Published Journal Articles:

“Consideration of intercondylar angles in determining a maxillo-mandibular relationship for intraoral sleep appliances”, Sleep Diagnosis and Therapy, June, 2012, Vol 7 No 3, pp 41-49

"Oral Appliance Design" Technical Corner Dialogue, Issue 2, 2011, pp. 27-30

"Sleepy Drivers" Sleep Diagnosis and Therapy, Vol 6.5, September 2011

"Evolution of Theory on Oral Appliances and Exercises for Sleep Apnea and Snoring" Sleep Diagnosis and Therapy, Vol 5 No 7 November/December 2010, pp 22-25

"A Case Study of the Anatomic Changes Effected by a Mandibular Advancement Device in a Sleep Apnea Patient" Sleep Diagnosis and Therapy, January/February 2010, Vol 5 No. 1 pp 30-34

“Protocol for Primary Treatment of Snoring by Dentists” Sleep Diagnosis and Therapy, Oct 2008,  Vol 3(6) pp 21-23

“Pilot Study Testing the Concept of Intraoral Nasal Dilation” with Klockow RG, and Lieberman M, accepted for publication Sleep Diagnosis and Therapy, May-June, Vol 3(3) pp 58-60

"What’s New in Oral Appliances for Snoring and Sleep Apnea” Sleep Diagnosis and Therapy, Dec 2007, Vol. 2(6) pp 19-24

"Computer Aided Diagnoses of Chronic Headaches: Explanation, Preliminary Data and Implications" with Lieberman M, Kittay I, Learetta JA. Accepted for publication Journal of Craniofacial Pain

"The Tongue Retaining Device: A New Look at an Old Device" Sleep Review, Nov 2003, Vol 4 (7), p 34 - 38, with Alvarez RM.

"Study of the Effect of External Nasal Dilators on Blood Oxygen Levels in Dental Patients", Journal of the American Dental Association, Jan 2003, Vol. 134, p97 - 101, with Lieberman M.

"Computer Aided Diagnosis of Pain in the Head: A Paradigm for Construction of the Software" Journal of Craniomandibular Practice, July 02, Vol. 2(3), pp 222-230

"Nasal breathing strips as clinical aids in the treatment of mouth breathers" Journal of the American Dent Assoc, Vol. 132, pp 1555-1556, Nov 2001.

"They Just Don't Understand TMD", Editorial, JOURNAL OF PROSTHETIC DENTISTRY, July, 1999, pp 117-120

"Politics, Philosophy and TMD", chapter in textbook, "Neuromuscular Dentistry In the Next Millennium", ed. D. Hickman, Herman Printing Inc/ICCMO, 1999, pp 171-185

"Cephalometric Variation in Patients, With and Without Intraoral Neuromuscular Orthotics", co-authored with Learreta, J, JOURNAL OF GENERAL ORTHODONTICS, Vol. 10 summer 1999, pp 14-21

"Daubert, Pain, Evidence and Inference in Treating TMD", DEFENSE COUNCIL JOURNAL, vol.64, no. 4, October 1997, pp. 613-616

"Controversy in TMD: Putting the Issues in Perspective" DENTISTRY TODAY, vol. 16, April 1997, pp. 92-97

"Good Science, Bad Science, and Scientific Double-talk" ed. CRANIO- JOURNAL OF CRANIOMANDIBULAR PRACTICE, vol. 14, no. 3, July 1996, pp. 170-173

"Objective Electronic Measurement: Part II" DENTISTRY TODAY, vol. 15, No. 4, April 1996, pp. 102-105

"Methodology of Clinical Research in Temporomandibular Disorders" ed. DENTAL ABSTRACTS, vol. 41, no. 2, 1996, pp. 56-59

"The Clinical Use of Objective Measurement in TMD" DENTISTRY TODAY, vol.14, no. 10, October 1995, pp. 70-73

"Scientific Methodology in Temporomandibular Disorders: Part III, Diagnostic Reasoning" JOURNAL OF CRANIOMANDIBULAR PRACTICE, vol. 12, no. 4, October 1994, pp. 259-265

"Understanding the Problems in Defending TMD cases", DEFENSE COUNSEL JOURNAL, vol. 61, no. 4, October 1994, pp. 593-596

"Scientific Methodology in Temporomandibular Disorders: Part II, Ethology", JOURNAL OF CRANIOMANDIBULAR PRACTICE, vol. 12, no. 2, April 1994, pp. 114-119

