Within two or three miles of most dental offices in America there must be at least a thousand people who snore loud enough to reduce the quality of life of someone near and dear to them.  It is not known what this exact number is, but consider the statistics gathered by questioning 23 consecutive patients at a family practice clinic in Toronto.¹ Eighty-six percent of the women said their husband snored and 15% were troubled by it.  Similar surveys taken throughout the world indicate these figures are not aberrations.²  A household without a snorer is in the minority.
      Why is valuable space being taken in a dental journal to discuss  a common domestic interpersonal problem?  It is because dentists, especially  those  who have had experience with functional orthopedic appliances, can now do something to relieve the wide spread trauma caused by this noxious nocturnal noise.  Medicine has no simple cure for simple snoring, but dentistry now has.  The potential demand is enormous. 
      In 1983 it was discovered that a modified functional orthopedic appliance can not only suppress the auditory assaults of the snorers, but can prevent life threatening obstructive sleep apnea (OSA).³  This discovery has opened a vast new field for dentistry.  Dr. Alan A. Lowe, professor and head of the department of clinical dentistry at the University of British Columbia stated that these devices will occupy more dental office time in the 1990s than TMD splints did in the 1980s.⁴
      What exactly is snoring and OSA and how can a dental device prevent them?  Everyone is familiar with how snoring's cacophony can replace domestic harmony, but few are aware of how this nocturnal  nuisance can detract from the perpetrator's awake performance.  Understanding the mechanism of this sleep breathing disorder will make clear the cause of the noise,  its after effect on the snorer, its relation to OSA, and what can be done to prevent it.
      Snoring occurs as a result of a constriction in the airway.  According to the Bernoulli effect, the velocity of a fluid passing through a tube is increased by decreasing the size of the lumen--- as occurs when turning down the nozzle of a garden hose.  This accelerated air passing through the airway causes the tissues of the pharynx, mainly the soft palate and uvula, to vibrate like the reed of a bassoon.

