Published ahead of print on April 30, 2003, doi:10.1164/rccm.200211-1275OC
© 2003 American Thoracic Society
Effect of Oral Appliance Therapy on Upper Airway Collapsibility in Obstructive Sleep ApneaDepartment of Respiratory and Sleep Medicine, St. George Hospital, University of New South Wales, Sydney, Australia Correspondence and requests for reprints should be addressed to Peter Cistulli, M.D., Ph.D., Department of Respiratory Medicine, St. George Hospital, Belgrave Street, Kogarah, NSW 2217, Australia. E-mail: p.cistulli{at}unsw.edu.au
Oral appliance therapy is emerging as an alternative to continuous positive airway pressure for the treatment of obstructive sleep apnea (OSA). However, its precise mechanisms of action are yet to be defined. We examined the effect of a mandibular advancement splint (MAS) on upper airway collapsibility during sleep in OSA. Ten patients with proven OSA had a custom-made MAS incrementally adjusted during an acclimatization period until the maximum comfortable limit of mandibular advancement was reached. Polysomnography with the splint was then performed. After a 1-week washout period, upper airway closing pressures during sleep (with and without MAS) were determined. Significant improvements with MAS therapy were seen in the apnea/hypopnea index (25.0 ± 3.1 vs. 13.2 ± 4.5/hour, p < 0.03) and upper airway closing pressure in Stage 2 sleep (–1.6 ± 0.4 vs. –3.9 ± 0.6 cm H2O, p < 0.01) and in slow wave sleep (–2.5 ± 0.7 vs. –4.7 ± 0.6 cm H2O, p < 0.02) compared with no therapy. These preliminary data indicate that MAS therapy is associated with improved upper airway collapsibility during sleep. The mediators of this effect remain to be determined.
Key Words: mandibular advancement splint • obstructive sleep apnea • upper airway collapsibility Obstructive sleep apnea (OSA) is a common disorder occurring in around 4% of men and 2% of women in the middle-aged workforce (1). It is characterized by recurrent obstruction of the upper airway during sleep (2). The current treatment of choice is continuous positive airway pressure delivered via a nasal mask to the upper airway during sleep (3). This is an extremely effective treatment, but its cumbersome nature often leads to reduced tolerance and compliance (4–6). An emerging treatment alternative is oral appliance therapy (7), which has potential advantages over continuous positive airway pressure because it is less obtrusive, does not make noise, and is more portable. Of the five randomized crossover trials comparing continuous positive airway pressure with oral appliances (8–12), all but one (12) demonstrated a patient preference in favor of oral appliances. However, although oral appliance therapy has been shown to be effective across all grades of OSA severity (13, 14), a key limitation is reduced effectiveness compared with continuous positive airway pressure (8–12). Current understanding of the precise mechanisms of action of oral appliances in OSA is incomplete. A better understanding of these mechanisms could improve our ability to predict treatment outcome, a key unresolved issue. Intuitively, one would believe that mandibular advancement should improve the anteroposterior dimension of the oropharynx. However, recent studies suggest that increases in upper airway caliber occur in the lateral dimension at the level of the velopharynx (15, 16). Hence, the anatomic changes induced by mandibular advancement appear to be quite complex, presumably due to the intricate linkages between upper airway structures. Regardless of these anatomic changes, the ultimate determinant of upper airway closure is the degree of upper airway collapsibility during sleep. Abnormal upper airway collapsibility during sleep has been clearly documented in both snorers and patients with OSA compared with normals (17, 18). Furthermore, treatment of OSA by weight loss or surgery has been shown to improve upper airway collapsibility in responders (19, 20). We postulate that oral appliance therapy reduces upper airway collapsibility during sleep. Hence, our aim was to examine the effect of oral appliance therapy on upper airway collapsibility during sleep.
Study Population Adult patients were recruited from a multidisciplinary Sleep Disorders Clinic in a University Teaching Hospital. Inclusion criteria were the presence of at least two symptoms of OSA (snoring, fragmented sleep, witnessed apneas, daytime sleepiness) and evidence of OSA on polysomnography, with an apnea/hypopnea index (AHI) of 10/hour or more. Patients were excluded if there was evidence of periodontal disease, dental caries, edentulism, an exaggerated gag reflex, or predominant central sleep apnea on polysomnography. The study was approved by the institutional Ethics Committee, and written informed consent was obtained from all patients before commencement. We used a mandibular advancement splint (MAS) as described previously by our group (13, 14).
Study Design
Outcome Measures
UACP.
Treatment Outcome Complete response was defined as a resolution of symptoms and reduction in AHI to less than 5/hour. Partial response was defined as improved symptoms plus a 50% reduction or more in AHI but remaining 5/hour or more. Failure was defined as less than 50% reduction in AHI.
Statistical Analysis
Study Population The study sample consisted of 10 patients (nine males and one female), all of whom completed the protocol. Patient characteristics at baseline are presented in Table 1 . There was no significant difference between baseline and treatment regarding weight. The mean mandibular advancement with the MAS was 4.6 ± 1.4 mm (range, 3.0–8.0) from centric occlusion.
Outcomes The MAS was well tolerated. Only mild side effects were experienced, which included excessive salivation, gum irritation, mouth dryness, and jaw discomfort. These did not preclude use of the MAS. Polysomnographic outcomes are summarized in Table 2 . MAS treatment resulted in a significant reduction in AHI and a significant increase in minimum SaO2. The MAS resulted in complete response in five patients (50%), partial response in two patients (20%), and treatment failure in three patients (30%). Six patients (60%) achieved an AHI of less than 10/hour.
