Journal of Sleep Medicine & Disorders

Cite this article: Romero MM, Samalea PV, César EC, Marfil NR, Sánchez MCV (2016) Efficacy of Orthoapnea Mandibular Advance Device in Patients with Mild and Moderate Obstructive Sleep Apnea Syndrome. J Sleep Med Disord 3(6): 1065.

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*Corresponding authorM. Martín Romero, Department of Pulmonology, Unit of Sleep Respiratory Diseases, Virgen de la Victoria Hospital, Málaga, Spain, C/ Císter nº 5, 2ºA. 29015 Málaga, Spain, Tel: :34-951032445; 34610701653; Email.

Submitted: 01 July 2016

Accepted: 27 August 2016

Published: 29 August 2016

ISSN: 2379-0822

Copyright© 2016 Romero et al.

OPEN ACCESS

Keywords•Mandibular advancement devices (MAD)•Oral appliance (OA)•Orthoapnea MAD•Sleep apnea-Hypopnea Syndrome (SAHS)

Short Communication

Efficacy of Orthoapnea Mandibular Advance Device in Patients with Mild and Moderate Obstructive Sleep Apnea SyndromeM. Martín Romero1*, P. Valiente Samalea3, E. Cabrera César1, N. Reina Marfil2, and MC Vera Sánchez2 1Department of Pulmonology, Sleep Respiratory Diseases, Virgen de la Victoria hospital, Spain2Department of Pulmonology, Virgen de la Victoria hospital, Spain3Valiente Dental Clinic, Spain

Abstract

Rationale: Continuous positive airway pressure (CPAP) is the treatment of choice in patients with Symptomatic Obstructive Sleep Apnea Syndrome (OSAS). Recently, Mandibular Advancement Devices (MAD) are used in the treatment of OSAS.

Objective: Investigate the efficacy of the Orthoapnea MAD in patients with mild or moderate OSAS in adults.

Methods: This is a prospective study. Patients diagnosed with mild or moderate OSAS by Respiratory Polygraphy were included. A Basal Polygraphy and 3D scan was performed and repeated after four weeks of treatment. The treatment was considered effective when an AHI lower than 5 or a significant reduction was reached.

Results: 103 patients were included: 84 men and 19 women; average age of 46.47 9.71; Body Mass Index average of 27.36 2.45 kg/m2. The airway area patency and volume increased after the treatment (area from 256 to 308 mm2; volume from 4533 to 6356 mm3). After treatment statistically significant decreases (p<0.05) were obtained in average AHI (from 16.2 to 6), both in supine (from 25.1 to 6.9) and prone position (from 7.8 to 3.9); Desaturation per hour Index Average (from 13.7 to 5.5); average CT90 (from 1.6 to 0.6). In 72.80% of the cases the AHI was halved. In 90.30%, an AHI under 10 was reached and, in 61.2%, under 5.

Conclusions: The use of Orthoapnea MAD proves to be an efficient therapeutic alternative, increasing airway area patency and volume, thus reducing the AHI and desaturation for patients with mild and moderate OSAS.

ABBREVIATIONSASAM: American Academy of Sleep Medicine; AHI: Apnea-

Hypopnea; BMI: Body Mass Index; Cpap: Continuous Positive Airway Pressure; Ct 90: % Time Whit Oxygen Saturation Below 90% ; ODI: Oxygen Desaturation Index; ESS: Epworth Sleepiness Scale; MAD: Mandibular Advance Device; TMJ: Temporomandibular Joint; OA: Oral Appliances; OSAS: Obstructive Sleep Apnoea Syndrome ; SAHS: Sleep Apnea-Hypopnoea Syndrome ; Sao2: Blood Oxygen Saturation

INTRODUCTIONObstructive Sleep Apnea Syndrome (OSAS) is a common

disorder characterized by repetitive episodes of nocturnal breathing cessation due to upper airway collapse that produce intermittent hypoxia and sleep fragmentation affecting the function of different organs and systems, mainly the brain and the cardiovascular system, and alter the body´s metabolic balance [1,2].