"Understanding Whiplash and TMD", DEFENSE COUNCIL JOURNAL, Vol. 61, no. 3, July 1994. Pp. 442-445

"Scientific Methodology in Tempromandibular Disorders: Part I, Epidemiology", JOURNAL OF CRANIOMANDIBULAR PRACTICE, vol. 12, no. 2, April 1994, p. 114-119

"Understanding Temporomandibular Disorders", DEFENSE COUNSEL JOURNAL, vol. 61, no. 2, April 1994, pp. 279-282

"Understanding Temporomandibular Disorders and Whiplash: Part II, Diagnosis and Treatment", CLAIMS, vol. 41, no. 9, September 1993, pp. 36-37 with Cooper BC.

"Legal Perspectives on TMJ/Whiplash", JOURNAL OF CRANIOMANDIBULAR PRACTICE, vol. 11, no. 3, July 1993, pp. 237-240

"Understanding Temporomandibular Disorders and Whiplash: Part I, Mechanism & Patient Presentation", CLAIMS, vol.41, no. 7, July 1993, pp. 32-34 (with Dr. B. C. Cooper)

"Analysis of a Functional Appliance", Chicago Dental Society REVIEW, 1991, vol. 84, pp. 24-29

"Functional Analysis of a Functional Appliance", Frontiers of Oral Physiology, Pathophysiology of Head and Neck Musculoskeletal Disorders, Bergamini, M. (ed.), 1990, vol. 7, pp. 122-131

"Airways and Appliances", Chicago Dental Society REVIEW, 1989, vol. 82, pp. 50-57

"Thumb Sucking or Thumb Propping?", Chicago Dental Society REVIEW, 1987, vol. 80, pp. 40-42

"Cervical Whiplash and TMJ", reprinted BASAL FACTS, 1986, vol. 8, pp. 61-63

"Cervical Whiplash and TMJ", TRIAL, 1986, vol. 22, pp. 63-66

"Viewpoint: Advertising May Improve Our Image", DENTAL ECONOMICS, 1978, pp. 33-36


Dr. Moses' article published in "Sleep Diagnosis and Therapy", Vol 5 No 7 November/December 2010, pp 22-25

Evolution of Theory on Oral appliances and Exercises for Sleep Apnea and Snoring

by Allen J. Moses, DDS

Assistant Professor
Rush University College of Medicine
Chicago IL

Patient exercises have been shown in two randomized controlled studies to be effective for reducing both the symptoms and severity in patients with moderate obstructive sleep apnea syndrome. A study by Puhan,1 et. al. involved lessons to practice and play the didgeridoo, a wind instrument that involves voice control as well as breath control. Regularly playing the didgeridoo, 5.9 days per week for an average
playing time of 25.3 minutes per day, for a four month period of time reduced the average Apnea/Hypopnea Index (a measure of severity) by almost 50% (22.3 to 11.6) and lowered the sleepiness (symptom) from an average Epworth Sleepiness Scale score of 11.8 to 7.4.

Guimares,2 et. al. showed in a randomized controlled trial that oropharyngeal exercises developed for the treatment of OSAS significantly reduced the AHI (severity) and subjective symptoms as well. The exercises, derived from speech therapy, consisted of isometric and isotonic involvement of muscles of the tongue, soft palate, and lateral pharyngeal wall. The exercise set consisted of activities simulating suction, swallowing, chewing, breathing and speech. The target effects are soft palate elevation, tongue protrusion and mandibular elevation to keep the lips together. This study was not designed to explore the exact mechanism by which the signs and symptoms were improved. It does demonstrate that daytime exercises alter muscle tone during sleep.

Reflex Activity
The oral cavity, the tongue and the pharynx are functionally integrated to perform such vital and complex life functions as breathing, drinking, masticating, swallowing, and speaking. The sensory receptors that innervate these parts are constituents of reflex systems that reflect a huge range of complexity. These oropharyngeal reflexes are in fact critical to maintaining life. Reflexes in the upper airway are protective by preventing aspiration, facilitating vocalization, transporting boluses of food and water and protective of breathing by maintaining a patent airway.

Genioglossus, the main tongue muscle, is a protruder. It has an important role in airway protection and maintenance of airway patency, especially in patients with obstructive sleep apnea. Styloglossus and hyoglossus are tongue retruders. Activation of genioglossus under hypoxic and hypercapnic conditions brings about tongue protrusion and pharyngeal airway dilation.3,4 In a study by Mateika,5 et. al. the styloglossus and hyoglossus were also coactivated in response to hypoxia and hypercapnia. This coactivation is the response of complex reflex activity between tongue protruders, tongue retruders and chemical sensors in the central nervous system.

