Case Report, Issue 5.4

Cessation of Snoring Without Apnea-Hypopnea Improvement During Oral Appliance Therapy for Obstructive Sleep Apnea

Arisa Ebato, DDS1; Satoru Tsuiki, DDS, PhD2,3,4; Yuuya Kohzuka, DDS3; Tatsuya Fukuda, DDS2; Hiroshi Suzuki, DDS, PhD1; Yoichiro Takei, RPSGT2; Fernanda Almeida, DDS, MSc, PhD3; Yuichi Inoue, MD, PhD2

1Department of Oral Function and Rehabilitation, Nihon University School of Dentistry at Matsudo, Matsudo, Japan, 2Japan Somnology Center, Institute of Neuropsychiatry, Tokyo, Japan, 3Department of Oral Health Sciences, Faculty of Dentistry, The University of British Columbia, Vancouver, Canada, 4Division of Aging and Geriatric Dentistry, Faculty of Dentistry, Tohoku University, Sendai, Japan


We encountered the case of a 41-year-old male patient with mild obstructive sleep apnea (OSA) treated with a mandibular advancement oral appliance (OAm) that highlights the fact that cessation of snoring is not always associated with an improvement of the apnea-hypopnea index (AHI).  Follow-up polysomnography revealed that snoring improved from 14.8% to 0.4% of total sleep time, whereas AHI slightly increased from 8.5 to 11.6/h and the nadir percutaneous oxygen level fell from 93% to 87%.  This case emphasizes the following three points: (1) cessation of snoring does not always indicate a reduction in AHI during OAm therapy for OSA; (2) objective follow-up evaluation of the efficacy of OAm treatment using sleep testing is necessary to avoid suboptimal outcomes; and (3) a follow-up sleep evaluation provides dentists and physicians with proper information for discussing not only treatment success but also the modification and/or replanning of OAm treatment.


follow-up polysomnography; obstructive sleep apnea; oral appliance; snoring


Ebato A, Tsuiki S, Kohzuka Y, et al. Cessation of snoring without apnea-hypopnea improvement during oral appliance therapy for obstructive sleep apnea. J Dent Sleep Med. 2018;5(4):131-135.


Snoring is a typical chief complaint in patients with obstructive sleep apnea (OSA). The cessation of snoring after the prescription of a mandibular advancement oral appliance (OAm) can often be assumed to reflect a patent upper airway following mandibular advancement, which would simultaneously support the effectiveness of the OAm. However, we recently experienced a case of mild OSA in which snoring disappeared with the use of an OAm, with little change in the apnea-hypopnea index (AHI). This case highlights the necessity of objective follow-up to evaluate the efficacy of OAm treatment.1


A 41-year-old male patient visited the Yoyogi Sleep Disorder Center, Tokyo, Japan.  He complained of mild insomnia and shallow sleep, and his wife reported loud snoring with episodes of apnea. The patient did not complain of dozing off during work. Mild OSA was diagnosed in this patient based on a nocturnal polysomnographic study (AHI = 8.5/h), and the patient was referred to the Sleep Apnea Dental Clinic in the same center for treatment with an OAm2 (Table 1). A custom-made monobloc OAm was fabricated at 50% of the maximum mandibular protrusion (3 mm advancement). After 3 months of acclimatization to the OAm and treatment with additional advancement of the mandible (1.5 mm) to stop his snoring, the patient used the OAm 6 to 7 nights a week. Consequently, the final amount of mandibular advancement was 4.5 mm.  Although the patient’s body weight increased by 2.6 kg, his wife no longer reported that he was snoring. When we proposed that the patient undergo follow-up sleep testing with the OAm in place, he was initially opposed; he thought that he had not made a remarkable subjective improvement in the quality of his sleep.

Table 1

Effects of an oral appliance on respiratory and sleep variables.
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A follow-up polysomnographic evaluation revealed that OAm treatment was effective with respect to snoring; the patient’s snoring had indeed improved from 67.4 to 1.6 minutes (from 14.8% to 0.4% of the total sleep time) (Figure 1). Nevertheless, there was no significant reduction in apneic and hypopneic episodes. The apnea index changed from 0.3 to 0.7/h and the hypopnea index slightly increased from 8.2 to 10.6/h. Consequently, the AHI increased from 8.5 to 11.4/h, whereas the nadir percutaneous oxygen (SpO2) fell from 93% to 87%. There was no regular intake of hypnotics nor alcohol throughout the treatment period or during the polysomnographic studies.