The aetiology of OSA is multi-factorial, consisting of a complex

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interplay between anatomic, neuromuscular factors and an underlying genetic predisposition toward the disease [1,3]. Risk factors include snoring, male gender, middle age, menopause in women, obesity and a variety of craniofacial and oropharyngeal features such as a large neck circumference, retro- or micrognatia, nasal obstruction, enlarged tonsils adenoids, macroglossia and low-lying soft palate [1,3].

If untreated, OSAS can cause severe symptoms, such as excessive daytime sleepiness, cognitive and neurobehavioral dysfunction, inability to concentrate, memory impairment and mood changes such as irritability, depression, impairs performance at work, motor vehicle accidents and loss of quality of life [4]. Sleep-related intermittent hypoxia has also been associated with a low-grade systemic inflammation and metabolic disorders independently from the body weight: insulin resistance, type II diabetes, and altered serum lipid profile, which in turn may contribute to initiate or accelerate the process of atherogenesis [5]. It is a major determinant of cardiovascular morbidity and mortality [6]: drug-resistant systemic hypertension (>50% of the patients), ischemic heart disease, cardiac arrhythmias and stroke [2,8] and is associated with a significant cardiovascular morbidity and mortality [6-8].

OSA is defined as the occurrence of 5 or more episodes of complete (apnea) or partial (hypopnea) upper airway obstruction per hour of sleep and is estimated to occur in around 24% of middle-aged men and 9% of women [9,10]. The diagnosis of OSAS is made through different levels of nocturnal monitoring of respiratory, sleep and cardiac parameters (polysomnographic or nocturnal cardio-respiratory polygraphy), aimed to detect the obstructive events and the following changes in blood oxygen saturation (SaO2) [11,12]. The most commonly used index to define the severity of OSA is the apnoea/hypopnoea index (AHI), calculated as the number of obstructive events per hour of sleep and obtained by nocturnal cardiorespiratory monitoring [11,12].

Different treatment options are now available for an effective management of this disease. The gold standard treatment for OSA is the continuous positive airway pressure (CPAP), the most effective and commonly used treatment. Alternative options include weight control, mandibular advancement devices and a number of upper airway surgical approaches. Oral appliances (OA) are designed to improve upper airway configuration and prevent collapse through alteration of jaw and tongue position. MAD is the OA most effective and commonly employed in the treatment of OSAS as an alternative in patients with mild or moderate OSAS or even in severe patients who do not tolerate the CPAP or refuse surgery [13-19]. These devices attach to both the upper and lower dental arches in order to advance and retain the mandible in a forward position. This will relocate laterally the pharyngeal fat pads from the airway and the tongue base will move forward. Consequently, the upper airway will be widened, and the function of upper airway dilator muscles, particularly the genioglossus, will improve [20]. As the pharyngeal collapsibility is reduced, the risk of apneic events will be lowered.

The main objectives of this study are to evaluate the effectiveness and tolerance of the MAD designed by Orthoapnea in adult patients with mild or moderate OSAS, and determine whether there is an improvement or not in the airway area

patency and volume, and if the number of respiratory events and desaturations decreases.

MATERIALS AND METHODSThe Orthoapnea device is a custom made, adjustable

mandibular advancement device that allows lateral and vertical jaw movement during sleep, as well as a controlled regulation of the millimetrically accurate advance.

The following data was recorded before and after treatment with MAD: specific anamnesis (typical symptoms, ESS, sleeping habits, drugs consumption, cardiovascular or neuropsychiatric problems), anthropometric exploration (blood pressure, weight, height, BMI, neck perimeter), examination of the oropharynx, dental exam, radiological examination of Airway by 3-D scanner, cardiorespiratory polygraphy, and informed consent. After the treatment with MAD hours of use and side effect were registered.

The diagnosis of OSAS was made by polygraphy, which also provides an indication of severity (AASM 2012). OSAS is considered to be mild when the AHI ranges from 5 to under 15, Moderate when AHI is between 15 to under 30 and Severe when is more than 30.

The following variables were registered: sex, age, total apnoea-hypopnoea index (AHI), AHI in supine and AHI in non-supine position, total amount of apneas, amount of obstructive apneas and hypopneas, desaturation per hour index and percentage of time during which the saturation was under 90% (CT90).