A reflex is defined as the sum total of any particular involuntary activity.6 Specific sensory inputs can subconsciously induce motor responses that have reciprocal effects on different motoneuron pools. Reflexes provide relatively hard wired circuits through the central nervous system to control a set of often antagonistic muscles for co-ordination of a given response, such as a swallow. The motor neurons and the Golgi tendon system are part of a neurologic feedback loop for maintaining muscle tone.

A reflex reaction is conditioned not by one reflex arc but many. Coordination is part of the reflex. According to Sherrington,7 “the main secret of nervous coordination lies in the compounding of reflexes”. Learning is involved in establishing many reflexes. Reflexes elicited from stimulating the oral region alter recruitment of lip, tongue and jaw muscles. The type of sensory stimulus determines the type of reflex
elicited – from simple reflexes to complex behavior affecting oral and pharyngeal regions. Motor neurons responsible for the reflex activity of the head and neck are located in the brainstem – medulla, pons and midbrain.

The tongue is a complex muscular organ. Extrinsic tongue muscles attach to at least one bone and function to alter the shape of the tongue. Intrinsic tongue muscles have both their origin and insertion in muscle. They protrude, retrude and move the tongue laterally. The chief tongue protruder, the
genioglossus muscle is extrinsic.
The electromyographic activity of genioglossus has been shown to be in phase with respiration when awake or in a resting state.8 Changes in mandibular posture have a direct effect on tongue activity and may relate to the role of the tongue in airway maintenance.9 Reflexes elicited from stimulating the oral region alter recruitment of lip, tongue and jaw muscles. The type of sensory stimulus determines the type of reflex elicited – from simple reflexes to complex behavior affecting oral and pharyngeal regions.

An important part of the research of A. J. Miller10 has been description and study of reflexes controlling orofacial function. Relative to tongue protrusion Miller has identified five tongue reflexes. Tongue reflexes are activated from motoneurons from three cranial nerves: hypoglossal, trigeminal and glossopharyngeal.

Jaw-Hypoglossal Reflex7
The hypoglossal nerve (XII) is the only motor nerve to the genioglossus muscle. Stimulation of the medial branch of the hypoglossal nerve causes genioglossus protrusion. The jawhypoglossal
reflex is that stimulation of the inferior alveolar
nerve (VIII) causes firing of hypoglossal motoneurons, a phenomenon that could not be activated by direct stimulation of the hypoglossal nerve. The hypoglossal motoneurons in this reflex protrude the tongue. Passive opening of the mandible by a sleep appliance increases the activity of genioglossus muscle. The position of the mandible in a sleep appliance affects tongue posture and the amount of protrusion. Forward protrusion of the tongue helps maintain a patent airway. Oral appliances for sleep apnea should be conceived to facilitate this reflex by a non-restrictive, open anterior design.

Masseter-Hypoglossal Reflex7
Direct stimulation of the masseteric nerve (VIII) contracts the masseter muscle. The masseter-hypoglossal reflex is that masseteric nerve stimulation also inhibits polysynaptic firing of hypoglossal motoneurons to retrusive tongue muscles. A passive jaw opening beyond rest position stimulates the
masseter to shorten, eliciting reproducible inhibition of tongue muscle retrusion that lasts as long as the jaw is open. Stimulation of this reflex can be easily incorporated into oral sleep appliances to inhibit tongue retrusion while the appliance is worn in the mouth.

Lingual-Hypoglossal Reflex7
The lingual nerve is a branch of the third and largest division of the trigeminal nerve (V) with a mostly sensory function. Mechanical stimulation of the surface of the tongue by light probing or scraping can induce multiple reflexes involving such functions as opening the jaws, closure of the glottis, elevation of the palate and some degree of tongue retrusion, but mostly tongue protrusion. The lingual-hypoglossal
reflex, triggered by tongue stimulation, depends on the site of the sensory input. Stimulation of the medial branch of the hypoglossal nerve innervates intrinsic tongue muscles and brings about protrusion. The lingual-hypoglossal reflex can be facilitated by a prior conditioning reflex and thus trained
by exercise. Stimulation of this reflex can also be incorporated into oral appliance design.

