Sleep bruxism and associated physiological events in children with obstructive sleep apnea: a polysomnographic study

Abstract

Study Objectives:

The aim of this study was to evaluate the physiological events associated with sleep bruxism (Sleep Bruxism [SB]; presence of mandibular movement activity) and the control window (4 minutes prior to SB event, where no mandibular movement activity was detected) in a polysomnography study in children with mild sleep apnea.

Methods:

Polysomnography data from children aged 4 to 9 years old diagnosed with mild sleep apnea were analyzed by 2 trained examiners. The mandibular movement activity (bruxism event; SB) was classified into phasic and tonic. The control window was selected 4 minutes prior to the SB event. All physiological events were recorded in both bruxism and control windows, including sleep phase (N1, N2, N3, and rapid eye movement), arousal, leg movements, tachycardia, bradycardia, oxygen desaturation, and number of obstructive and central sleep apnea events. The moment in which those phenomena occurred when associated with SB was also analyzed (before/after). Data were analyzed using 95% confidence intervals (α = 5%).

Results:

A total of 661 mandibular movements were analyzed and classified as tonic (n = 372) or phasic (n = 289). The mean apnea-hypopnea index was 1.99 (SD = 1.27) events/h. The frequency of leg movements, microarousal, and tachycardia was increased in SB events when compared with the control window (P < .05). There was an increase in bradycardia frequency in the control window when compared with SB (in both tonic and phasic events). The frequency of obstructive and central apnea during SB was lower when compared with the other physiological phenomena.

Conclusions:

There is a difference in the physiological parameters evaluated in children with mild sleep apnea when comparing the 2 windows (SB and control). Sleep bruxism is associated with other physiological phenomena, such as leg movements, tachycardia, and microarousal. The use of a control window (where no mandibular activity was detected) was representative since it did not show activation of the sympathetic nervous system.

Citation:

Bonacina CF, Soster LMSFA, Bueno C, et al. Sleep bruxism and associated physiological events in children with obstructive sleep apnea: a polysomnographic study. J Clin Sleep Med. 2024;20(4):565–573.

BRIEF SUMMARY

Current Knowledge/Study Rationale: Studies on the physiological phenomena that occur during sleep and their temporal relationship with sleep bruxism are nonexistent in children, especially in those with obstructive sleep apnea.

Study Impact: This knowledge is fundamental for understanding this condition, which is common in this age group since investigating parameters of sleep architecture revealed that episodes of sleep bruxism are related to phases of arousals, activation of the sympathetic nervous system, and changes in heart rate, and that physiological occurrences are synchronized with changes in cortical activity, which are typical of sleep bruxism.

INTRODUCTION

Sleep is an essential brain activity for an organism’s biological and homeostatic regulation and reflects an individual’s physiological and behavioral characteristics. The observation of different phenomena that occur during sleep, such as arousal events, leg movements, tachycardia, bradycardia, desaturation, obstructive apnea, central apnea, and mandibular movement activity, can be an important tool for the diagnosis of adverse conditions.

Sleep activity is divided into 2 distinct and alternating phases, each with a unique neurological physiology and distinct electrophysiological and behavioral parameters. One of the phases is characterized by the absence of eye movements (non–rapid eye movement [non-REM]), subdivided into stages N1, N2, and N3, and the other by rapid eye movements (REM). During the sleep period, it is common to observe arousal events, which can be defined as the intrusion of wakefulness, being associated with superficialization and consequent fragmentation of sleep.¹

Some of the common respiratory dysfunctions that occur during sleep and that can impact children’s quality of life include obstructive sleep-disordered breathing and central apnea. The first is considered an airway dysfunction syndrome that occurs during sleep characterized by snoring and/or respiratory efforts due to difficulty in the air passage. Sleep-disordered breathing comprises several clinical entities with increasing degrees of intermittent upper airway obstruction, including primary snoring, airway resistance syndrome, obstructive hypoventilation, and obstructive sleep apnea (OSA).² OSA occurs as a consequence of intermittent upper airway obstruction caused mainly by an increase in lymphoid tissue or alteration in muscle tone. Central sleep apnea, however, presents as an absence or reduction in respiratory effort. In OSA, breathing impairment occurs regardless of continuous ventilatory effort.³ In addition to respiratory changes, sleep in children also exhibits limb motor activities, which may be within physiological patterns or pathological, mainly involving leg movements.⁴