All patients diagnosed with mild or moderate OSAS by respiratory polygraphy were recruited, following the recommendations of indication for treatment with MAD [17-19].

Those with serious comorbidity, severe obesity, anatomic problems that prevent MAD placing, high gag reflex, pregnant women and those who would not participate in the study or did not sign the informed consent were excluded.

A basal polygraphy was performed and repeated after four weeks of treatment. During the treatment, two 3-D scans were performed with and without MAD to measure airway area and volume, defined by Dolphin 3-D imaging airway analysis tool.

The treatment was considered effective when an AHI lower than 5 or a significant reduction was reached. Other criteria were also considered: significantly reduced to 10 or bellow, if the AHI was halved, significant decrease or improvement of apneas/hypopneas, significant decrease or improvement of episodes of oxyhaemoglobin desaturation, significant decrease or improvement of snores and subjective improvement of clinical symptoms.

The results were analyzed by Student’s T-test for paired data, nonparametric Wilcoxon test and McNemar test. Significant difference was considered when the significance level obtained was less than 5% (p < 0.05). Data sampling: 103 patients were included in the research: For sampling, a difference was initially considered significant when it reached 50% before and after treatment. With this sample size (103 patients) a 99% level of confidence and power was obtained.

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RESULTS AND DISCUSSION103 patients were included in the research: 84 men (81.6%)

and 19 women (18.4%); average age of 46.47 ± 9.71; neck perimeter average: 39,73 ± 3,16; body mass index average of 27.36 ± 2.45 kg/m2. The BMI without MAD was: 27,3 ± 2,41; and the BMI with MAD was: 27,46 ± 2,39. That means that the results of the MAD treatment are not influenced by losing weight. The Mallampati grade was: I in 5,7%, II in 25,7%, III in 28,6% and IV in 34,3% of patients.

In this study, we did not obtain significant differences in blood pressure values after using MAD treatment. This could be due to the fact that it was not a long-term study and that the patients did not show high blood pressure values before treatment.

Statistically significant decreases (p<0.05) were obtained before the treatment in terms of the average number of snores (from 165,7 to 116,3).

The ESS was > 10 in 82 patients before the treatment. When comparing the before and after the treatment (Table 1), statistically significant decreases (p<0.05) were obtained in average ESS (from 13,1 to 8,3).

Statistically significant increases were obtained (Table 2, Figure 1) before the treatment in the airway area patency and volume after the treatment (area from 256 to 308 mm2; volume from 4533 to 6356 mm3).

When comparing the respiratory parameters before and after the treatment (Table 1), statistically significant decreases (p<0.05) were obtained in average AHI (from 16.2 to 6), both in supine (from 25.1 to 6.9) and prone position (from 7.8 to 3.9), as well as on total apneas average (from 69.2 to 9.5); obstructive apneas average (from 34 to 8.7); hypopneas average (from 70.1 to 24.8); desaturation per hour index average (from 13.7 to 5.5), and CT90 average (from 1.6 to 0.6).

In 72.80% of the cases the AHI was halved. In 90.30%, an AHI under 10 was reached and, in 61.2%, under 5.

The table 3 shows the evolution in the level of severity of AHI. After treatment, in 62 cases (60,19%) the AHI was normal

(without apneas), 81 cases improved (78,64%), and 22 cases remained stable (21,36%) and no cases (0%) were aggravated.

We found no differences in the results when analyzed according to separate sexes.

These side effects were minor and generally well tolerated: 37.6% of the patients reported dry mouth, 34.4 %, excessive salivation; 28 patients, gingivae irritation; 34 patients, teeth pain; and 20 patients reported discomfort in the temporomandibular joint. Most patients tolerated well the device, 98 % used it: 86% during 7 days / week; 51.6% for an average of 5-6 hours daily, 23.7% of patients for 7-8 hours daily.

There is clear evidence that effective treatment of OSA provides major benefit to patients. CPAP is the current treatment of choice, but with tolerance and compliance less than optimal in some cases. There is growing interest in the use of oral appliances as a useful alternative to CPAP for the treatment of patients with mild to moderate OSA and for those patients with severe disease intolerant to CPAP [21]. They are many such types of appliances for the treatment of sleep apnea. The results obtained in this study confirm the efficacy and good tolerance of Orthopnea MAD.

