a...
Treatment of Obs...
Biomarkers Assoc...
Obstructive Slee...
Obstructive Slee...

 Article Access Statistics
    PDF Downloaded290    
    Comments [Add]    
    Cited by others 1    

Recommend this journal