An Oral Elastic Mandibular Advancement Device for Obstructive Sleep Apnea

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An Oral Elastic Mandibular Advancement Device for Obstructive Sleep Apnea KATHE G. HENKE, DONALD E. FRANTZ, and SAMUEL T. KUNA Sleep Disorders Center of Virginia, Richmond, Virginia; Don E. Frantz, DDS,
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An Oral Elastic Mandibular Advancement Device for Obstructive Sleep Apnea KATHE G. HENKE, DONALD E. FRANTZ, and SAMUEL T. KUNA Sleep Disorders Center of Virginia, Richmond, Virginia; Don E. Frantz, DDS, PC, Webster, Texas; and Department of Internal Medicine, The University of Texas Medical Branch, Galveston, Texas Oral mandibular advancement devices are becoming an increasingly important treatment alternative for obstructive sleep apnea (OSA). The first aim of the study was to determine whether a new oral elastic mandibular advancement device (EMA) prevents pharyngeal airway closure during sleep in patients with OSA. The second aim of the study was to determine if the polysomnographic response to the oral mandibular advancement device was dependent on the site of airway closure. Overnight polysomnograms were performed in 28 untreated OSA subjects with and without EMA. A third polysomnogram was performed in 12 of the subjects to determine the site of airway closure without the device. Site of airway closure above or below the oropharynx was determined by measuring the respective presence or absence of respiratory fluctuations in oropharyngeal pressure during induced occlusions in non rapid eye movement (NREM) sleep. Mean apnea hypopnea index (AHI) was (SD) events/h without the device and events/h with the device. Nineteen subjects (68%) had at least a 50% reduction in AHI with the device. The change in AHI with the device (AHI without device AHI with device) was directly related to the AHI without the device. All three subjects with airway closure in the lower pharyngeal airway had a greater than 80% reduction in AHI with the device. Two of the nine subjects with airway closure in the velopharynx had a similar therapeutic response. The results show the effectiveness of EMA in the treatment of OSA. The results also indicate that polysomnographic severity of OSA and the site of airway closure should not be used to exclude patients from this oral device treatment. Henke KG, Frantz DE, Kuna ST. An oral elastic mandibular advancement device for obstructive sleep apnea. AM J RESPIR CRIT CARE MED 2000;161: Oral mandibular advancement devices are becoming an increasingly important treatment alternative for obstructive sleep apnea (OSA). A variety of appliances are commercially available, differing widely in design and the manner in which they alter the oral cavity. Previous studies by other investigators have tested the ability of these devices to prevent pharyngeal airway closure during sleep in patients with OSA, and report that the apnea hypopnea index (AHI) decreases by 40 to 75% with the device (1 15). An oral mandibular advancement device has also been reported to be effective in treating upper airway resistance syndrome (16). Recently, a new oral mandibular advancement appliance (EMA) has been developed by one of the authors (D. Frantz) for the treatment of OSA. The device consists of two plastic trays custom molded to the patient s maxillary and mandibular teeth. Elastic straps attached to the upper and lower trays (Received in original form March 15, 1999 and in revised form July 22, 1999) Supported by a grant from The Moody Foundation, NIH HL and by the General Clinical Research Centers Program of the NIH Division of Research Resources Grant RR-73. Correspondence and requests for reprints should be addressed to Samuel T. Kuna, M.D., Pulmonary, Critical Care & Sleep Section, Philadelphia Veterans Affairs Medical Center (111P), University & Woodland Avenue, Philadelphia, PA Am J Respir Crit Care Med Vol 161. pp , 2000 Internet address: pull the mandible forward. The amount of advancement can be adjusted by altering the length and elasticity of the straps. The device allows lateral, vertical, and anteroposterior movement of the mandible while advancing the mandible in a ventral and caudal direction. The first aim of the current study was to determine whether this new appliance prevents pharyngeal airway closure during sleep in patients with OSA. While the effectiveness of nasal continuous positive airway pressure (CPAP) treatment of OSA is independent of the site of pharyngeal airway closure, studies indicate that the effectiveness of uvulopalatopharyngoplasty, a resection of soft tissue in the velo- and oropharynx, is dependent on the site of closure. Launois and coworkers (17) and Hudgel and coworkers (18) have shown that OSA patients with airway closure in the velopharynx are more likely to have an initial beneficial outcome. A recent study by Millman and coworkers (19) reported that patients with continued OSA after uvulopalatopharyngoplasty had a very favorable polysomnographic response to oral mandibular advancement device treatment. The