Efficacy of a mandibular advancement appliance on sleep disordered breathing in children



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EFFICACY OF A MANDIBULAR ADVANCEMENT APPLIANCE ON SLEEP DISORDERED BREATHING IN CHILDREN


Lay Summary

Sleep-Disordered Breathing (SDB) varies from habitual snoring to completely stopped breathing and can be found in up to 10% of New Zealand children. SDB can cause breathlessness and frequent waking during sleep due to partial or complete obstruction of the upper airway. It can also cause growth disorders, daytime sleepiness, educational concerns, and behavioral problems.

In the most severe cases, SDB can also lead to life-threatening events like heart failure. Therefore, SDB may have a significant impact on the well-being of children, and a considerable financial burden on the national health system. Thus, early diagnosis and treatment of SDB in children is vital to prevent health issues later.

Continuous positive air pressure and surgery (adenotonsillectomy) represent the primary treatment modalities for SDB in children. Mandibular Advancement Splints (MAS) represent an alternative treatment that is less invasive, cheaper, more comfortable and acceptable than other treatment modalities. While the efficacy of these appliances has been clearly demonstrated in adults, there is little information about their usefulness in children.

This project aims to determine the efficacy of mandibular advancement appliances for the management of SDB and related health problems in children. This project will utilise skills from multiple research groups, thus establishing a multidisciplinary research team for the study of SDB in children in New Zealand.

Children with SDB will be recruited and randomly assigned to two groups; both groups will receive the same treatment with active MAS and non-active MAS but in different sequences; the first group will receive three weeks treatment with active MAS, two weeks break, and three weeks treatment with non-active MAS, the second group will receive the appliances in a reversed order. Potential improvement in SDB symptoms and some other accompanied health related problems will be assessed using a portable breathing monitoring instrument, questionnaires, and collecting blood samples.



Researchers

Dr. Ghassan Idris (PhD Student)

PhD Student at Sir John Walsh Research Institute

Discipline of Orthodontics,

Department of Oral Sciences, Faculty of Dentistry,

University of Otago

A: Walsh Building 310 Great King Street Health Sciences Dental School, Dunedin, New Zealand

E: idrgh523@student.otago.ac.nz

Professor Mauro Farella (Main Supervisor)

Head of Discipline of Orthodontics,

Department of Oral Sciences,

Faculty of Dentistry,

University of Otago

A: Walsh Building 310 Great King Street Health Sciences Dental School, Dunedin, New Zealand

E: mauro.farella@otago.ac.nz
Associate Professor Barbara Galland (Co-supervisor)

Research Associate Professor,

Department of women’s & children’s health,

School of medicine

University of Otago.

A: 3rd Floor of the Children's Pavilion which is on the corner of Great King and Hanover Streets, Dunedin, New Zealand

E: barbara.galland@otago.ac.nz

Dr. Christopher John Robertson (Co-supervisor)

Professional Practice Fellow,

Discipline of Orthodontics,

Department of Oral Sciences, Faculty of Dentistry,

University of Otago

A: Walsh Building 310 Great King Street Health Sciences Dental School, Dunedin, New Zealand

E: c.robertson@clear.net.nz
EFFICACY OF A MANDIBULAR ADVANCEMENT APPLIANCE ON SLEEP DISORDERED BREATHING IN CHILDREN



Background

Sleep-disordered breathing (SDB) varies in a continuum spectrum from habitual snoring and upper airway resistance syndrome (UARS) to obstructive sleep apnea (OSA), due to either partial or complete airway obstruction, respectively.1,2

Obstructive Sleep Apnea (OSA) is characterized by recurring episodes of complete and/or partial obstruction of the upper airway during sleep, resulting in intermittent hypoxemia and hypercapnia, frequent arousals and sleep fragmentation.3-5 Snoring is the cardinal clinical symptom of OSA and the hallmark of all SDB syndromes. Those patients who snore but do not fulfil the criteria for OSA are considered to have habitual snoring.6,7