Most results obtained in previous studies showed an improvement in the average AHI when using a MAD, although the degree of improvement varied. There is great heterogeneity, which partly accounts for the different types of devices and for the variability in their benefit and side effects, and for the diverse methodology employed in different studies. Although 70% of the patients in these studies showed around a 50% reduction in AHI, many did not return to normal levels, whilst some patients showed no improvement or even became worse. The evidence available in the literature indicates that oral appliances successfully solve mild to moderate OSAS at least in 40-50% of the cases, and significantly improve it in an additional 10-20%. Their effectiveness is inferior to CPAP and similar to surgical procedures, but these are invasive and irreversible. Treatment with MAD is safe, producing common, but transitory and very mild, side effects [22- 24]. Better outcomes and a better compliance have been obtained with adjustable, custom made devices [10, 25]. MAD candidates require assessment by an expert dentist and

Figure 1 3D CT image of a patient’s airway before and after DAM placing.

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Table 1: Main respiratory parameters before and after MAD treatment.

P Mean Standard Deviation PERC 25 Median

AHI supine 0,000without DAM 25,2 15,2 14,3 22,6

with DAM 6,9 6,4 2,6 4,9

AHI non-supine 0,000without DAM 7,7 8,7 2,7 5,7

with DAM 3,7 5,6 0,6 1,9

AHI 0,000without DAM 14,7 5,9 10,0 13,2

with DAM 5,0 4,4 2,1 4,1

Desaturation index/hour 0,000without DAM 12,4 6,6 7,1 11,1without DAM 4,8 4,7 1,6 3,7

CT90 0,000without DAM 2,4 9,2 0,1 0,5without DAM 0,7 1,3 0,0 0,1

Nº of apneas 0,000without DAM 97,9 42,3 65,5 88,0

with DAM 31,3 28,5 10,0 24,0

Nº of obstructive apneas 0,000without DAM 32,0 31,6 9,0 20,0

with DAM 10,7 12,4 2,0 7,0

Nº of Hypopneas 0,000without DAM 64,5 34,1 37,5 59,5

with DAM 21,7 22,4 5,0 17,0

Nº of central apneas 0,925without DAM 1,1 3,7 0,0 0,0

with DAM 1,2 6,9 0,0 0,0

Nº of mixed apneas 0,000without DAM 1,1 4,2 0,0 0,0

with DAM 0,1 0,3 0,0 0,0

Epworth test 0,000without DAM 13,1 4,9 10,0 13,0

with DAM 8,3 4,6 5,0 8,0

Figure 2 Main respiratory parameters in men (dark blue ) and in women (light blue) before and after MAD treatment..

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Table 2: Main respiratory parameters before and after MAD treatment.

P Mean Standard Deviation Perc25 Median Perc75

AREA (mm2) 0,004 without 256 242 0 313 471

with 308 301 0 360 582

VOLUME (mm2) 0,000 without 4533 4531 0 4394 8485

with 6356 6486 0 7571 40580

Table 3: This table shows the evolution in the level of severity of AHI E.g, from the 60 patients who initially had a mild AHI, 41 of them had a normal AHI after treatment.

AHI (With MAD)Total

Normal Mild Moderate

AHI (Without MAD)

MildRecount 41 19 0 60

% 68,3% 31,7% 0,0% 100,0%

ModerateRecount 21 19 3 43

% 48,8% 44,2% 7,0% 100,0%

TotalRecount 62 38 3 103

% 60,2% 36,9% 2,9% 100,0%

are need to have sufficiently healthy teeth and alveolar ridge, a valid mandibular protrusion and absence of temporomandibular disorders. Generally, the best results treatment is achieved in younger, female patients without obesity and in milder OSA [26]. In addition, some cephalometric and physiologic upper airway variables (i.e. low nasal resistance at rhinometry) can predict the response to MAD [27,28]. Patients requiring high CPAP pressures (>13 cm H2O) to eliminate apneas will not respond to MAS.