Glossopharyngeal-Hypoglossal Reflex7
The glossopharyngeal nerve contains sensory fibers that innervate the lateral border of the posterior 1/3 of the tongue.Stimulation of the lateral border of the posterior 1/3 of the tongue induces reflex discharges in hypoglossal motoneurons that cause the tongue to protrude and that also inhibit retrusive hypoglossal motoneurons.

Tongue–Tongue Reflex7
The lingual nerve provides sensory innervations to the tip of the tongue. The tongue-tongue reflex is that touch or stroking on the tip of the tongue stimulates hypoglossal motoneurons that cause the tongue to orient toward the stimulus.11 The more intense the stimulation, the higher the probability of tongue movement toward the source. Mechanical stimulation of the dorsal surface of the tongue will induce the same reflex as direct stimulation of the lingual sensory nerve. Coordination of the tongue-tongue relies heavily on exteroceptors on the tongue surface. Stimulation of this reflex can be incorporated into the design of oral sleep apnea appliances.

Studies by Isono,12 Miki,13 Edmonds,14 Decker,15 Guilleminault16 and Schwartz17 have demonstrated that electrical stimulation directed at hypoglossal motoneurons stiffen the retroglossal airway. As a therapeutic approach electrical stimulation has failed to obtain satisfactory results. Too often the electrical stimulation caused cortical arousal resulting in poor sleep quality. The dilation effect only lasted as long as the electrical stimulation was on. Placement of the electrodes often caused pain.

A previous study by Moses18 demonstrated visually the effect of an oral appliance (Figure 1) to actually achieve airway dilation. Placing that oral device in the mouth gives the appearance of airway dilation similar to the splinting effect of CPAP (Figure 2). The dilation from the appliance however, occurred downstream from the actual site of the appliance in the mouth. Note in Figure 2 (right) the enlargement of the airway in the area of the pharyngeal constrictors. The pharyngeal constrictors are not attached to either the tongue or the mandible. The effect of the oral appliance sitting in the mouth is not as simple as tongue and/or mandibular advancement. It has a more complex effect on the entire airway, more closely resembling inflation of a balloon.

Fig. 1. The Moses™, an open anterior, adjustable, FDA cleared oral airway dilator.

It would seem to be a reasonable assumption based on the Moses study and the cited studies on exercises that the operative mechanism by which airway dilation works in both cases
is stimulation of hypoglossal reflexes. Reflex training during the day by exercises has a carryover effect during sleep. The reflex effect of oral appliances works as long as the appliance remains in the mouth. Hypoglossal reflexes operate at a site apart from the origin of the stimulus.

The effectiveness of oral appliances at treating OSA is well documented in the scientific literature.19,20,21,22,23 The effectiveness of exercise training is well demonstrated in the
two articles cited.1,2 Neither methodology alone appears to be better than CPAP when using PSG measures; however, in a recent paper, Chan & Cistulli24 presented data that patient compliance, acceptance and comfort is better with oral appliances than CPAP.

Fig. 2. Left image above is a posterior view of a three dimensional volumetric reconstruction of the patient’s airway without MAD.
Right image is a posterior view of a three dimensional reconstruction of the patient’s airway with MAD properly positioned in the mouth. The increase in size of the airway is substantial and obvious.
The appliance used in the figure on the right is The Moses™.


The old idea that oral appliances are merely mandibular advancement devices, moving the tongue forward to prevent its collapse on the airway is an oversimplification. It does not account for the dilation of the sides and back of the pharynx visible on the 3-D computerized cone beam image with The Moses™ in place. The multidimensional airway dilation cannot be accounted for solely by active anterior
movement of the mandible and the attendant passive pull forward of the tongue base. Consideration and testing of oral appliance therapy in terms of their effect on airway dilation by reflex stimulation is warranted.

It would seem that there is no downside or risk to a clinical strategy of a treatment protocol combining the two methodologies of oropharyngeal exercises and oral appliance therapy. It would also seem that future controlled trials to objectively evaluate the combined effects of oral appliances and exercises is warranted.