      A number of factors can cause the narrowing of the airway, such as: nasal constriction or congestion, enlarged tonsils and adenoids, micrognathia or retrognathia, macroglossia, and adipose tissue in the pharyngeal area.  These factors all predispose one to snore, but the main precipitating factor is a super relaxed tongue.  It is normal for the tonicity of all muscles in the pharyngeal area to decrease during sleep,  however, this tendency is greater in snorers.  Since the posterior of the tongue is the anterior wall of the airway (see Figure 1), its rearward movement obviously narrows this vital lumen. Therefore, when the diaphragm contracts, creating a vacuum, in an attempt to suck in air through the nose or mouth, it also sucks back the flaccid tongue.  The resultant narrowed airway accelerates the airflow which, in turn, causes the audible vibrations of the soft palate and uvula.
      When the tongue is sucked back into complete apposition with the posterior wall of the pharynx, as shown in Figure 2, the oral and nasal air cannot reach the lungs.  This is obstructive sleep apnea.  The term "apnea" literally means "without breath".  Once the tongue makes a seal with the posterior pharyngeal wall, the diaphragm intensifies its efforts to suck in air, however, it only succeeds in making the seal tighter.  This is analogous to sucking on a straw after contacting a lump of ice cream--- the greater the suction, the flatter the straw.
      The obstruction in the pharynx will not release until the blood carbon dioxide levels rise high enough to awaken the patient.  This usually occurs with a loud snort, and within seconds the patient is asleep again.  This can repeat hundreds of times per night with the patient completely unaware of its occurrence the following morning.  However, the main daytime symptoms of OSA are those of sleep deprivation, namely sleepiness.
      The astute observer will notice morphological differences between Figure 1, depicting a non-snorer, and Figure 2, an OSA patient.  The most important of these is the vertical level of the hyoid bone which is significant in the etiology and treatment of snoring and OSA.⁵  The discussion of these variations is beyond the scope of this introductory article, but will be dealt with in subsequent articles. 
      The first patient to wear a modified functional orthopedic appliance for the relief of snoring and/or OSA was a 45 year old man of Japanese decent.³  He had an apnea index of 79, i.e., an average of 79 apneas per hour during the entire night.  His breathing would stop for 10 to 60 seconds on the average of every 45 seconds.  He got practically no sleep, and during the day he was known to fall asleep while talking to a client sitting across the desk from him.  His physician advised him to have a tracheotomy with a valve which he could close during the day and open at bedtime.  When he refused, the physician suggested that an oral surgeon evaluate him for mandibular advancement.  The surgeon rejected the option of surgery when he found that the patient had a Class I occlusion with an ANB of only 3 degrees.
      During a discussion with the oral surgeon, details of this case came to the attention of this author who then suggested constructing a modified functional orthodontic appliance which could maintain his mandible in a protruded position only while sleeping.  the patient readily consented to trying this device.  The main modifications of the appliance were complete occlusal coverage to prevent movement of the teeth in any direction and clasps on upper and lower dentitions to preclude any functional movement of the mandible that might create an orthodontic effect.^6,7  The appliance as modified was named Nocturnal Airway Patency Appliance (NAPA) (Figures 3 and 4)
      It was originally believed that the only active component of the NAPA was the mandibular advancement and that the only purpose of the modifications was to prevent untoward side effects.  That proved to be simplistic.  It is now believed the modifications may contribute as much as the mandibular advancement to the Napa's ability to prevent snoring and apnea.⁸
      How the NAPA achieves its results is the subject of a future article, but briefly, the occlusal coverage provides a bite plane effect, and the clasps stabilize the mandible.  The bite plane has been shown in animal experiments to increase the tonicity of the genioglossus muscle⁹ which strengthens the tongue's resistance to the negative airway pressure.  Stabilization of the mandible prevents the retraction of the tongue via the anti-tongue biting reflex.¹⁰  Also, a stable mandible provides a firm attachment for the geniohyoid muscle to protect the hyoid bone which, in turn, enables the hyoglossus muscle to advance the posterior of the tongue.⁵
      The first NAPA was delivered on September 21, 1983 to Rodney Takeuhi.³  He has worn a NAPA practically every night since then.  The results were dramatic.  Subsequently, his snoring stopped immediately, he was no longer sleepy during the day, and his performance at work improved.  He and his family consider him a new man.  Objectively, an overnight  sleep study with polysomnography indicated his sleep apnea index dropped from 79 to 5.3 and his blood oxygen saturation markedly improved.
      Takeuchi's case was very closely monitored medically and dentally in the early years to determine if there might be any untoward side effects.  Dentally we took base line records including study models, intraoral photographs, and panoramic, transcranial and cephalometric radiographs.  New patients were slowly accepted until we were certain of the safety and efficacy of the NAPA.  After we had enough cases, we applied to the FDA for permission to market the NAPA for the treatment of snoring and OSA.  That permission was granted on September 19, 1990.
      The reason the accumulation of records took so long is that the overnight sleep test with polysomnography which is required for proof of efficacy in the treatment of OSA costs about $1,200, and many insurance companies will not pay for a second test.  Many patients who were diagnosed with sleep tests as having OSA refused to go back for a second test when they found their insurance would not cover it or would only pay for part of it especially when they felt for certain their symptoms had disappeared.  Most would comment that they could see no reason to pay to find out what they already knew.
      I have personally placed over 400 NAPAs.  The vast majority of them were for snoring only, but I have had 20 cases that show an average reduction of over 80% in RDI (see Table 1).  RDI stands for respiratory distress index and is the average number of apneas plus hypopneas per hour.  A Hypopnea is a decrease in airflow that results in an arousal and its effects are considered to be as detrimental as an apnea.
      The two most common manifestations of OSA are loud irregular snoring and daytime sleepiness.  Other signs and symptoms not uncommonly associated with this sleeping/breathing disorder are excessive motion during sleep, morning headache, irritability, cognitive impairment, nocturia, and impotence.  Long term consequences often associated with OSA are hypertension and increase incidence of myocardial infraction.  Recent studies indicate about a 12% increase in mortality rates among OSA patients.¹¹
      Treatment of snoring and OSA has provided the most gratifying experience on my 37 years in dentistry.  The objective data presented in Table 1 could be supplemented with many pages of heartwarming anecdotes.  In addition to the OSA results, the outcome of the treatment of simple snoring has been equally rewarding.  Snoring has long been the butt of many jokes, but it has been the source of tragedy, not humor, to those whose families have been broken because of it.  Equally gratifying has been the response of middle age men who assumed their vim and vigor was solely due to advancing age and not related to their snoring.
      How does a dentist get started in this therapy?  Since 1983, a large number of dental devices that claim to prevent snoring have been marketed.  Some are excellent, others are completely worthless.  In selecting a device for the prevention of snoring the first consideration should be efficacy.  There are some devices that are being advertised as 95% successful.  Find out how (or, if) they can make that claim.  Demand to see polysomnographic evidence of efficacy.  If you are told the device is only intended to prevent snoring, therefore, polysomnographic evidence is irelevalent, don't use it.  As explained above, snoring is caused by a constriction in the airway.  That same constriction can also cause OSA.  For instance to stop the snoring by stabilizing the soft tissue palate with out maintaining an open airway is like turning off an alarm while the fire burns.  This can be dangerous, even fatal.  The device that has the best record for preventing OSA will be the most effective and safest device for preventing snoring.
In addition to the above, be sure the device you select has: 1) Food and Drug Administration approval for marketing; 2) full occlusal coverage to prevent occlusal changes; and 3) long-term observation.  There are anti-snore devices that require that you only heat and adapt, but they are not the most effective, you should not be using them.
If you are a dentist with experience in functional orthodontics, you will have no difficulty with the technical aspects of this treatment.  However, anyone involved in this therapy should understand the scientific rationale for the use of dental devices.  It is most important to differentiate between simple snoring and OSA, be able to communicate properly with the patient's physician, and inform the patient accurately.
I strongly recommend that any dentist who elects to deliver this therapy join the Sleep Disorders Dental Society.  Membership information may be obtained by writing to SDDS, 11676 Perry Highway, Building 1, Wexford, PA 15090