The health impact of OSA has been increasingly recognized2 in both adults and children.8 Pediatric and adult OSA differ in prevalence, physiology, clinical presentation, polysomnographic characteristics and outcomes.2,5,9,10 The prevalence of OSA varies from 3 to 7%11-13 in adults. Epidemiological studies in New Zealand have shown that OSA affects over 15% of the adult males, and its prevalence is twice as high in Māori men than non-Māori men.14,15 In children, the prevalence of OSA varies from 1 to 4%,8,16-20 while that of habitual snoring varies from 0.7 to 10.3%; most authors have reported a 10% prevalence of habitual snoring in children.21-24 Habitual snoring is more common in Māori than non-Māori children19,25,26, but the exact prevalence of OSA in New Zealand children is still unknown.

SDB have been associated with growth disorders, daytime sleepiness,10 educational and behavioral problems,27-29 and nocturnal enuresis.30,31 In the most severe cases, OSA may have life-threatening consequences like cardiorespiratory failure, which can lead to death.2,10,32

Adenotonsilar hypertrophy or recurrent infection is the primary cause of pediatric OSA.10,33,34 Jaw anomalies and malposition also are associated with changes in airway morphology and respiratory problems,35,36 and an obstructed airways may affect craniofacial development.37-39 Orthodontic and craniofacial anomalies have often been reported in pediatric sleep-disordered breathing. A triad of narrow upper airway, maxillary constriction and mandibular retrusion is a common phenotype of pediatric OSA syndrome.33,34,40-43

There is an abnormal secretion of growth hormone (GH) during sleep and somatic growth impairment in children with OSA,44 which affects the craniofacial traits, especially the height of mandibular ramus.45-47 Studies have reported an accelerated ramus growth, and improved facial morphology after adenotonsillectomy in pediatric OSA patients.48 This improvement may be due to normalization in GH status, balance between tongue and cheeks, and nasal breathing after adenotonsillectomy.39,49 However, this growth acceleration is not sufficient to correct the malocclusion and the underlying skeletal discrepancy often requires dentofacial growth modification treatment.50

Polysomnography (PSG) is considered the gold standard in diagnosis of SDB, particularly OSA.2,9 Other diagnostic tools include portable monitoring devices,51 physical examination to detect anatomic risk factors, upper airway imaging using magnetic resonance imaging (MRI),52,53 endoscopy and cephalometry.43,54 Continuous positive air pressure (CPAP) and adenotonsillectomy are the primary treatment options for the adult and pediatric OSA patients, respectively.2,10 Surgery to increase the upper airway cross-sectional area, remove obstructive tissues, or ultimately bypass the upper airway10,55 is indicated in severe adult cases, or where CPAP is not tolerated.2,56 Oral appliances (OA) have also been widely used for the treatment of OSA, especially in adults.2,57-62 These appliances increase the posterior oropharyngeal airway by reducing upper airway collapsibility during sleep. They may also trigger stretch receptors, which in turn activate the airway supporting muscles.2 Previous studies have shown that use of OA are better tolerated than CPAP treatment,58 because of improved comfort, quietness, and portability.63,64 Mandibular advancement appliances are the most common type of oral appliances used in the treatment of SDB in adults, but their use in children is less common.

There is a significant relationship between pediatric OSA and craniofacial traits.34,43,65,66 It is generally accepted that advancing the mandible will increase the nasopharyngeal dimensions,67,68 thereby improving the symptoms of OSA.57,61,63 Mandibular Advancement Splints (MAS) can be used to advance the mandible in adults, and also for growth modification in children.69 MAS are suitable for both mixed and permanent dentition,70 relatively well tolerated by patients, with low failure rates,71 and may potentially be used for treatment of pediatric OSA64 by incremental advancement of the lower jaw71 and upper arch expansion,70 Although there is increasing evidence regarding the efficacy of MAS in adults with OSA,58,72 there is little information about their efficacy in children.73 The few studies on the subject suffer from important methodological flaws like heterogeneous samples; lack of randomization; limited power to detect a clinically relevant effect; and lack of an adequate control conditions such as the use of a placebo-like appliance.57,61,64,73 Therefore it is difficult to draw a conclusion regarding the efficacy of MAS appliances in treating children with SDB.