1. Puhan MA, Suarez A, Lo Cascio C, Zahn A, Heitz M, Braendli O,
Didgeridoo playing as alternative treatment for obstructive sleep
apnoea syndrome: randomized controlled study. BMJ, doi:1136/
bmj.38705.470590.55 (23 Dec. 2005).
2. Guimares KC, Drager LF, Genta PR, Marcondes BF, Lorenzo-
Filho G, Effects of oropharyngeal exercises on patients with
moderate obstructive sleep apnea syndrome. 179: 962–966, 2009.
3. McEvoy RD, Popovic RM, Saunders NA, White DP, Effects of sustain
ed and repetitive isotonic hypoxia on on ventilation and geniogloossal
and diaphragmatic EMGs. J APPL Physiol, 81:866–875, 1996.
4. Strohl KP, Hensley MJ, Hallet M, Saunders NA, Ingram RH,
Activation of upper airway muscles before onset of inspiration in
normal humans. J Appl Physiol. 49:638–642, 1980.
5. Mateika JH, Millrood DL, Kim J, Rodriguez HP, Samara GJ,
Response of human tongue protrudor and retractors to hypoxia
and hypercapnia. Am J Crit Care Med 160: 1976–1982, 1999.
6. Dictionary
7. Sherrington C, “The Integrative Action of the Nervous System”
Yale University Press, 1906.
8. Sabolsky JP, Butler JE, Fogel RB, Taylor JL, Trinder JA, White
DP, Gandevia SC, Tonic and phasic respiratory drives to human
genioglossus motoneurons during breathing. J Neurophysiol,
95:2213–2231, 2006.
9. Blom S, Afferent influences on tongue muscle activity. Acta
Physiol Scand. Vol 49 (Suppl 170) 1–97, 1960.
10. Miller AJ, Oral and pharyngeal reflexes in the mammalian
nervous system: Their diverse range in complexity and the pivotal
role of the tongue. Crit Rev Oral Biol Med, 13(5):409–425, 2002.
11. Weiffenbach JM, Discrete elicited motions of the newborn’s
tongue. In: “Oral sensation and Perception” ed. Bosma JF, US
Govt Printing Ofc , p232–243, 1972.
12. Isono S, Tanaka A, Nishino T, Effects of tongue electrical stimulation
on pharyngeal mechanics in anesthetized patients with
obstructive sleep apnea. Eur Respir J, 14:1258–1265, 1999.
13. Miki H, Hida W, Chonan T, Kikuchi Y, Takishima T, Effects of
submental electrical stimulation during sleep on upper airway
patency in patients with obstructive sleep apnea. Am Rev Respir
Dis, 140: 1285–1289, 1989.
14. Edmonds LC, Daniels BK, Stanson AW, Sheedy PF, Shepard JW,
The effects of transcutaneous electrical stimulation during wakefulness
and sleep in patients with obstructive sleep apnoea. 146:
1030–1036 , 1992.
15. Decker MJ, Haaga J, Arnold JL, Atzberger D, Strohl KP,
Functional electrical stimulation and respiration during
sleep. J Appl Physiol, 75:1053–1061, 1993.
16. Guilleminault C, Powell N, Bowman B, Stoohs R, the
effect of electrical stimulation on obstructive sleep apnoea syndrome.
Chest, 107:67–73, 1995.
17. Schwartz AR, Eisele DW, Hari A, Testerman R, Erickson
D, Smith PL, Electrical stimulation of the lingual musculature
in obstrudctive sleep apnoea. J Appl Physiol,
81:643–652, 1996.
18. Moses AJ, Bedoya JA, Learreta JA, Case study of the anatomic
changes effected by a mandibular advancement device
in a sleep apnea patient. Sleep Diagnosis and Therapy 5:1,
30–34, 2010.
19. Schmidt-Nowara WW, Mead TE, Hayes MB, Treatment of
snoring and obstructive sleep apnea with a dental orthosis.
Chest, 99:1378–1385, 1991.
20. IchiokaM, Tojo N, Yoshizawa M, et.al. A dental device
for the treatment of sleep apnea: a preliminary study.
Otolaryngol head Neck Surg, 104: 555–558, 1991.
21. Eveloff SE, Rosenberg CL, Carlisle CC, Millman RP,
Efficacy of a Herbst mandibular advancement device in
obstructive sleep apnea. Am J Resp Crit Care Med 149:
905–909, 1994.
22. Clark GT, Arand D Chung E, Tong D, Effect of anterior
mandibular positioning on obstructive sleep apnea. Am Rev Resp
Dis 147: 624–629, 1993.
23. Bonham PE, Currier GF, Orr WC, Othman J, Nanda RS,
The effect of a modified functional appliance on obstructive
sleep apnea. Am J Orthod Dentofacial Orthop, 94:
384–392, 1988.
24. Chan ASL, Cistulli PA, Oral appliance treatment of
obstructive sleep apnea: an update. Current Opinion in
Pulmon Med, 2009, 15: 591–595.