Table 1

*All tests were done in Honolulu at the sleep disorders centers of: Queen's Hospital, Straub Clinic, and Kuakini Medical Center.
1. Number of apneas + hypopneas per hour of sleep
2. After uvulopalatopharygoplasty
3. Half night

References

1. Lipman, D.S. "Stop Your Husband From Snoring", Emmans, Pa Rodale Press, 1990:13-14
2. Lugraresi, E, Cirignotta, F., Montagna, P. "Snoring: Pathogenic, Clinical and Therapeutic Aspects" Kryger MS, Roth T., Dement W.C., eds. Principles and Practice of Sleep medicine, Philadelphia W.B. Saunders, 1989:495
3. Soll, B.A. and George, P.T. "Treatment of Obstructive Sleep Apnea with a Nocturnal Airway Patency Appliance" (Letter), New England Journal of Medicine 313:6. 1985
4. Lowe, A.A. "Tongue Muscle Activity and Obstructive Sleep Apnea"  Pacific Coast Society of Orthodontics Bulletin, 61:4:38-41,1989
5. George, P.T., Pearce, J.W., Kapunani, L.E., Crowell, D.H., "Stabilization of the mandible in the Prevention of Snoring and Obstructive Sleep Apnea", Sleep Research, 21:202, 1992
6. George, P.T., "A Modified Functional Appliance for Treatment of Obstructive Sleep Apnea", Journal of Clinical Orthodontics 21:171-175, 1987
7. George, P.T. , "Still More on Obstructive Sleep Apnea: A Dentist's Perspective" (Letter) Arch Otolaryngol 113:12. 1987
8. George, P.T., "Still more on Obstructive Sleep Apnea" (Letter), Am I Orthod. Dentofac. Orthop. 96:A29, 1989
9. Lowe, A.A.  "Effects of Posterior Bite Block Therapy on Genioglossus Muscle Activity", Pacific Coast Society of Orthodontics Bulletin 60:1:41, 1988
10. Sauerland, E.K. and Mizuno, J. "Protective Mechanism for the Tounge: Suppression of Genioglossus Activity Induced by Stimulation of Trigeminal Proprioceptive Afferents" Experienta 26:1226-7, 1970
11. Westbrook, P.R. "Apnea " Carskadon, M.A. ed Encyclopedia of Sleep and Dreaming, Macmillan, New York: 1993:49
    Reprint July/August 1993 The Functional Orthodontist
    
    This article is reproduced with the kind permission of the American Association for Functional Orthodontics  original copies may be obtained  by calling:
     (800) 441-3850 

        Request a copy of this document.

Return To Top