Jaw protrusion device – open the airway before using C-PAP

C-pap (continuous positive airway pressure – think a “reverse” vacuum cleaner blowing air down your mouth) is a treatment device which many people credit with saving their lives BUT   many, many more patients hate these devices.

Why the dispairity?

In my clincal experience, those that hate the C-PAP do so bcause they aren’t working.

Makes sense?

But WHY doesn’t the C-PAP work on those people?

Usually the problem is that the machine is pushin air into the mouth and up against a “cork” in the throat i.e.  the jaw and tongue  are collapsed back (especially if you sleep on your back and snore) against the airway and causing an obstruction.   Until you move that blockage and open up the airway, the C-PAP just makes things worse.

That is what I recommend a jaw protrusion device to open the airway before prescribing a C-PAP machine.

Effect of Mandibular and Tongue Protrusion on Upper Airway Size During Wakefulness

Kathleen A. Ferguson, Leslie L. Love, and C. Francis Ryan
Department of Medicine, University of British Columbia, Vancouver, British Columbia, Canada
Published in American Journal of Respiratory and Critical Care Medicine Vol. 155, pp 1748-1754, 1997

Summary

The authors describe oral (dental) appliances as “an interesting new approach to the treatment of OSA.” They refer to at least 15 different devices now available, most of which are designed to hold either the mandible (lower jaw) or the tongue in a protruded (pulled forward) position. This may benefit OSA by increasing the size of the upper airway. Alternatively, these measures might activate the muscles that hold the airway open, or decrease the collapsibility of the upper airway. The authors hoped that systematic study of the effects of two mechanisms (mandibular vs. tongue protrusion) on upper airway size and shape would lead to better understanding of how they might work. They thought that mandibular and tongue protrusion might both increase upper airway size, but in different parts of the upper airway. They also thought that obesity or severity of OSA might influence these effects. They used videoendoscopy to measure airway size at the end of expiration.

They studied 10 patients with OSA and 9 normal controls. They excluded subjects with gross abnormalities of upper airway anatomy. All subjects had standard overnight laboratory polysomnography. Afterwards, while lying on their backs but awake, subjects had videoendoscopy. At the same time, esophageal pressures were measured. Subjects were instructed to voluntarily position their lower jaw and their tongue in five ways: (1) full retrusion (pulled back as much as possible); (2) resting position, with the upper and lower molar teeth lightly in contact; (3) with the upper and lower front teeth aligned (mandibular protrusion) or the tongue tip resting between the front teeth (tongue protrusion); (4) half the maximal protrusion of the lower jaw or tongue; (5) maximal protrusion of the lower jaw or tongue.

Patients and controls had similar weights, neck circumferences, and Body Mass Indices (BMI: 29 for patients, 25 for controls, SD=1.5-1.6). Patients had Apnea Indices (AI) of 13.5 (SD=4) and Apnea/Hypopnea Indices (AHI) of 34 (SD=5.2). Comparative figures for controls were 0.1 (SD=0.1) and 2.7 (SD=0.7). Because the patients and controls showed no differences in effects of mandibular or tongue protrusion on upper airway cross-sectional area (CSA) or on airway shape (and presumably also because of the small numbers of subjects) the data for patients and controls were pooled for most analyses.

Over all three sections of the pharynx where CSA was measured (in descending anatomical order: velopharynx, oropharynx, and hypopharynx), the average effects of mandibular and tongue protrusion on CSA were a 33% increase with half-maximal protrusion and a 90% increase with maximal protrusion. Correspondingly, retrusion of the mandible and tongue decreased CSA, but this reached significance only in the oropharynx (the middle level, between the soft palate and the epiglottis).

Maximal mandibular protrusion doubled the CSA (102% SD=72%) in the hypopharynx (the lowest level, from the larynx to the esophagus) and increased it significantly by 50% (SD=29%) in the oropharynx, but nonsignificantly increased it by 44% (SD=65%) in the velopharynx (the highest level, at the soft palate and nasopharyngeal wall). (Note the extreme variation in the last figure; some subjects actually decreased their CSA in this area with maximal mandibular protrusion.) Mandibular protrusion increased CSA in the hypopharynx significantly more than in the oropharynx or velopharynx.

