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Compendium
January 2018
Volume 39, Issue 1
Peer-Reviewed

Treatment of Obstructive Sleep Apnea: Current Strategies to Maximize Oral Appliance Therapy

B. Gail Demko, DMD

Obstructive sleep apnea (OSA) is a chronic disease that is progressive with time and can have a severe medical impact on a person. The medical field has now embraced the use of oral appliance therapy (OAT) for the treatment of patients who have OSA,1 and the majority of medical insurers provide coverage for this therapy. Recent research has focused on how OAT creates physiologic improvement, how to predict who is most likely to benefit from the use of an oral appliance (OA), the importance of combining various therapies to improve compliance and medical outcomes, and the amount of mandibular advancement needed to remain an effective therapy.

Modifications to Degree of Titration

OAs appear to work by anatomically increasing the size of the upper airway (UA). Advancing the mandible is required for effectiveness2 and predominantly increases the airway in a lateral direction behind the palate, and less so behind the tongue.

The US Food and Drug Administration (FDA) now has a list of more than 100 different OAs, all of which work on similar principles of mandibular advancement and they also increase the interincisal distance (simply called “vertical”). While published data on various appliances show total control of OSA in 34% to 55% of patients, there is ongoing research on how far the mandible must be moved forward. Older studies often determined that reduction in the number of breathing events improved the further forward the mandible was moved,3 however these studies had an initial advancement of 75% to 80% of the patient's overall range. Because the average patient has a 10-mm range of protrusive movement, authors believed that a protrusive range of less than 6 mm was a contraindication for OAT. Updated research, in which the initial setting of the OA is minimal, shows that many patients need mandibular advancement of only 2 mm to 5 mm for a drop in apnea-hypopnea index (AHI) of 60%.4 Older studies frequently used appliances that had a significant vertical opening (>10 mm), which may relate to the need to advance the mandible to 100% of protrusive range. Opening the interincisal distance to 10 mm was shown to negatively impact the improvement in UA size5 but not necessarily the number of breathing events.6 Due to high inter-individual variability in response to mandibular advancement, the severity of OSA may actually increase with continued mandibular advancement.7

In light of these findings, dentists are starting to assess the overall design of devices with an eye toward limiting vertical opening as well as initial mandibular advancement, while titrating the device based on the individual patient's dental anatomy and response to treatment.

Efforts to Predict Efficacy

Dentists and physicians are increasingly making observational and clinical efforts to determine predictors of patient treatment success before fabricating an OA. For example, use of anatomical correlates such as retrognathia, a long soft palate, or a steep mandibular plane angle has not been found to predict success or failure. Mechanized advancement of the mandible during overnight sleep recording (ie, polysomnography) has shown good correlation with treatment success, but it is not very accurate at determining which patients will not be successful with OAT or identifying the appropriate effective mandibular position.8

Increase in Combination Therapy

The most common medical approach to chronic disease, and one that has seen an increase in use, is combination therapy in patients who have a subtherapeutic response to monotherapy. Cancer is often treated with a combination of chemotherapy, radiation, and surgery; diabetic control may require insulin as well as oral hyperglycemic medications; hypertension may require multiple medications. It is becoming more apparent to sleep medicine practitioners that for many patients the overall control of OSA may require combination therapy.

Weight loss can lessen the severity of OSA, but it does not “cure” it.9 Positive airway pressure (PAP) can control OSA in more than 90% of patients, but adherence to therapy has remained consistently poor for decades.10 OA monotherapy is ineffective in patients with epiglottic collapse. These factors have led to the use of OAs in combination with other standard therapies to improve adherence and medical outcomes.

Patients who are adherent to PAP but unable to tolerate the high pressures necessary to fully correct their sleep-disordered breathing events can combine OAT with their PAP11; this allows for a significant decrease in therapeutic pressures. Patients with positional OSA often have epiglottic collapse, which is incompletely controlled with an OA. Providing positional therapy, which helps the patient avoid the supine position, in combination with OAT may be needed to control the OSA.12,13Alerting agents may be required in patients who remain clinically sleepy regardless of control of their OSA,14,15 and nasal steroids may be necessary for those with high nasal resistance.16

Providers who treat patients with OSA must be cognizant of the multiple options of therapy available, verify the level of effectiveness of any monotherapy, and be willing to guide the patient toward combination therapy as necessary. Because combination therapy requires effective communication and collaboration between dentists and medical providers, being part of a medical team is critical.