Sleep bruxism (SB), defined as the presence of mandibular muscle activity, has also been reported in children, with an increased prevalence in children with respiratory disorders.^5–7 SB can be characterized by rhythmic (phasic) or nonrhythmic (tonic) movements. In healthy individuals, it is not considered a sleep disorder.⁸ This muscular activity can be protective in situations in which movement favors the re-establishment of the airways and/or salivary production.⁹ However, SB also has undesirable consequences for the individual, such as tooth wear and an increased risk of developing temporomandibular disorders.¹⁰ Individuals with SB may also have other comorbid conditions, including parasomnias, restless legs syndrome, mandibular myoclonus, and REM disorders.¹¹

As occurs during sleep, the activities of the mastication muscles are interconnected with other phenomena that occur in the body. Investigating parameters of sleep architecture revealed that episodes of SB are related to phases of arousals, activation of the sympathetic nervous system, and changes in heart rate, and that physiological occurrences are synchronized with changes in cortical activity, which are typical of SB.¹² With regard to temporality, it was found that the sequence of physical events that determine SB begins approximately 4 minutes before tooth contact and is initially triggered by activation of the sympathetic nervous system, followed by increased cortical activity, heart rate, and respiratory and muscle tone.¹³

One of the most used methods to accurately detect SB (mandibular movement activity) and other physiological phenomena that occur during sleep in children is sleep polysomnography (PSG) studies. However, very little is known about the temporal relationship of these phenomena and SB, especially in those with OSA. The objective of this study was to evaluate the physiological events associated with SB in children diagnosed with OSA during a sleep PSG study when compared with a control window (4 minutes before the SB PSG window, where no mandibular movement activity occurred). As a secondary outcome, the present study investigated the association of those factors with OSA events during event and control windows.

METHODS

This observational case-control study evaluated, by means of video PSG, physiological parameters presented at the moment of SB (case window) and compared with the moment without SB, 4 minutes before each event (control window) (Figure 1).

Figure 1. Two 30-second type 1 polysomnography windows showing the control window (without sleep bruxism) and case window (with sleep bruxism).

We assessed mandibular movements, both tonic and phasic, from children with sleep-disordered breathing complaints who underwent overnight video PSG for neurophysiological complementary diagnosis. Those PSG recordings were from patients enrolled in a previous study of otherwise healthy children with a clinical history of sleep-disordered breathing.¹⁴ The local Ethics Committee from the Children's Institute of the Clinical Hospital at the University of Sao Paulo Medical School reviewed and approved the present study protocol (approval number: 4.863.256). Only children whose parents agreed to participate and signed the informed consent form were included.

PSGs of children diagnosed with sleep apnea, with no other relevant health conditions, were consecutively selected from the waiting lists for adenotonsillectomy between August 2015 and January 2019. The PSG sample was composed of Brazilian children (4.0–9.0 years old) with nasopharynx obstruction (> 60%), tonsil enlargement (Brodsky’s grades 2, 3, or 4), parental complaints of snoring (> 3 nights/wk), mouth-breathing, and/or witnessed apnea episodes. All children were surgical candidates for adenotonsillectomy,¹⁵ as stated in a previous study by Bozzini et al.¹⁴ Incomplete examinations were excluded.

The recordings were performed at the Children’s Institute of the Clinical Hospital at the University of Sao Paulo Medical School with Embla N700 (Natus Neurology, EUA). Recordings were performed in a comfortable room, without sedative drugs and accompanied by caregivers. Electrophysiological and cardiopulmonary parameters were registered in RemLogic software (version 3.2, Natus Neurology, USA). This included electroencephalogram, electromyogram (anterior tibialis, chin), electrooculogram, electrocardiogram, nasal airflow, input and output nasal air pressure, thoracic and abdominal movement, microphone for snoring, oxyhemoglobin saturation, and video recording for body position and movements. Sleep stages, hypopnea events, and central, obstructive, or mixed apneas were scored according to the American Academy of Sleep Medicine parameters following the 10–20 system for electrode disposal.¹⁶ An extra pair of electrodes was placed over the masseter.