aforementioned studies raise the possibility that the ability of an oral mandibular advancement device to prevent pharyngeal airway closure during sleep is also dependent on the site of airway closure. The second aim of the study was to determine if the polysomnographic response to EMA was dependent on the site of airway closure. We hypothesized that OSA subjects with airway closure in the lower pharyngeal airway would be more likely to respond to an oral device owing to the ventral Henke, Frantz, and Kuna: Mandibular Advancement Device 421 displacement of the tongue and hyoid apparatus with mandibular advancement. METHODS Subject Selection The protocol was performed on 28 untreated subjects with OSA (24 males and 4 females): age yr (mean SD), mean body mass index kg/m 2, mean neck circumference cm. During the subject recruitment phase of the study, consecutive patients evaluated in the sleep laboratory with untreated OSA were asked to participate. The criterion for inclusion in the study was an AHI 10 events/h on an overnight polysomnogram. Exclusion criteria included edentulous patients and patients who had an oxygen saturation 85% for more than 20% of the total sleep time. Patients with a previous history of temporomandibular joint pain (n 4) were not excluded. All subjects presented with complaints of excessive daytime hypersomnolence but no measures were used to quantify this symptom. None of the subjects had evidence on physical examination of right-sided congestive heart failure. The protocol was approved by the institutional review board of The University of Texas Medical Branch at Galveston and written informed consent was obtained from all subjects. Nighttime Polysomnograms All subjects were asked to perform three nighttime polysomnograms in the following order: polysomnogram 1 established the diagnosis of OSA and led to subject recruitment into the study, polysomnogram 2 (n 28) was performed with the subjects using EMA, and polysomnogram 3 (n 12) determined the site of pharyngeal airway closure. Body position was not controlled in the first two polysomnograms, but polysomnogram 3 was performed with the subjects in the supine position. Using standard techniques, the following signals were recorded during the polysomnograms with a computer data acquisition and analysis system (Mallinckrodt, Plymouth, MN): C3A2 and O2A1 electroencephalogram (EEG), bilateral electro-oculograms, chin muscle activity, impedance plethysmography of the rib cage and abdomen (Respitrace; Ambulatory Monitoring, Ardsley, NY), airflow at the nose and mouth (Neurosupplies, Waterford, CT), body position, oxygen saturation by pulse oximetry (Ohmeda, Louisville, CO), and presence or absence of tracheal breath sounds. The time interval between polysomnograms 1 and 2 was days (range 49 to 262). The time interval between polysomnograms 2 and 3 was d (range 23 to 84). Paired t tests found no statistically significant differences in body weight between polysomnograms 1 and 2 or between polysomnograms 2 and 3. Oral Elastic Mandibular Advancement Device After the diagnostic polysomnogram, the subjects were fitted with EMA (Frantz Design, Austin, TX) (Figures 1 and 2). The oral device consists of two plastic trays custom molded to the patient s maxillary and mandibular teeth. The trays remain securely in place by snapping into undercut areas of the teeth. The trays are made of a hard material which does not allow tooth movement and prevents the device from falling off during sleep. On the buccal side of the device, bilateral plastic button hooks are located on the maxillary tray at the level of the cuspids and on the mandibular tray at the molar region. Bite planes are located bilaterally on the occlusal surface of the mandibular tray at the molar region. The amount of bite opening was just sufficient to allow clearance of the upper and lower incisors during mandibular advancement. The amount of bite opening in the oral devices was not altered during the course of the study. To activate the appliance, elastic straps are attached to the right and left pairs of button hooks so that the stationary maxilla pulls the mandible forward. The amount of mandibular advancement can be adjusted by varying the length and elasticity of the straps connecting the upper and lower dental trays. Straps of three different lengths (21 mm, 17 mm, and 13 mm) and three different elastic strengths (60, 70, and 80 durometers) were used. Before performing polysomnogram 2, the subjects were instructed to wear the appliance at home during sleep. Initially they used the longest strap with the lowest elastic strength. The mandible was then progressively advanced by substituting elastics of shorter length and greater strength. Polysomnogram 2 was obtained at a mandibular advancement that eliminated or greatly reduced snoring and/or daytime hypersomnolence based on history from the patient and bed partner (n 19), advancement equal to or greater than maximal voluntary advancement (n 5), or the greatest advancement that could be tolerated by the subject owing to