Study design

This study will be designed as a randomized clinical trial with crossover administration of two appliances (active MAS and non-active/sham MAS). Each appliance will be worn for three weeks, followed by two-week washout period.



Objectives:

The aims of the study are: (1) to test the efficacy of MAS in the treatment of children with SDB; and (2) to assess the effect of MAS treatment on quality of life, behavior, growth hormone levels, and nocturnal enuresis in SDB children.



Research hypothesis

The mandibular advancement splints are effective in reducing SDB symptoms in children.



Experimental Approach

Participants

Sample size estimation

A reduction of 50% in Apnea/Hypopnea Index AHI (number of apnea and hypopnea events recorded per hour of sleep) is generally considered clinically relevant.58 This change corresponds to a large effect size (Cohen’s d= 1.5). To detect this effect size, and setting α error to 0.05 and β error to 0.80 (one-tail test), we have estimated that at least 13 participants are needed. We will recruit 16 children to avoid problems occur from possible dropouts.



Recruitment

We will advertise in newspapers to invite children to participate in the study according to the following eligibility criteria: age 8-12 years; snore three times or more per week; no previous orthodontic treatment.

Eligible patients should meet the following inclusion/ extrusion criteria.

Inclusion criteria: SDB diagnosis.

Exclusion criteria: severe OSA AHI more than ten events per hour;74 craniofacial syndromes and genetic syndromes; neuromuscular diseases; body mass index at or above 95th percentile of normative values.

Methods

Portable unit for SDB monitoring

Home-based abbreviated polysomnography (PSG)51 will be performed using a portable monitoring unit (Visi Black Shadow, Stowood Scientific Instruments Ltd, Oxford, UK). This unit records nasal airflow, respiratory efforts, oximetry, pulse profile, snoring sounds, body movement, body position, and electrocardiographic signals.


Oral appliances


The oral appliance that will be used in the study is a Twin-block design consisting of two removable plates; one is worn on the upper arch, the other on the lower. Each plate has matching pieces which encourage the lower jaw to posture or slide forward as the teeth come together(active MAS).70 To ensure keeping the mandible in an advanced position during sleep a fastener (MDSA Ltd., Victoria, Australia), will be imbedded in the splints.75 The new sagittal and vertical position of the mandible will be determined by taking the bite records and the construction bite using George Gauge™,76,77 which provides an aid in determining the amount of protrusion needed in construction of the mandibular protruding devices.

The non-active appliance (sham MAS) will consist of an upper and lower acrylic plate resembling the design of the active MAS, but without any component to protrude the mandible.

Participant in the study will be asked to wear the appliances at night and for two to three hours during the daytime. Wearing time will be recorded by parents using diaries.

Outcome measurements Apnea/Hypopnea Index (AHI – primary outcome)

This is defined as number of apnea and hypopnea events recorded per hour of sleep.78 An apnea episode is defined as cessation of breathing for 10 seconds or longer.78 A hypopnea episode is defined as reduced respiratory airflow by 30% with a 4% decrease in oxygen saturation.78

AHI will be assessed using the portable monitoring device.51 This monitoring will be carried out four times. (Figure 1)

Sleep Questionnaires

SDB associated symptoms will be assessed using the Pediatric Sleep Questionnaire. Daytime sleepiness and related behavioral disturbances will be assessed using the Epworth Sleepiness Scale (ESS).79-81 A questionnaire of sleep related breathing disorder scale (PSQ-SRBD scale) will also be completed by parents to ascertain the quality of the child’s sleep including difficulties in getting to sleep, frequency of waking during the night, and alertness in the morning and daytime signs of sleepiness. It will also include questions about the history of the breathing difficulties during sleep, snoring, family history of SDB, and levels of household smoking.82 These questionnaires will be administered before and after each treatment period.