Long-term Patient Follow-up

For decades, OAT has been discussed in terms of a “lifetime” therapy. Data has shown that up to 50% of patients abandon therapy (both OAT and PAP) within the first year. This is predominantly because they do not feel the treatment is effective in addressing their symptoms of excessive daytime sleepiness or continued snoring,17,18 while others discontinue therapy because they find the OAs “bothersome to use,” which may underscore patients' lack of understanding as to how serious OSA can be. Attali noted that OAs became less effective with time, which may be related to the natural progression of OSA or wear and loosening of the OA.18

Of utmost concern is data from 2015 that showed patients who continued to use an OA for more than 10 years, while pleased with the continued control of symptoms, actually had exacerbation of their OSA when wearing their OA.19 Thus, it seems as if OAT requires ongoing patient follow-up to evaluate efficacy and determine if changes, such as device adjustments, combination therapy, or a different therapy, are needed.

All of these developments in the field of dental sleep medicine reinforce the need for dentists who provide OAT for treatment of OSA to remain aware of new and emerging data that will help improve patient adherence to therapy, understand that OA design changes may improve outcomes, and know that continued follow-up is needed for all patients who receive an OA.

References

1. Ramar K, Dort LC, Katz SG. Clinical practice guideline for the treatment of obstructive sleep apnea and snoring with oral appliance therapy: an update for 2015. J Clin Sleep Med. 2015;11(7):773-827.

2. Marklund M, Verbraecken J, Randerath W. Non-CPAP therapies in obstructive sleep apnoea: mandibular advancement device therapy. Eur Respir J. 2012;39(5):1241-1247.

3. Gindre L, Gagnadoux F, Meslier N, et al. Mandibular advancement for obstructive sleep apnea: dose effect on apnea, long-term use and tolerance. Respiration. 2008;76(4):386-392.

4. Anitua E, Durán-Cantolla J, Almeida GZ, Alkhraisat MH. Minimizing the mandibular advancement in an oral appliance for the treatment of obstructive sleep apnea. Sleep Med. 2017;34:226-231.

5. Piskin B, Karakoc O, Genc H, et al. Effects of varying mandibular protrusion and degrees of vertical opening on upper airway dimensions in apneic dentate subjects. J Orofac Orthop. 2015;76(1):51-65.

6. Vroegop AV, Vanderveken OM, Van de Heyning, PH, Braem MJ. Effects of vertical opening on pharyngeal dimensions in patients with obstructive sleep apnoea. Sleep Med. 2012;13(3):314-316.

7. Bartolucci ML, Bortolotti F, Raffaelli E, et al. The effectiveness of different mandibular advancement amounts in OSA patients: a systematic review and meta-regression analysis. Sleep Breath. 2016;20(3):911-919.

8. Sutherland K, Ngiam J, Cistulli PA. Performance of remotely controlled mandibular protrusion sleep studies for prediction of oral appliance treatment response. J Clin Sleep Med. 2017;13(3):411-417.

9. Olson EJ, Courcoulas AP. Obstructive sleep apnea, obesity, and bariatric surgery. In: Kryger MH, Roth T, Dement WC. Principles and Practice of Sleep Medicine. 5th ed. St. Louis, MO: Elsevier Saunders; 2011:chap 115.

10. Rotenberg BW, Murariu D, Pang KP. Trends in CPAP adherence over twenty years of data collection: a flattened curve. J Otolaryngol Head Neck Surg. 2016;45(1):43.

11. El-Solh AA, Moitheennazima B, Akinnusi ME, et al. Combined oral appliance and positive airway pressure therapy for obstructive sleep apnea: a pilot study. Sleep Breath. 2011;15(2):203-208.

12. Dieltjens M, Vroegop AV, Verbruggen AE. A promising concept of combination therapy for positional obstructive sleep apnea. Sleep Breath. 2015;19(2):637-644.

13. Marques M, Genta PR, Sands SA, et al. Effect of sleeping position on upper airway patency in obstructive sleep apnea is determined by the pharyngeal structure causing collapse. Sleep. 2017;40(3):1–8.

14. Roth T, Rippon GA, Arora S. Armodafinil improves wakefulness and long-term episodic memory in nCPAP-adherent patients with excessive sleepiness associated with obstructive sleep apnea. Sleep Breath. 2008;12(1):53-62.

15. Verbruggen AE, Dieltjens M, Wouters K, et al. Prevalence of residual excessive sleepiness during effective oral appliance therapy for sleep-disordered breathing. Sleep Med. 2014;15(2):269-272.

16. Zeng B, Ng AT, Qian J. Influence of nasal resistance on oral appliance treatment outcome in obstructive sleep apnea. Sleep. 2008;31(4):543-547.

17. Nishigawa K, Hayama R, Matsuka Y. Complications causing patients to discontinue using oral appliances for treatment of obstructive sleep apnea. J Prosthodont Res. 2017;61(2):133-138.

18. Attali V, Chaumereuil C, Arnulf I, et al. Predictors of long-term effectiveness to mandibular repositioning device treatment in obstructive sleep apnea patients after 1000 days. Sleep Med.2016;27-28:107-114.

19. Marklund M. Long-term efficacy of an oral appliance in early treated patients with obstructive sleep apnea. Sleep Breath. 2016;20(2):689-694.

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