A. J. Moses – Assistant Professor, Rush University College of Medicine, Chicago IL, USA Department of Sleep Disorders.
J. A. Bedoya – Universidad Diego Portales, Santiago, Chile Department of Oral Surgery.
J. A. Learreta – Universidad Catolica de Salta, Buenos Aires, Argentina Department of Orthodontics and Temporomandibular Pathologies.
An imaging study is presented to advance understanding of how a Mandibular Advancement Device (MAD) used as therapy for Obstructive Sleep Apnea (OSA) changes the shape and volume of the oral airway.
In lower animals the uvula overlaps the epiglottis. This anatomic arrangement separates the oropharynx from the nasopharynx and allows the animal to swallow and breathe at the same time. Human babies have this same anatomic configuration. At about six to nine months of age the epiglottis begins to descend and the uvula ascends such that by two years of age there is a vertical gap between them. Subsequent to age two in humans, the foodway and the airway share the same passage from the uvula to the epiglottis, and the boundaries of this area are all soft tissues. This creates a compliant, collapsible oropharynx. The front wall is the tongue and the side and rear boundary is the pharyngeal wall.1
Humans are the only animals to have a collapsible oropharynx and the only animals with the ability to articulate speech. All vowel sounds are formed in this compliant, collapsible area. Speech is the advantage. The disadvantages in humans are the possibility of obstructive sleep apnea and choking.
The MAD actively repositions and supports the mandible in a more anterior and open position than the position of maximum interarch occlusion of teeth or physiological rest position of the mandible. The tongue is attached to the mandible on the lingual side of the symphysis, below the apex of the roots of the mandibular central incisors. As the mandible is actively advanced by the MAD, the tongue at its attachment is passively pulled anteriorly away from the back wall of the oropharynx.
MADs are approved by the American Academy of Sleep Medicine for use as primary therapy in cases of mild to moderate OSA and in patients with more severe OSA who cannot tolerate Continuous Positive Air Pressure (CPAP) therapy.3
What remains problematic is how MADs work. Studies report that MADs increase posterior airway space,4, 5 and at least one that demonstrates no change in posterior airway space.6 Passive tongue advancement during general anesthesia has been reported to increase both retropalatal and retroglossal areas.7 Studies of the effect of protrusion consistently report that increased protrusion produces greater reductions in restricted respiratory events.8,9,10,11 Studies differ however on the impact of vertical opening related to device efficiency and the amount of jaw discomfort reported using the MAD.12,13,14,15
The hydrostat theory of tongue function was proposed by Keir and Smith in 1985.16 It has been supported by scientific testing for almost a quarter of a century.17,18,19 The most important biomechanical characteristic of a muscular hydrostat is that it is a structure of constant volume. Muscle tissue is composed primarily of an aqueous liquid which is practically incompressible at physiological pressures. Contraction of muscle does not change its volume. Any decrease in one dimension will cause a compensatory increase in at least one other dimension in a muscular hydrostat.
The tongue being a hydrostat, in reasoning the mechanism of action of a MAD, one must assume that tongue volume is a constant. A tongue might change its shape but the volume remains the same. MADs move the tongue out of the airway at night but to accommodate this change it must increase the volume of space for the tongue in the oral cavity.
An open gantry cone beam 3 D computerized tomography scanner, the ICAT™ by Imaging sciences International was used for this study. High resolution, 360 scans produced images at .2mm voxel size. 14 bit grayscale quality along all x, y, and z-axes produced clear images in cross-sectional views. A scan time of 40 seconds was used with beam collimation at full height. The x-ray source was a high frequency, constant potential, pulse mode at 120kVp and 3-8mA. The focal width is .5mm and the image detector is an amorphous silicon flat panel of 20cm. x 25cm.
The MAD used for this study was the Moses Appliance, a two piece open-anterior device. The upper element is a .3mm polypropylene-ethylene copolymer vacuum-formed splint covering all maxillary teeth and trimmed to not touch the gingiva. The lower element is made of methyl-methylacrylate and built to maintain the dental arches in a position at the maximum vertical height at which the patient can comfortably close the lips, and the maximum protrusive position that the patient can comfortably tolerate.
The effectiveness of MADs used as treatment for OSA have been thoroughly referenced in an updated (2006) American Academy of Sleep Medicine review paper.20 That MADs work is well established. How they work is a subject of continuing research.
This case report demonstrates that the MAD studied, constructed to a jaw position of increased vertical and sagittal position substantially increases the size of the airway lumen in the retroglossal and palatal regions in all possible dimensions. The term oral airway dilator may be a more suitable descriptor than simply mandibular advancement device.
This study was done with the patient awake and seated upright. A preliminary study by the lead author using a different CT scanner with the patient in the supine position did not show any appreciable changes in awake airway measurements. Sleep could certainly affect the airway dynamics from upright and awake to the sleep state. The actual role of the tongue during sleep was not directly dealt with in this study. It is certainly an excellent subject for a future research study.
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