Figure 1

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The current case is probably typical of cases that are often encountered by sleep dentists and physicians. Users of an OAm sometimes do not consent to follow-up sleep testing if, for example, the cessation of snoring is witnessed by a bed partner and/or the resolution of subjective OSA symptoms is confirmed. However, the recent clinical practice guidelines from the American Academy of Sleep Medicine suggest that “sleep physicians conduct follow-up sleep testing to improve or confirm the treatment efficacy, rather than conduct follow-up without sleep testing, for patients” fitted with an OAm.1 Physicians should also consider follow-up testing for OAm users “who develop recurrent symptoms, show substantial weight changes, or receive diagnoses of comorbidities relevant to OSA”.1 Although barriers to polysomnographic sleep studies, including cost, waiting time, accessibility to the sleep clinic, and disease severity, have always been argued, the follow-up sleep study in this patient played a role in the avoidance of suboptimal treatment by further adjustment of OAm while encouraging weight control by explaining for an interaction between consumption of nighttime snack and likely increase in body weight.3

The OAm predominantly enlarges the velopharynx, which is both where snoring originates and the primary site of upper airway occlusion.4,5 However, it is clinically crucial to speculate why apnea and hypopnea remained despite the cessation of snoring. First, the favorable effects on the velopharynx due to mandibular advancement were maintained with OAm because the ventral displacement of the tongue associated with advancement of the mandible could stiffen the velopharynx through the palatoglossal arch6 more than the oropharynx because snoring was well controlled throughout the follow-up sleep study. In addition, the sleep-related atonia of the genioglossus muscle that maintains the tongue in position may offset the effect of mandibular protrusion on the oropharynx.7 Second, fat deposits in the tongue per se (a heavier tongue weight), despite representing only a slight change, may be a factor in increasing the vulnerability of the oropharyngeal space, because body weight was the only parameter that changed during the treatment period (2.6 kg). These speculations can be more easily tested without laborious imaging and/or endoscopic approaches by further refinements of a method for determining the site of upper-airway occlusion by focusing solely on the shape of inspiratory flow limitations.8Finally, the reduction in stage N3 sleep along with an increase in stage N2 sleep as shown in Table 1 would result in the absence of a remarkable subjective improvement in the quality of patient’s sleep, although it should be investigated in additional studies.


1. Ramar K, Dort LC, Katz SG, et al. 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(1):773-827.

2. Iber C, Ancoli-Israel S, Chesson AL, Jr, Quan SF for the American Academy of Sleep Medicine. The AASM Manual for the Scoring of Sleep and Associated Events: Rules, Terminology and Technical Specifications. 1st ed. Westchester, IL: American Academy of Sleep Medicine; 2007.

3. Liu XY, Zheng CL, Xu C, et al. Nighttime snacking is associated with risk of obesity and hyperglycemia in adults: a cross-sectional survey from Chinese adult teachers. J Biomed Res. 2017 Jun 20. [Epub ahead of print]

4. Kato J, Isono S, Tanaka A, et al. Dose-dependent effects of mandibular advancement on pharyngeal mechanics and nocturnal oxygenation in patients with sleep-disordered breathing. Chest. 2000;117(4):1065-1072.

5. Tsuiki S, Almeida FR, Bhalla PS, A Lowe AA, Fleetham JA. Supine-dependent changes in upper airway size in awake obstructive sleep apnea patients. Sleep Breath. 2003;7(1):43-50.

6. Isono S, Tanaka A, Tagaito Y, Sho Y, Nishino T. Pharyngeal patency in response to advancement of the mandible in obese anesthetized persons. Anesthesiology. 1997;87(5): 1055-1062.

7. Almeida FR, Tsuiki S, Hattori Y, Takei Y, Inoue Y, Lowe AA. Dose-dependent effects of mandibular protrusion on genioglossus activity in sleep apnoea. Eur Respir J. 2011;37(1):209-212.

8. Genta PR, Sands SA, Butler JP, et al. Airflow shape is associated with the pharyngeal structure causing OSA. Chest. 2017;152(3):537-546.


Submitted for publication February 26, 2018
Submitted in final revised form April 17, 2018
Accepted for publication May 22, 2018
Address correspondence to: Satoru Tsuiki, DDS, PhD, Division of Dental Sleep Medicine, Japan Somnology Center, Institute of Neuropsychiatry, 5-10-10, Yoyogi, Shibuya-ku, Tokyo, Japan 151-0053, Tel: +81-3-6804-8995, Fax: +81-3-6804-8996, Email:


This work was performed at the Institute of Neuropsychiatry, Tokyo, Japan.  All authors have seen and approved the final version of this manuscript.  This report was supported in part by a Grant-in-Aid for Scientific Research (15H05301 and 17K11793) from the Japanese Society for the Promotion of Science and was not an industry supported report. Written informed consent was obtained from the patient regarding the anonymous use of the patient’s data for presentation and/or publication.  The authors have indicated no conflicts of interest.