Sleep data were recorded and stored on a hard disk using the same PSG system (RemLogic). Sleep stages, leg movement, and apnea/hypopnea events were scored using American Academy of Sleep Medicine parameters.¹⁷ The presence of OSA was established when the apnea-hypopnea index value per hour was higher than or equal to 1 and/or the minimal oxygen saturation was lower than 92%, according to the criteria of Uliel et al.¹⁸ For SB, muscular activity was detected by bilateral electrodes on masseter muscles, with a duration between 0.25 and 2 seconds, and at least 3 bursts of 1 Hz was considered a phasic event when detected on the electromyograph. In the “tonic event” diagnosis, electromyography should be sustained for a duration greater than 2 seconds.¹⁹ The control time frame was assessed 4 minutes before the main event, which would be immediately prior to the start of sympathetic activity.¹³ The associated variables (presence of arousal, central and obstructive apnea, blood oxygen saturation, bradycardia/tachycardia, and leg movement) were analyzed. Data analysis was performed at the Children's Institute of the Clinical Hospital at the University of Sao Paulo Medical School by 2 trained researchers (C.F.B. and J.S.D.) supervised by a specialist of the children's polysomnography service (L.M.S.F.A.S.).

Data were tabulated using Excel (Microsoft Corporation, Redmond, WA, USA). Descriptive and statistical analyses were performed using Stata software version 17.0 (StataCorp, College Station, TX, USA). The Kolmogorov–Smirnov test was used to evaluate the normal distribution of data. A t test was used to compare the number of events between phasic and tonic mandibular movements. Chi-square and Fisher’s exact tests were used to evaluate the associations between categorical variables. The McNemar test was performed to assess the difference between the experimental and control groups and the sleep phase (paired data). Cluster-adjusted logistic regression analysis was used to assess the association between independent variables and the presence of OSA.

RESULTS

A total of 781 bruxism episodes were identified in 21 PSG recordings from children aged 4–9 years (male = 52.38%; female = 47.62%), with a mean age of 5.81 (SD =1.99) years, apnea-hypopnea index of 1.99 events/h (SD =1.27), were assessed. From these, 120 episodes were excluded from analysis. The mean ± SD apnea-hypopnea index in the present sample was 4.8 ± 7.6 events/h. Oxygen saturation varied between 72% and 98% (mean: 86.8 ± 5.2).

The main reason for exclusion was the presence of mandibular muscular activity present in the control window (phasic = 41; tonic = 79). The final analysis included a total of 661 SB episodes (tonic n = 372; phasic n = 289).

The number of tonic events ranged from 4 to 30 (mean = 17.71; SD = 6.91) and phasic events ranged from 3 to 33 per child (mean = 13.6; SD = 8.92). No differences were found between the number of phasic and tonic events (P = .116).

Table 1 shows the differences between tonic and phasic SB and sleep phase. Approximately 40% of SB episodes occurred in the N2 phase. No differences were found between sleep phases and bruxism type (tonic and phasic; P = .100).

Table 1.

Comparison between tonic and phasic activity of the mandibular muscles and sleep phase.

	Event Group
	Tonic, n (%)	Phasic, n (%)	χ2, P
Sleep phase
N1	66 (17.74)	45 (15.57)	.100
N2	160 (43.01)	118 (40.83)
N3	71 (19.09)	78 (26.99)
REM	75 (20.16)	48 (16.61)
Total	372 (56.28)	289 (43.72)

REM = rapid eye movement.

Conversely, when comparing the event window (mandibular movements) and their control window (4 minutes before the event), the sleep phase was significantly different between the groups (P < .001). The sleep phase between all analyzed windows (control and event) changed in 33.28% (441/661) of the cases. When comparing the changes (n = 220) in the sleep phases, it was noted that 75% changed from superficial to deeper phases, while only 25% changed from deeper to superficial sleep phases. This phenomenon is illustrated in Figure 2.