Snoring frequency and intensity

Snoring sounds will be assessed using the portable PSG equipment at the beginning and the end of each treatment period. Reports of snoring frequency and intensity will also be collected by parents using daily diaries.



Growth hormone levels

Blood samples will be taken from SDB children twice in the middle of each treatment period. A specialist in venipuncture will collect the samples to minimize discomfort and potential complications of venipuncture. Growth hormone will be assessed indirectly by determination of insulin-like growth factor-1 (IGF-1) levels.



Parent-report of nocturnal enuresis

A child will be diagnosed as having urine incontinence when it occurs at least one night per week.31 This will be assessed during both treatment periods using diaries.



Neurobehavioral assessment

Behavioral changes will be assessed using the BASC-2 rating scale, which has been widely used in studying behavioral differences in pediatric SDB patients.8384



Quality of life

Quality of life in SDB children will be assessed using the OSA-18 and the Pediatric Quality of Life Inventory™ (PQoL).85 Parents or caregivers will rate the frequency of symptoms before treatment and at the end of each treatment period.



Clinical procedure

Assessments will be taken at baseline (T0) and four times (T1, T2, T3, T4) during the study period. Details about assessments are described in Figure 1.



Significance of the research

Early treatment of SDB in children is vital to prevent significant health issues that may develop later, including behavioral and learning concerns. In the most severe cases, OSA may have life-threatening consequences like cardio-respiratory failure, which can ultimately lead to death. SDB may therefore have a significant impact on the wellbeing of many New Zealand children, as well as direct and indirect cost the health system.

The use of MAS in selected children may represent an effective treatment that is less invasive and better tolerated than other treatment modalities such as CPAP or surgery.

This project will utilise skills from multiple research groups, thus establishing a multidisciplinary team for treatment of SDB in children in New Zealand. The expertise of orthodontists, pulmonologists, pediatricians will be combined to conduct much-needed clinical research into a condition that may affect up to 4% of New Zealand children.19



d:\phd otago\figures and shapes\protocol to anzctr\protocol to anzctr جديد1.jpg

Figure 1 The study is designed as a crossover randomized controlled trial. Sixteen patients will be randomly assigned to two treatment sequences, each including the use of an active or non-active (sham) mandibular advancement appliance in a reverse order. Active and non-active treatment periods will be separated by a two-week washout period. Assessments will be taken at baseline (T0) and four times (T1, T2, T3, T4) during the study period. PSG data will be collected during home-based recordings, whereas all the other data will be collected in a clinic environment.

List of abbreviations: Abbreviated polysomnography (PSG), Cephalograms (Ceph), Behavior assessment system for children, second edition (BASC-2) the quality of life questionnaire (OSA-18), pediatric quality of life inventory (PQoL), and the Epworth sleepiness scale (ESS).



References:
1. Panossian L, Daley J. Sleep-disordered breathing. Continuum (Minneap Minn) 2013;19:86-103.

2. Casale M, Pappacena M, Rinaldi V, Bressi F, Baptista P, Salvinelli F. Obstructive sleep apnea syndrome: from phenotype to genetic basis. . Current Genomics 2009:119-126.

3. Goldstein N, Stefanov D, Graw-Panzer K, Fahmy S, Fishkin S, Jackson A et al. Validation of a clinical assessment score for pediatric sleep-disordered breathing. Laryngoscope 2012;122:2096-2104.

4. Redline S, Tishler PV. The genetics of sleep apnea. Sleep Medicine Reviews 2000;4:583-602.

5. Certal V, Catumbela E, Winck JC, Azevedo I, Teixeira-Pinto A, Costa-Pereira A. Clinical assessment of pediatric obstructive sleep apnea: A systematic review and meta-analysis. LARYNGOSCOPE 2012;122:2105-2114.

6. Marcus CL. Sleep-disordered breathing in children. Am J Respir Crit Care Med 2001;164:16-30.

7. Loghmanee DA, Sheldon SH. Pediatric obstructive sleep apnea: an update. Pediatr Ann 2010;39:784-789.

8. Bixler EO, Vgontzas AN, Lin H-M, Liao D, Calhoun S, Vela-Bueno A et al. Sleep disordered breathing in children in a general population sample: prevalence and risk factors. Sleep 2009;32:731-736.