temporomandibular joint pain (n 4). The latter four subjects were those who had a prior history of temporomandibular joint pain. History from the patient and/or bed partner was used to assess snoring and daytime hypersomnolence. Gradual advancement of the mandible appeared to be important in preventing temporomandibular joint pain. When unilateral temporomandibular joint pain developed in a subject, it could usually be alleviated by removing the ipsilateral elastic strap for several days. When the joint pain was bilateral, the straps were changed to decrease Figure 1. EMA shown off (left panel) and on (right panel) a cast of one subject s upper and lower teeth. Elastic straps attach the upper and lower trays. The maxilla pulls the mandible forward. Different degrees of advancement are achieved by using straps of different elasticity and length. 422 AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE VOL Figure 2. The maxillary (left panel) and mandibular (right panel) trays of EMA. the amount of advancement. None of the subjects had to discontinue wearing the device because of temporomandibular joint pain. The subjects were instructed to replace the elastic straps every week to avoid stretching. The elastic straps were also replaced by the laboratory technician just prior to polysomnograms 2 and 3. Both the subjects and technicians were shown how to change the straps when the device was out of the subject s mouth. This was easily accomplished manually and required no special instruments. The amount of advancement and bite opening with the device using the elastics worn during polysomnograms 2 and 3 and maximal voluntary mandibular advancement were measured during wakefulness with a caliper and ruler. Determination of Site of Airway Closure Polysomnogram 3 was performed to determine the site of airway closure without the oral device. During the polysomnogram, the subjects were placed on nasal CPAP (Respironics, Murrysville, PA) to eliminate snoring and apneas and hypopneas. In addition to the standard polysomnographic parameters recorded during polysomnograms 1 and 2, nose mask pressure, nasal air flow, and oropharyngeal pressure were recorded during polysomnogram 3. Nose mask pressure was measured with a pressure transducer (Spectramed, Oxnard, CA) attached to a port in the nose mask. Nasal air flow was measured with a pneumotachograph (Hans Rudolph, Kansas City, MO) and symmetrical differential pressure transducer (Validyne, Northridge, CA) interposed between the nose mask and the expiratory port of the nasal CPAP circuit. Oropharyngeal pressure, i.e., airway pressure below the level of the soft palate, was measured with a saline filled 8-Fr catheter attached to a pressure transducer (Spectramed). After topical anesthesia of one nasal passage with 1 ml of 1% lidocaine spray, the catheter was advanced transnasally into the oropharynx and secured to the nose. Correct position of the catheter below the level of the soft palate and above the tip of the epiglottis was confirmed at the beginning and end of the study by direct visualization of the oropharynx. The pharyngeal catheter was not bothering once in place. Pressure was measured at the side holes near the sealed distal tip of the catheter. Pressure was calibrated in cm H 2 O with a water manometer and flow was calibrated in L/min with a rotameter (Fischer & Porter, Warminster, PA). To determine if the site of pharyngeal airway closure was above or below the tip of the oropharyngeal catheter, airway closure was induced during stable periods of stages 2 4 non rapid eye movement (NREM) sleep by abruptly lowering nose mask pressure to atmospheric pressure. To achieve this abrupt decrease in pressure, the tube connecting the nose mask to the machine was disconnected at the machine end. Airway closure was determined by the absence of fluctuations in nose mask pressure and absence of nasal air flow. The absence of respiratory-related fluctuations in oropharyngeal pressure during the induced apnea indicated that the site of closure was below the catheter tip, i.e., below the velopharynx. The presence of respiratoryrelated fluctuations in the pressure signal during the induced apnea indicated that the site of closure was above the catheter tip, i.e., at the velopharynx. Mask pressure was restored to control pressure after 3 to 5 occluded efforts. Approximately 5 min separated three consecutive trials. Trials associated with an arousal before restoration of nasal CPAP were eliminated. Data Analysis In a given subject, the polysomnograms were analyzed manually with the aid of computer software by the same polysomnographic technologist. The technologist scoring the polysomnograms was not informed whether or not the subject was wearing the oral device during the recording. Data in polysomnograms 1 and 2 from the entire sleep period and from the NREM and rapid eye movement (REM) sleep periods were used for statistical analysis. Change in a polysomnographic outcome parameter was calculated as (parameter value without device parameter value with device). Percent change in a