Maximal tongue protrusion showed a different pattern of increase in CSA: greatest in the velopharynx (160% SD=153%), next greatest in the hypopharynx (126% SD=115%), and least in the oropharynx (79% SD=44%), again highly variable (at least at the first two levels) though significant at all levels. There were no statistically significant differences between the effects of tongue protrusion at different levels, probably due to the high variability. Maximal tongue protrusion had significantly greater effect on the CSA at the levels of the oropharynx and velopharynx than did maximal mandibular protrusion.

In obese subjects, both mandibular and tongue protrusion made for greater increases in CSA at the level of the oropharynx than in normal-weight subjects. Neck circumference showed no such relationship.

The shape of the airway, measured by the ratio of its anteroposterior or AP (front-to-back) diameter to its lateral or L (side-to-side) diameter, was expressed as AP/L. This was similar for patients and controls, obese and non-obese subjects. Mandibular and tongue protrusion both increased this measure, representing a change from a laterally oriented ellipse (i.e., side-to-side measure greater than front-to-back) to a more circular contour (i.e., side-to-side measure more similar to front-to-back). Mandibular protrusion produced this effect to the maximum degree in the oropharynx, tongue protrusion in the oropharynx and velopharynx. These changes were associated with a ventral movement (towards the front side of the body) of the anterior (front) airway structures. Thinking of the subject lying on his back, this means that tongue and lower jaw protrusion both expanded the airway by moving upwards those parts of the airway which lie on top in this body position.

Generally, the maneuver of lower jaw protrusion seemed to have its greatest effects on the lower part of the airway, while the maneuver of tongue protrusion had its greatest effects on the upper parts of the airway.

The authors acknowledged that studying these effects in the waking state provides “only an approximation of their effects during sleep” but the waking state makes them much easier to study and possibly apply the findings to regional effects of oral appliances on the upper airway in sleep. They suggest that oral appliances that move the lower jaw or tongue forward may help OSA by increasing the cross-sectional area of the airway. They noted that substantial beneficial effects on airway size seem to require maximal mandibular protrusion, consistent with the observation of others that any appliance resulting in less than 75% of maximal mandibular protrusion was associated with treatment failure. Tongue retaining devices probably don’t exceed 50% of maximal protrusion, but data here indicates significant increases in airway size with this degree of protrusion, at least in the hypopharynx and oropharynx. For clinical purposes, the appropriate comparison is not one of maximal mandibular protrusion with maximal tongue protrusion, but what is achievable with current devices: maximal mandibular protrusion vs. 50% of maximum tongue protrusion. In this realm, both tongue and mandibular protrusion exerted their main effects at the lowest level, the hypopharynx, with some effects also at the next highest level, the oropharynx. Obese subjects had their greatest response to both maneuvers at this level and seemed to have especially small airways at this level due to a large tongue base, often with large tongue tonsils.

At the highest level, the velopharynx, mandibular protrusion had little effect but tongue protrusion did increase area here.

With regard to airway shape, both mandibular and tongue protrusion “circularized” the original elliptical shape. Other studies have shown that OSA patients typically have this elliptical shape of airway, versus normals where the shape is also elliptical but with the longest diameter from front to back rather than side-to-side as in OSA.

In this study, no differences were seen in the effects of mandibular or tongue protrusion on OSA patients vs. normal controls, perhaps because the groups were matched on various measures of body weight. When subjects were divided according to BMI, differences did emerge, especially in the oropharynx.

The authors concluded by suggesting that oral appliances may be useful for patients with OSA whose main site of obstruction is in the oropharynx or hypopharynx. Both types of oral appliances–those the protrude the lower jaw and those that protrude the tongue–probably act to increase the size of the airway mainly in these areas. Near-maximal protrusion of the lower jaw is necessary for therapeutic effect, whereas lesser degrees of tongue protrusion may be effective.

The design of this study has many drawbacks, most prominent among them being the small numbers of subjects studied and the testing of these maneuvers only in a waking state which is not really that of clinical interest. However, as the authors suggest, I think it does help us to understand how dental/oral devices might work to alleviate symptoms of OSA, and even some situations where they might be particularly effective.