9. Wise MS, Nichols CD, Grigg-Damberger MM, Marcus CL, Witmans MB, Kirk VG et al. Executive summary of respiratory indications for polysomnography in children: an evidence-based review. Sleep 2011;34:389-398.

10. Li HY, Lee LA. Sleep-disordered breathing in children. Chang Gung Med J 2009;32:247-257.

11. Young T, Palta M, Dempsey J, Skatrud J, Weber S, Badr S. The Occurrence of Sleep-Disordered Breathing among Middle-Aged Adults. The New England Journal of Medicine 1993;328:1230-1235.

12. Gislason T, Benediktsdóttir B, Björnsson JK, Kjartansson G, Kjeld M, Kristbjarnarson H. Snoring, hypertension, and the sleep apnea syndrome. An epidemiologic survey of middle-aged women. Chest 1993;103:1147-1151.

13. Kripke DF, Ancoli-Israel S, Klauber MR, Wingard DL, Mason WJ, Mullaney DJ. Prevalence of sleep-disordered breathing in ages 40-64 years: a population-based survey. Sleep 1997;20:65.

14. Mihaere KM, Harris R, Gander PH, Reid PM, Purdie G, Robson B et al. Obstructive sleep apnea in New Zealand adults: prevalence and risk factors among Maori and non-Maori. Sleep 2009;32:949-956.

15. Harris R. Obstructive sleep apnoea syndrome: symptoms and risk factors among Maori and non-Maori adults in Aotearoa Wellington School of Medicine and Health Sciences. Wellington: University of Otago; 2003.

16. Li AM, So HK, Au CT, Ho C, Lau J, Ng SK et al. Epidemiology of obstructive sleep apnoea syndrome in Chinese children: a two-phase community study. Thorax 2010;65:991-997.

17. Guilleminault C, Lee JH, Chan A. Pediatric Obstructive Sleep Apnea Syndrome. Archives of Pediatrics & Adolescent Medicine 2005;159:775-785.

18. Kaditis AG, Gourgoulianis K, Molyvdas PA, Finder J, Alexopoulos EI, Starantzis K et al. Sleep-disordered breathing in 3,680 Greek children. Pediatric pulmonology 2004;37:499-509.

19. Lucas C, Campbell A, Elder D. Prevalence of obstructive sleep apnoea symptoms in children whose parents have diagnosed obstructive sleep apnoea. Summer studentship scientific report university of Otago 2013:1-17.

20. Rosen CL, Larkin EK, Kirchner HL, Emancipator JL, Bivins SF, Surovec SA et al. Prevalence and risk factors for sleep-disordered breathing in 8- to 11-year-old children: association with race and prematurity. J Pediatr 2003;142:383-389.

21. Castronovo V, Zucconi M, Nosetti L, Marazzini C, Hensley M, Veglia F et al. Prevalence of habitual snoring and sleep-disordered breathing in preschool-aged children in an Italian community. J Pediatr 2003;142:377-382.

22. Montgomery-Downs HE, Gozal D. Sleep habits and risk factors for sleep-disordered breathing in infants and young toddlers in Louisville, Kentucky. Sleep Med 2006;7:211-219.

23. Brockmann PE, Bertrand P, Pardo T, Cerda J, Reyes B, Holmgren NL. Prevalence of habitual snoring and associated neurocognitive consequences among Chilean school aged children. Int J Pediatr Otorhinolaryngol 2012;76:1327-1331.

24. Lumeng JC, Chervin RD. Epidemiology of pediatric obstructive sleep apnea. Proc Am Thorac Soc 2008;5:242-252.

25. Gill AI, Schaughency E, Galland BC. Prevalence and factors associated with snoring in 3-year olds: early links with behavioral adjustment. Sleep Med 2012;13:1191-1197.