Figure 2. Alluvial diagram showing differences in sleep phase between movement and control windows.

REM = rapid eye movement.

The tonic event window exhibited a higher number of arousal episodes, tachycardia, central apnea, and leg movements when compared with their own control window, whereas the control window exhibited a higher number of bradycardia events than the event window (P < .05).

The phasic event window presented a higher number of arousal, tachycardia, and leg movements when compared with their own control window, while the control window presented a higher number of OSA and bradycardia events (Table 2).

Table 2.

Comparison between the physiological events occurring in the 30-second window between mandibular muscle activity (tonic and phasic bruxism) and its respective control window (occurring 4 minutes before).

	Tonic			Phasic
	Control, n (%)	Tonic Bruxism, n (%)	P	Control, n (%)	Phasic Bruxism, n (%)	P
Microarousal	7 (2.63)	259 (97.37)	<.001*	7 (3.61)	187 (96.39)	<.001*
Obstructive apnea	22 (64.71)	12 (35.29)	.079	23 (76.67)	7 (23.33)	.003*
Central apnea	6 (22.22)	21 (77.78)	.003*	8 (40.00)	12 (60.00)	.363
Desaturation	23 (53.49)	20 (46.51)	.637	27 (39.13)	42 (60.87)	.054
Tachycardia	160 (44.94)	196 (55.06)	.008*	133 (43.75)	171 (56.25)	.002*
Bradycardia	153 (72.86)	57 (27.14)	<.001*	116 (67.44)	56 (32.56)	<.001*
Leg movement	49 (13.84)	305 (86.16)	<.001*	48 (17.84)	221 (82.16)
Total	372 (50.00)	372 (50.00)		289 (50.00)	289 (50.00)

P values were calculated using chi-square test (χ²). *P < .05.

The numbers of physiological events that occurred before and after SB, both phasic and tonic, were evaluated in order to establish temporality in the same 30-second window (Table 3).

Table 3.

Temporality of physiological occurrences in relation to the type of muscle activity in the same analysis window (30 seconds) of the events.

	Group, n (%)			χ2, p	OR (95% CI)
	Tonic	Phasic	Total
Micro-arousal
Before	199 (61.61)	124 (38.39)	323 (72.42)	.014*	1.68 (1.10–2.56)
After	60 (48.78)	63 (51.22)	123 (27.58)
Total	259 (58.07)	187 (41.93)	446
Obstructive apnea
Before	5 (50.00)	5 (50.00)	10 (55.56)	.278a	0.33 (0.04–2.52)
After	6 (75.00)	2 (25.00)	8 (44.44)
Total	10 (55.56)	8 (44.44)	18
Central apnea
Before	7 (63.64)	4 (36.36)	11 (33.33)	.645a	1.00 (0.22–4.50)
After	14 (63.64)	8 (36.36)	22 (66.67)
Total	21 (63.64)	12 (36.36)	33
Desaturation
Before	12 (38.71)	19 (61.29)	31 (50.00)	.277	1.81 (0.61–5.35)
After	8 (25.81)	23 (74.19)	31 (50.00)
Total	20 (32.26)	42 (67.74)	62
Tachycardia
Before	107 (54.86)	88 (45.13)	195 (53.13)	.549	1.13 (0.75–1.71)
After	89 (51.74)	83 (48.26)	172 (46.87)
Total	196 (53.41)	171 (46.59)	367
Bradycardia
Before	45 (50.56)	44 (49.44)	89 (78.76)	.961	1.02 (0.41–2.51)
After	12 (50.00)	12 (50.00)	24 (21.24)
Total	57 (50.44)	56 (49.56)	113
Leg movement
Before	179 (56.83)	136 (43.17)	315 (59.89)	.510	0.88 (0.62–1.26)
After	126 (59.72)	85 (40.28)	211 (40.11)
Total	305 (57.98)	221 (42.02)	526

P values were calculated using chi-square test (χ²). ^aFisher’s exact test. *P < .05. CI = confidence interval, OR = odds ratio.