Comments

Many of the audience would probably find the anatomy and anatomical changes described in this abstract much easier to grasp with a good 3-dimensional model of the upper airway and surrounding structures. Abstracts of this sort, however, generally include only a two-dimensional graphic outline of a “slice” of the head, and in this particular case not even that; moreover, I lack the skill to either accurately depict or portray such a 3-dimensional model. The best I can do is try to simplify a word picture of the situation:

Lying on their backs, these subjects had airways which were flattened from side-to-side, one might imagine as a result of overlying tissues pressing down, since these waking subjects didn’t have the usual sleep-related muscular relaxation. Consistent with this being a normal phenomenon, there was no difference in this respect between OSA patients and normal controls. When the lower jaw is pushed forward or the tongue is pushed out, they pull the structures on the ventral (in this position, the upper) side of the airway outwards, enlarging the airway and making it more circular. These changes appear mostly in the middle and lower part of the airway, as one might expect.

So what is the relevance of all this to patients with OSA? Dental appliances for OSA are a relatively recent development and less often used than CPAP and probably even than surgery. Using one’s dentist as the primary treater for one’s sleep apnea has some disadvantages. There is more “distance” from the sleep laboratory with its many measures essential for diagnosing a variety of sleep disorders which may coexist, as well as for following up the results of any treatment to make sure it is working adequately. Furthermore, the dentist is ill equipped to diagnose and treat such commonly coexisting conditions as periodic leg movements of sleep or narcolepsy, not to mention the many medical and medication-related factors which may affect sleep. The focus of the dentist is rather narrowly anatomical and his expertise is probably limited to factors which obstruct the upper airway, when in fact sleep disorders are often multifactorial in origin even if anatomy is the primary predisposing factor to obstructive apneas and hypopneas.

On the other hand, consider some countervailing factors. Few people ever see a sleep medicine specialist, but almost everyone sees a dentist and a primary care physician. Of the two, the dentist may be easily supposed more sensitive to the possibility of sleep apnea and the existence of anatomical factors which predispose to it.

To give a little personal example, when I was a child and young adolescent, I saw the dentist frequently because of many problems with my teeth. The dentist noticed that I had a receding jaw and thought it might have something to do with my dental problems. He even took some photographs of my facial features! This was about 40 years ago, before any treatments (except tracheostomy) were available for sleep apnea, and when the disease was considered rare and unfamiliar. But nowadays that same dentist would probably be quite ready to think of sleep apnea as a possible complication of my facial bone construction. He would probably ask the right questions to make the diagnosis, quite early in life and early in the course of the disease, before an accumulation of complications such as obesity and chronic obstructive pulmonary disease and attentional and memory deficits had arisen. In fact, he might be in an excellent position to help prevent all these things from happening but initiating early intervention.

Whether the earliest intervention should be a dental appliance (as it might likely be, if the dentist were the first to detect the OSA) is, to my mind, very questionable. I still consider CPAP as the main treatment for all but the mildest cases of OSA or those with a predominant positional component. However, many people still turn to surgery quite early in the course of their treatment, presumably because they don’t want to accept the prospect of life-long treatment with CPAP with the implication of a life-long chronic illness, and hope instead for a “cure” that will leave them indistinguishable from people who never had OSA. Hopefully, they do not turn to UPPP but the odds are this is what they will first get; then when this doesn’t work, they will go on to more complex procedures. These procedures are aimed at opening the airway further, much as the dental devices are intended to do; even, in a sense, CPAP is directed at the same goal. However, these surgical procedures are (a) very expensive, much more so than CPAP; (b) quite painful to recover from; (c) often ineffective, especially in reference to the commonest procedure, UPPP alone; (d) capable of worsening OSA and impeding later response to CPAP; and (e) irreversible. With all these considerations against surgery, it makes good sense to try achieving the same goal with a less expensive, painless, reversible treatment such as a dental appliance. Furthermore, in cases where a surgical intervention has left (or even created) another area of obstruction in the airway, the dental appliances might be helpful in remedying this situation without needing to resort to further surgery. Many people, one would think, could accept the idea of wearing a dental appliance at night who would shrink from the image of wearing a mask attached to a machine something like a respirator, with all its connotations of chronic and even terminal disease.

For more information on Sleep Apnea, please see our Sleep Apnea Section.

Share This Post

C-pap (continuous positive airway pressure – think a “reverse” vacuum cleaner blowing air down your mouth) is a treatment device which many people credit with saving their lives BUT   many, many more patients hate these devices. Why the dispairity? In my clincal experience, those that hate the C-PAP do so bcause they aren’t working. Makes…
&source=WeeksMD">