26. Mitchell EA, Thompson JMD. Snoring in the first year of life. Acta paediatrica (Oslo, Norway : 1992) 2003;92:425-429.

27. Ali NJ, Pitson DJ, Stradling JR. Snoring, sleep disturbance, and behaviour in 4-5 year olds. Arch Dis Child 1993;68:360-366.

28. Blunden S, Lushington K, Kennedy D, Martin J, Dawson D. Behavior and neurocognitive performance in children aged 5-10 years who snore compared to controls. J Clin Exp Neuropsychol 2000;22:554-568.

29. Chervin RD, Archbold KH, Dillon JE, Panahi P, Pituch KJ, Dahl RE et al. Inattention, hyperactivity, and symptoms of sleep-disordered breathing. Pediatrics 2002;109:449-456.

30. Stone J, Malone PS, Atwill D, McGrigor V, Hill CM. Symptoms of sleep-disordered breathing in children with nocturnal enuresis. J Pediatr Urol 2008;4:197-202.

31. Sakellaropoulou AV, Hatzistilianou MN, Emporiadou MN, Aivazis VT, Goudakos J, Markou K et al. Association between primary nocturnal enuresis and habitual snoring in children with obstructive sleep apnoea-hypopnoea syndrome. Arch Med Sci 2012;8:521-527.

32. Capua M, Ahmadi N, Shapiro C. Overview of obstructive sleep apnea in children: exploring the role of dentists in diagnosis and treatment. J Can Dent Assoc 2009;75:285-289.

33. Guilleminault C, Li KK, Khramtsov A, Pelayo R, Martinez S. Sleep disordered breathing: surgical outcomes in prepubertal children. Laryngoscope 2004;114:132-137.

34. Kawashima S, Peltomaki T, Sakata H, Mori K, Happonen RP, Ronning O. Craniofacial morphology in preschool children with sleep-related breathing disorder and hypertrophy of tonsils. Acta Paediatr 2002;91:71-77.

35. McNamara JA. Influence of respiratory pattern on craniofacial growth. Angle Orthod 1981;51:269-300.

36. Sosa FA, Graber TM, Muller TP. Postpharyngeal lymphoid tissue in Angle Class I and Class II malocclusions. Am J Orthod 1982;81:299-309.

37. Moss M. The functionalmatrix:vistasinorthodontics. Philadelphia: Lea& Febinger; 1962.

38. Stellzig-Eisenhauer A, Meyer-Marcotty P. [Interaction between otorhinolaryngology and orthodontics: correlation between the nasopharyngeal airway and the craniofacial complex]. Laryngorhinootologie 2010;89 Suppl 1:S72-78.

39. Zettergren-Wijk L, Forsberg CM, Linder-Aronson S. Changes in dentofacial morphology after adeno-/tonsillectomy in young children with obstructive sleep apnoea--a 5-year follow-up study. Eur J Orthod 2006;28:319-326.

40. Tasker C, Crosby JH, Stradling JR. Evidence for persistence of upper airway narrowing during sleep, 12 years after adenotonsillectomy. Arch Dis Child 2002;86:34-37.

41. Guilleminault C, Partinen M, Praud JP, Quera-Salva MA, Powell N, Riley R. Morphometric facial changes and obstructive sleep apnea in adolescents. J Pediatr 1989;114:997-999.

42. Arens R, Marcus CL. Pathophysiology of upper airway obstruction: a developmental perspective. Sleep 2004;27:997-1019.

43. Flores-Mir C, Korayem M, Heo G, Witmans M, Major MP, Major PW. Craniofacial morphological characteristics in children with obstructive sleep apnea syndrome: a systematic review and meta-analysis. Journal of the American Dental Association (1939) 2013;144:269.

44. Nieminen P, Lopponen T, Tolonen U, Lanning P, Knip M, Lopponen H. Growth and biochemical markers of growth in children with snoring and obstructive sleep apnea. Pediatrics 2002;109:e55.