The place of oral appliances in the spectrum of the treatment options for OSAS was extensively discussed in various reviews and guidelines [14-21]. Direct comparisons with CPAP indicate the superiority of CPAP overall, although similar outcomes between the two treatments appear to be achieved in a substantial subgroup of patients, since patient acceptance has, in general, been in favour of oral appliances.

In spite of the expanding role of oral appliance therapy, there are a number of limitations that are yet to be overcome, such as an ideal patient selection, the inability to reliably predict treatment outcome, the apparent need for an acclimatization period to attain maximal efficacy of treatment, the appropriate level of mandibular advancement required to control OSA in the individual patient, the uncertainty about the influence of appliance design on treatment outcome and its adverse effects and adherence to treatment, and potential long-term complications of therapy.

They are a marked variability of individual responses to oral appliance therapy, and therefore the necessity to approach each patient on an individual basis. The patients should be informed about the different treatment options.

Therefore, a multidisciplinary approach is fundamental and, after the diagnosis of OSA is made, collaboration between dentists and sleep physicians is required in order to establish the indication for MAD, the choice of the best device, and the titration procedure.

CONCLUSIONIn this study, the use of Orthoapnea MAD resulted in an

important improvement of clinical symptoms such as snoring or daytime sleepiness, increased airway area patency and volume, thus reducing the number of respiratory events, and improving some of its pathophysiological consequences, such as nocturnal desaturation. For these reasons it was well tolerated by patients, as such we consider that the Orthoapnea MAD could be a good choice therapy for mild or moderate OSAS.

ACKNOWLEDGEMENTSD. Ramón Hidalgo Sánchez. Area of Biostatistics, Department

of Preventive Medicine and Public Health, University of Málaga. D. José Antonio Carmona Martín. Licenciado en Traducción e Interpretación.

REFERENCES1. Guilleminault C, Quo SD. Sleep-disordered breathing. A view at the

beginning of the new Millennium. Dent Clin North Am. 2001; 45: 643-656.

2. Bradley T. and Floras J. Obstructive sleep apnoea and its cardiovascular consequences. Lancet. 2009; 373: 82–93.

3. Dempsey J, Veasey S, Morgan B. O’Donnel C. Pathophysiology of sleep apnea. Physiol Rev. 2010; 90: 47–112.

4. Vaessen, T., Overeem, S., and Sitskoorn, M. Cognitive complaints in obstructive sleep apnea. Sleep Med Rev 2014; 19: 51–58.

5. Jordan, A., McSharry, D. and Malhotra, A. Adult obstructive sleep apnoea. Lancet 2014; 22: 736–747.

6. Young T, Finn L, Peppard P, Szklo-Coxe M, Austn, D., Nieto, F. et al. Sleep disordered breathing and mortality: eighteen-year follow-up of the Wisconsin sleep cohort. Sleep. 2008 ; 31: 1071–1078.

7. Marin J, Carrizo S, Vicente E, Agusti A. Long-term cardiovascular outcomes in men with obstructive sleep apnoea-hypopnoea with or without treatment with continuous positive airway pressure: an observational study. Lancet 2005; 365: 1046–1053.

Romero et al. (2016)Email:

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Romero MM, Samalea PV, César EC, Marfil NR, Sánchez MCV (2016) Efficacy of Orthoapnea Mandibular Advance Device in Patients with Mild and Moderate Obstructive Sleep Apnea Syndrome. J Sleep Med Disord 3(6): 1065.

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8. Kendzerska T, Gershon A, Hawker G, Leung R, Tomlinson G. Obstructive sleep apnea and risk of cardiovascular events and all-cause mortality: a decade-long historical cohort study. PLoS Medicine 2014; 11: 1–15.

9. 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 ; 32: 1230–1235.

10. Sutherland K, Vanderveken O, Tsuda H, Marklund M, Gagnadoux F, Kushida C, et al. Oral appliance treatment for obstructive sleep apnea: an update. J Clin Sleep Med. 2014; 10: 215–227.

11. Richard B Berry, Rita Brooks, Charlene E Gamaldo, Susan M Harding, Carole L, Marcus Bradley V. Vaughn, et al. The AASM Manual for the Scoring of Sleep and Asociate Events. Rules, Therminology and Thecnical Specifications. 2012.