Dr. Moses' article published in "Sleep Diagnosis and Therapy", January/February 2010, Vol 5 No 1, pp 30-34

Case Study of the Anatomic Changes Effected by a Mandibular Advancement Device in a Sleep Apnea Patient
Allen J. Moses DDS, ABCFP, ABDSM
Assistant Professor, Rush University College of Medicine, Chicago IL, USA
Department of Sleep Disorders
Juan A. Bedoya, DDS
Universidad Diego Portales, Santiago, Chile
Department of Oral Surgery
Prof. Dr. Jorge A Learreta, ABCFP
Universidad Catolica de Salta, Buenos Aires, Argentina
Department of Orthodontics and Temporomandibular Pathologies

Case Study of the Anatomic Changes Effected by a Mandibular Advancement Device in a Sleep Apnea Patient
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.

Figure 1.  Anatomic rendering of a 36 week old child showing the overlap of uvula and epiglottis  
Figure 2.  Anatomic rendering of sagittal section of 36 week old infant showing uvula-epiglottis overlap shunting milk to the sides of the pharynx and the patent nasal airway.  This arrangement allows an infant to swallow and breathe at the same time.2

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 .

What remains problematic is how MADs work.  Studies report that MADs increase posterior airway space   , and at least one that demonstrates no change in posterior airway space .  Passive tongue advancement during general anesthesia has been reported to increase both retropalatal and retroglossal areas .  Studies of the effect of protrusion consistently report that increased protrusion produces greater reductions in restricted respiratory events.  Studies differ however on the impact of vertical opening related to device efficiency and the amount of jaw discomfort reported using the MAD.

The hydrostat theory of tongue function was proposed by Keir and Smith in 1985 .  It has been supported by scientific testing for almost a quarter of a century.  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.


Figure 3.  The left photo above shows a frontal view of the patient’s study models in centric occlusion.  The right photo above shows the MAD positioned on the study models.

Figure 4.  The left photo above shows a rear view of the study models in centric occlusion.  The right photo above shows a rear view of the MAD positioned on the study models.  Note the dramatic increase in volume of space for the tongue in the right photo.

Figure 5.  The left CT image is a midline sagittal view of the head without MAD.  The patient is instructed to keep lips together, teeth slightly apart in a resting position and tongue in the roof of the mouth.  This is a typical posture for a nose breather.  The marker measuring sagittal airway space (10.75 mm) was taken at the base of the second cervical vertebrae for accuracy and consistency of scientific measurement.  It is obvious that the airway is narrower above the marker but not based on a reproducible fixed landmark.  The right CT image is taken with the MAD in proper position in the mouth.  The patient is instructed to keep lips together, teeth where they fit ito the appliance and tongue in the roof of the mouth.  This image clearly shows a dramatic increase in the sagittal airway dimension (14.75 mm), approximating 40%.

Figure 6.  Both CT sectional views above are at the same level at the base of the second cervical vertebrae as those shown in Figure 5.  The left image of the patient without appliance has the same anteroposterior measurement of 10.75 mm (not marked) and a lateral measurement of 31.00 mm.  The image on the right above (again at the same level as Figure 5 – 14.75 mm) shows a lateral measurement of the airway of 39.75 mm.  Noteworthy is that the apparent sagittal effect of the MAD is accompanied by a lateral expansion of the airway approximating 25% at this level.

Figure 7.  Frontal CT scans measure the lateral dimensions of the airway without appliance (left) and with appliance in place in mouth (right).  The wider airway on the right with the appliance in place is obvious.  The markers appear to be at different levels on the right and on the left but that is because with the appliance in place the position of the mandible, head and airway has moved relative to the vertebrae.  The three measurements shown in each scan are at the same level in the airway.
18.75mm. to 29.75 mm.
21.00mm. to 38.25mm.
24.00mm. to 34.25mm.

Figure 8.  Left image above is a posterior view of a three dimensional volumetric reconstruction of the patient’s airway without MAD.  Right image is a posterior view of a three dimensional reconstruction of the patient’s airway with MAD properly positioned in the mouth.  The increase in size of the airway is substantial and obvious.


The effectiveness of MADs used as treatment for OSA have been thoroughly referenced in an updated (2006) American Academy of Sleep Medicine review paper .  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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