45. Lowe AA, Santamaria JD, Fleetham JA, Price C. Facial morphology and obstructive sleep apnea. Am J Orthod Dentofacial Orthop 1986;90:484-491.

46. Andersson L, Brattstrom V. Cephalometric analysis of permanently snoring patients with and without obstructive sleep apnea syndrome. Int J Oral Maxillofac Surg 1991;20:159-162.

47. Solow B, Skov S, Ovesen J, Norup PW, Wildschiodtz G. Airway dimensions and head posture in obstructive sleep apnoea. Eur J Orthod 1996;18:571-579.

48. Agren K, Nordlander B, Linder-Aronsson S, Zettergren-Wijk L, Svanborg E. Children with nocturnal upper airway obstruction: postoperative orthodontic and respiratory improvement. Acta Otolaryngol 1998;118:581-587.

49. Woodside DG, Linder-Aronson S, Lundstrom A, McWilliam J. Mandibular and maxillary growth after changed mode of breathing. Am J Orthod Dentofacial Orthop 1991;100:1-18.

50. Peltomaki T. The effect of mode of breathing on craniofacial growth--revisited. Eur J Orthod 2007;29:426-429.

51. Polese JF, Santos-Silva R, Kobayashi RF, Pinto IND, Tufik S, Bittencourt LRA. Portable monitoring devices in the diagnosis of obstructive sleep apnea: current status, advantages, and limitations. JORNAL BRASILEIRO DE PNEUMOLOGIA 2010;36:498-505.

52. Schwab RJ, Pasirstein M, Pierson R, Mackley A, Hachadoorian R, Arens R et al. Identification of Upper Airway Anatomic Risk Factors for Obstructive Sleep Apnea with Volumetric Magnetic Resonance Imaging. American Journal of Respiratory and Critical Care Medicine 2003;168:522-530.

53. Okubo M, Sugawara J, Suzuki M, Horiuchi A, Okabe S, Ikeda K et al. Morphologic analyses of mandible and upper airway soft tissue by MRI of patients with obstructive sleep apnea hypopnea syndrome. Sleep 2006;29:909-915.

54. Borek RC, Thaler ER, Kim C, Jackson N, Mandel JE, Schwab RJ. Quantitative airway analysis during drug-induced sleep endoscopy for evaluation of sleep apnea. LARYNGOSCOPE 2012;122:2592-2599.

55. Franklin KA, Anttila H, Axelsson S, Gislason T, Maasilta P, Myhre KI et al. Effects and side-effects of surgery for snoring and obstructive sleep apnea--a systematic review. Sleep 2009;32:27-36.

56. Baptista PM. [Surgery for obstructive sleep apnea]. An Sist Sanit Navar 2007;30 Suppl 1:75-88.

57. 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 Respir Crit Care Med 2002;165:123-127.

58. Ferguson KA, Cartwright R, Rogers R, Schmidt-Nowara W. Oral appliances for snoring and obstructive sleep apnea: a review. Sleep 2006;29:244-262.

59. Deane SA, Cistulli PA, Ng AT, Zeng B, Petocz P, Darendeliler MA. Comparison of mandibular advancement splint and tongue stabilizing device in obstructive sleep apnea: a randomized controlled trial. Sleep 2009;32:648-653.

60. Carra MC, Huynh NT, El-Khatib H, Remise C, Lavigne GJ. Sleep bruxism, snoring, and headaches in adolescents: short-term effects of a mandibular advancement appliance. Sleep Med 2013;14:656-661.

61. Cozza P, A P, Ballanti F. A modified monobloc for the treatment of obstructive sleep apnoea in paediatric patients. Eur J Orthod 2004; Oct;26:523-530.

62. Lawton HM, Battagel JM, Kotecha B. A comparison of the Twin Block and Herbst mandibular advancement splints in the treatment of patients with obstructive sleep apnoea: a prospective study. Eur J Orthod 2005;27:82-90.

63. Poon KH, Chay SH, Chiong KF. Airway and craniofacial changes with mandibular advancement device in Chinese with obstructive sleep apnoea. Ann Acad Med Singapore 2008;37:637-644.