12. Berry R, Budhiraja R, Gottlieb D, Gozal D, Iber C, Kapur V, et al. Rules for scoring respiratory events in sleep: update of the 2007 AASM Manual for the Scoring of Sleep and Associated Events. J Clin Sleep Med. 2012; 8: 597–619.

13. Kushida CA, Morgenthaler TI, Littner MR, Alessi CA, Bailey D, Coleman J Jr, et al. Practice parameters for the treatment of snoring and obstructive sleep apnea with oral appliances: an update for 2005. Sleep. 2006; 29: 240-243.

14. Hoffstein V. Review of oral appliances for treatment of sleep-disordered breathing. Sleep Breath. 2007; 11: 1-22.

15. Lim J, Lasserson TJ, Fleetham J, Wright J. Aparatos bucales para la apnea obstructiva del sueño. Biblioteca. Cochrane Plus. 2009.

16. Ramar K, Dort LC, Katz SG, Lettieri CJ, Harrod CG, Thomas SM, et al. Clinical practice guideline for the treatment of obstructive sleep apnea and snoring with oral appliance therapy: an update for 2015. J Clin Sleep Med. 2015; 11: 773–827.

17. Patricia Lloberes, Joaquín Durán Cantolla, Miguel Angel Martínez García, José María Marín, Antoni Ferrer, Jaime Corral, et al. Normativa sobre el diagnóstico y tratamiento del síndrome de apnea obstructiva durante el sueño (SAOS). Arch. Bronconeumol. 2011; 47: 143-156.

18. Consenso nacional sobre Síndrome de Apneas-Hipopneas del sueño (SAHS). Arch Bronconeumol. 2005; 4: 1-80.

19. Documento de consenso sobre Síndrome de Apneas-Hipopneas del sueño en Andalucía. Rev Esp Patol Torac 2012; 24: 214-254.

20. Chan AS, Sutherland K, Schwab R, Zeng B, Petocz P, Lee R, et al. The effect of mandibular advancement on upper airway structure in obstructive sleep apnoea. Thorax. 2010; 65: 726–732.

21. Ngiam J, Balasubramaniam R, Darendeliler M, Cheng A, Waters K, Sullivan C. Clinical guidelines for oral appliance therapy in the treatment of snoring and obstructive sleep apnoea. Aust Dent J. 2013; 58: 408–419.

22. Marklund M, Sahlin C, Stenlund H, Persson M, Franklin K. Mandibular advancement device in patients with obstructive sleep apnea: longterm effects on apnea and sleep. Chest. 2001; 20: 162–169.

23. Marklund M, Stenlund H, Franklin KA. Mandibular advancement devices in 630 men and women with obstructive sleep apnea and snoring. Tolerability and predictors of treatment success. Chest. 2004; 125:1270-1278.

24. Cistulli P, Gotsopoulos H, Marklund M, Lowe A. Treatment of snoring and obstructive sleep apnea with mandibular repositioning appliances. Sleep Med Rev. 2004; 8: 443–446.

25. Vanderveken O, Devolder A, Marklund M, Boudewyns A, Braem M, Okkerse W, et al. Comparison of a custom-made and a thermoplastic oral appliance for the treatment of mild sleep apnea. Am J Respir Crit Care Med. 2008; 178: 178–197.

26. Mehta A, Qian J, Petocz P, Darendeliler MA, Cistulli PA. A randomized, controlled study of a mandibular advancement splint for obstructive sleep Apnea. Am J Respir Crit Care Med. 2001; 163: 1457–1461.

27. Liu Y, Lowe A, Fleetham J, Park Y. Cephalometric and physiologic predictors of the efficacy of an adjustable oral appliance for treating obstructive sleep apnea. Am J Orthod Dentofacial Orthop. 2001; 120: 639–647.

28. Zeng B, Ng A, Qian J, Petocz P, Darendeliler M,Cistulli P. Influence of nasal resistance on oral appliance treatment outcome in obstructive sleep apnea. Sleep. 2008; 31: 543–547.