MAS treatment resulted in significant improvements in UACP during Stage 2 non-REM sleep and slow wave sleep (Table 2). Improvement was noted in all subjects, albeit to different degrees. Nine patients had the type 1 response with and without MAS. One patient had the type 2 response without MAS, converting to a type 1 response with MAS. A significant positive correlation was found between the change in AHI and change in UACP in Stage 2 non-REM sleep (r = 0.64, p < 0.05). A median improvement in UACP (Stage 2 non-REM sleep) of 2.8 cm H2O (25th, 75th percentiles 1.9, 5.7) was observed in the complete responders, and this was significantly greater than the median of 1.1 cm H2O (25th, 75th percentiles: 0.6, 1.2) seen in the combined group of partial responders and treatment failures (Mann–Whitney U: z = -2.41, p < 0.01). No significant correlation was found between baseline UACP and AHI or between the degree of mandibular advancement and change in UACP.
Despite the increasing use of oral appliances in the treatment of OSA, considerable uncertainty about their precise mechanisms of action exists. This is the first study to examine the influence of an oral appliance on UACP during sleep. We found that the MAS improved upper airway collapsibility and suggest that this is one mechanism through which OSA is improved. Upper airway patency is complex and involves a number of interrelated factors. A balance exists between its tendency to collapse, induced by the subatmospheric intraluminal pressure during inspiration, and upper airway dilator muscle activity, which is influenced by upper airway dimensions and complex neuromuscular reflex interactions (2). Upper airway collapsibility measured by the UACP is likely to reflect the net effect of all these factors. Our patients had a baseline average UACP of –1.6 ± 0.4 cm H2O in Stage 2 sleep and –2.5 ± 0.7 cm H2O in slow wave sleep during supine sleep. These results are consistent with previous findings in patients with OSA by Issa and Sullivan (17). This study demonstrated a relationship between the magnitude of improvement in UACP during Stage 2 sleep and the improvement in AHI. In addition, the improvement in UACP during Stage 2 sleep in the group of complete responders was significantly greater than that found in the other two groups combined. However, an interesting finding in our study was that UACP improved after MAS treatment even in the failures, albeit to a lesser extent. This suggests that it is the magnitude of improvement in UACP that determines treatment outcome. How mandibular advancement improves upper airway collapsibility, however, remains unclear. Anatomic improvements in the anteroposterior dimension of the oropharynx have been postulated, although recent studies (15, 16) suggest that it is the lateral dimensions of the velopharynx that improve. Another mechanism proposed by Isono and coworkers (23) is that mandibular advancement stretches the soft palate, thus stiffening the velopharynx because of the connection of the lateral wall of the soft palate to the base of the tongue through the palatoglossal arch. Improved upper airway collapsibility has been seen when other treatment alternatives have been successful. Schwartz and coworkers (19, 20) have demonstrated improvements in upper airway collapsibility after treatment success with weight loss and also with uvulopalatopharyngoplasty using a technique called the pharyngeal critical pressure. This technique, which is different from the closing pressure technique used in our study, examines pressure–flow relationships during sleep using the Starling resistor model (flow through a collapsible conduit) of the upper airway. Pharyngeal critical pressure is the pressure below which occlusion and cessation of airflow occurs. This pressure is found by measuring maximal airflow at different nasal mask pressures and then extrapolating to the pressure at which no airflow occurs (24). Therefore, pharyngeal critical pressure is a derived value and is believed to represent the pressure surrounding the locus of pharyngeal collapse. This model predicts that when pharyngeal critical pressure is positive relative to atmospheric nasal pressure, the upper airway should close. The closing pressure technique that we used measures the airway suction pressure at which pharyngeal closure occurs in response to complete external nasal occlusion, which is fundamentally different from the pharyngeal critical pressure technique. We chose the closing pressure technique because it provides a direct measure of the pressure at which airway collapse occurs. In our study, the average mandibular protrusion of 4.6 mm is less than that seen in other studies (13, 14). This was the maximum comfortable limit tolerated by our study patients and was 65% of the maximum possible protrusion on average. One potential limitation of our study was treatment order bias because UACP measurements were made with and without MAS during a single night. This was reduced by randomizing the treatment order during the closing pressure determination study. As a result of the unpredictability of achieving REM sleep during the overnight protocol, only two patients had reliable UACP determinations in this sleep stage. Another limitation was the inability of the technique to localize the site(s) of obstruction within in the upper airway. This could be overcome in future studies by using a catheter measuring pressure at different levels in the upper airway during a closing pressure determination study. Although the sample studied was small, there was uniformity of the direction of effect in all patients. In conclusion, we have demonstrated that oral appliance therapy improves upper airway collapsibility during sleep in patients with OSA. The magnitude of improvement in UACP was greater in patients who achieved a complete response to treatment. Given that treatment success with MAS is not achievable in every patient, further research is needed to determine whether UACP can be used as a predictor of treatment outcome.
The authors thank Carol Chen and Michael Lazaris for assisting with patient management and technical support. The oral appliance used in this study was designed by Dr. Richard Palmisano (patents pending). Received in original form November 4, 2002; accepted in final form April 28, 2003
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