64. Zhang C, He H, Ngan P. Effects of twin block appliance on obstructive sleep apnea in children: a preliminary study. Sleep Breath 2013.

65. Vig KW. Nasal obstruction and facial growth: the strength of evidence for clinical assumptions. Am J Orthod Dentofacial Orthop 1998;113:603-611.

66. Miles PG, Vig PS, Weyant RJ, Forrest TD, Rockette HE, Jr. Craniofacial structure and obstructive sleep apnea syndrome--a qualitative analysis and meta-analysis of the literature. Am J Orthod Dentofacial Orthop 1996;109:163-172.

67. Restrepo C, Santamaria A, Pelaez S, Tapias A. Oropharyngeal airway dimensions after treatment with functional appliances in class II retrognathic children. J Oral Rehabil 2011;38:588-594.

68. Ozbek MM, Memikoglu TU, Gogen H, Lowe AA, Baspinar E. Oropharyngeal airway dimensions and functional-orthopedic treatment in skeletal Class II cases. Angle Orthod 1998;68:327-336.

69. Clark WJ. twin blook functional therapy U.K: Mosby; 2002.

70. Clark WJ. The twin block technique. A functional orthopedic appliance system. Am J Orthod Dentofacial Orthop 1988;93:1-18.

71. Birnei D, Harradine N. Functional appliances Excellence in Orthodontics lecture course. Amman-Jordan; 2012: p. 321-348.

72. Sutherland K, Deane SA, Chan AS, Schwab RJ, Ng AT, Darendeliler MA et al. Comparative effects of two oral appliances on upper airway structure in obstructive sleep apnea. Sleep 2011;34:469-477.

73. Carvalho FR, Lentini-Oliveira D, Machado MA, Prado GF, Prado LB, Saconato H. Oral appliances and functional orthopaedic appliances for obstructive sleep apnoea in children. Cochrane Database Syst Rev 2007:Cd005520.

74. Association ASA. Children's Sleep Apnea. Washington, DC , United States American Sleep Apnea Association; 2013.

75. Barnes M, McEvoy RD, Banks S, Tarquinio N, Murray CG, Vowles N et al. Efficacy of positive airway pressure and oral appliance in mild to moderate obstructive sleep apnea. Am J Respir Crit Care Med 2004;170:656-664.

76. George PT. A new instrument for functional appliance bite registration. J Clin Orthod 1992;26:721-723.

77. George PT. Selecting sleep-disordered-breathing appliances. Biomechanical considerations. J Am Dent Assoc 2001;132:339-347.

78. Myers KA, Mrkobrada M, Simel DL. Does this patient have obstructive sleep apnea?: The Rational Clinical Examination systematic review. Jama 2013;310:731-741.

79. Manni R, Politini L, Ratti MT, Tartara A. Sleepiness in obstructive sleep apnea syndrome and simple snoring evaluated by the Epworth Sleepiness Scale. J Sleep Res 1999;8:319-320.

80. Johns MW. A new method for measuring daytime sleepiness: the Epworth sleepiness scale. Sleep 1991;14:540-545.

81. Johns MW. Daytime sleepiness, snoring, and obstructive sleep apnea. The Epworth Sleepiness Scale. Chest 1993;103:30-36.

82. Spruyt K, Gozal D. Pediatric sleep questionnaires as diagnostic or epidemiological tools: a review of currently available instruments. Sleep Med Rev 2011;15:19-32.

83. Reynolds CRK, R.W. BASC2 Behavioral assessment system for children manual. Pearson; 2004.

84. Tripuraneni M, Paruthi S, Armbrecht ES, Mitchell RB. Obstructive sleep apnea in children. Laryngoscope 2013;123:1289-1293.



85. Reinfjell T, Hjemdal O, Aune T, Vikan A, Diseth TH. The Pediatric Quality of Life Inventory (PedsQL) 4.0 as an assessment measure for depressive symptoms: a correlational study with young adolescents. Nord J Psychiatry 2008;62:279-286.




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