polysomnographic parameter was calculated as the change in the parameter divided by the parameter s value without the device. Depending on whether or not the data were normally distributed, the paired t test was used for within-group comparisons of the following polysomnographic outcome parameters with and without the oral device: AHI, apnea index (AI), hypopnea index (HI), desaturation index, minimal oxygen saturation, and the amount of sleep time spent below 90% oxygen saturation. Nonparametric tests were used to validate the paired t test results in cases where the normality test failed. The results were the same in both cases. A desaturation event was defined as a 4% drop in oxygen saturation. Comparisons with p 0.05 were considered statistically significant. RESULTS Amount of Mandibular Advancement and Bite Opening The elastic straps used by the subjects during polysomnograms 2 and 3 advanced the mandible by mm (range 3.3 to 17.0) during wakefulness. This amount of mandibular advancement was % (range 72 to 109) of maximal voluntary advancement. In three subjects, the device advanced the mandible further forward than maximal voluntary advancement. The devices increased bite opening by mm (range 8.8 to 16.5). Polysomnographic Results with and without the Oral Device No significant differences were present between polysomnograms 1 and 2 with regard to total sleep time, time in NREM sleep, time during sleep in a particular body position, or body weight. There was a significant difference (p 0.03) in the amount of time in REM sleep between polysomnograms 1 and 2 ( min and min, respectively). In the analysis of the effect of the oral device on the polysomnographic data, the statistical results presented subsequently for the entire sleep period were the same as those obtained from NREM sleep or REM sleep, unless otherwise specified. The effect of the oral device on AHI and other polysomnographic parameters is shown in Figures 3 and 4 and Table 1. For the entire group, EMA reduced the AHI from events/h (range 10.2 to 112.2) to events/h (range 0 Henke, Frantz, and Kuna: Mandibular Advancement Device 423 Figure 3. AHI and AI without and with EMA. The largest reductions in AHI and AI with the device occurred in subjects who had an AHI 40 events/h without the device. to 91), a % improvement (range 40 to 100%) (p 0.001). Similar statistically significant differences were present for AI, HI, and desaturation index. Nineteen subjects (68%) had at least a 50% reduction in AHI with the device. AHI with the oral device was 15 events/h in 12 (43%) subjects and 10 events/h in nine (32%) subjects. The AHI without the device in these subjects was and events/h respectively. Subjects with an AHI 40 events/h on polysomnogram 1 had a % improvement in AHI with the device, whereas subjects with an AHI 40 events/h on polysomnogram 1 had a % improvement. Five of the seven subjects who had greater than 80% improvement in AHI with the device had an AHI greater than 40 events/h without the device. Four subjects had a higher AHI with the device. Careful review of the data from these subjects found no explanation for this finding. For the entire group, the change in AHI with the device was linearly related to the AHI without the device (Figure 5). A straight line fit to the data using least squares linear regression explained 60% of the variance (coefficient of determination [R 2 ] 0.60). Similar statistically significant relationships were present for other polysomnographic outcome parameters: AI (R ), HI (R ), minimal oxygen saturation (R ), and amount of time spent below 90% oxygen saturation (R ). All the p values of these linear regressions were The change in a given polysomnographic outcome parameter (AHI, HI, AI, minimal oxygen saturation, time below 90% oxygen saturation) with and without the device was not related to the amount of mandibular advancement, amount of bite opening, neck circumference, body weight, and body mass index. The amounts of variance explained by these relationships were all less than 15% and the p values were The amount of polysomnographic improvement with the device could not be predicted on the basis of whether the amount of advancement had been determined by symptomatic improvement or limited by maximal anatomic advancement or temporomandibular joint pain. Effect of Site of Airway Closure on Efficacy of the Oral Appliance The AHI of the 12 subjects who agreed to perform the third polysomnogram was events/h (range 28.3 to Figure 4. Minimal oxygen saturation and percent sleep time spent below 90% oxygen saturation without and with EMA. 424 AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE VOL TABLE 1 EFFECT OF EMA ON POLYSOMNOGRAPHIC PARAMETERS* Without Device With Device NREM and REM sleep AI, events/h HI, events/h AHI, events/h Minimal oxygen saturation, % Sleep time below 90% oxygen saturation, % NREM sleep AI, events/h HI, events/h AHI, events/h REM sleep AI, events/h HI, events/h AHI, events/h * Values are expressed as mean SD. p p p Figure 6. Percent c
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