The graphical presentation illustrates the temporal distribution of the different phenomena that occur before (blue) and after (orange) the mandibular muscular activity in tonic (Figure 3) and phasic (Figure 4) events.

Figure 3. Temporality of physiological occurrences in relation to tonic activities of the masticatory muscles, in the same analysis window (30 seconds).

Figure 4. Temporality of physiological occurrences in relation to the phasic activities of the masticatory muscles, in the same analysis window (30 seconds).

In this analysis, there was a difference between tonic and phasic events in relation to arousal, and tonic events had a significantly higher numbers of arousals before SB (P = .014). All other variables analyzed showed no differences between the groups (P > .05).

It was observed that leg movements and tachycardia were the most frequent phenomena associated with bruxism, both in tonic and phasic events, and no difference was noted in their frequency before and after SB.

Although the present study included only PSGs from children diagnosed with sleep apnea, the frequency of obstructive and central apneas during the SB 30-second window and desaturation was lower when compared with the other physiological phenomena. Logistic regression analysis was used to evaluate the associated factors with OSA (Table 4). When merging all phasic and tonic events and their respective control windows (n = 1,322), OSA was present only in 4.84%. The control window (4 minutes before the SB event) presented significantly higher numbers of OSA when compared with the SB event window (P = .034). Sleep phase, desaturation, and bradycardia were the other physiological phenomena associated with OSA (P < .05).

Table 4.

Logistic regression analysis investigating obstructive apnea and associated factors in SB and control windows.

	Obstructive Apnea		Univariate		Adjusted
	No, n (%)	Yes, n (%)
			OR (95% CI)	P	OR (95% CI)	P
Group
Control (ref)	616 (93.19)	45 (6.81)	0.40 (0.20–0.78)	.008	0.22 (0.05–0.88)	.034*
Event (tonic + phasic)	642 (97.13)	19 (2.87)
Sleep phase
REM (ref)	132 (89.80)	15 (10.20)
N1	514 (93.97)	33 (6.03)	0.56 (0.32–0.98)	.046*	0.29 (0.15–0.57)	<.001*
N2	348 (99.15)	3 (0.85)	0.07 (0.01–0.57)	.012*	0.07 (0.01–0.47)	.006*
N3	264 (95.31)	13 (4.69)	0.43 (0.10–1.72)	.235	0.22 (0.06–0.72)	.013*
Movement type
Tonic (ref)	710 (95.43)	34 (4.57)	1.14 (0.60–2.15)	.680	0.59 (0.30–1.16)	.131
Phasic	548 (94.81)	30 (5.19)

Cluster-adjusted (patient) logistic regression analysis. *P < .05. CI = confidence interval, OR = odds ratio, ref = reference, REM = rapid eye movement, SB sleep bruxism.

DISCUSSION

To the best of our knowledge, this is the first study to investigate the physiological phenomena associated with masticatory muscle activity in children with OSA. Furthermore, this research established the temporal relationship between events, which is an important aspect to be considered when analysing causality of the events. The control window was evaluated with the intention of investigating phenomena that occurred at the beginning of the sequence of events culminating in masticatory muscle activities.¹³

In previous studies, both in children and young adults, most episodes of muscle activity occurred in the early stages of the non-REM phase (N1 and N2).^20,21 In the present study, the sleep phase in which the greatest number of masticatory muscle activities was observed was N2, although there was no statistically significant difference in relation to the occurrence in the other phases.

However, in relation to order (before/after mandibular muscular activity) of occurrence of the events, most of them did not affect sleep phase (441/661, 66.7%).

It was observed that, in 25% (165/661) of the events, there was a record of change from the current sleep phase to more superficial phases, contrary to what was observed in 8.3% (55/661) of the events, where there was a record of change in sleep phase to deeper stages. To the best of our knowledge, this sleep phase shift has not been explored previously in the literature. However, there are studies on the occurrence of rhythmic movements of the muscles of mastication in moments of more superficial sleep (N1 and N2), associated with arousals.²² Hence, the stage shift for superficial phases in 25% of our sample, alongside previous literature data on arousals,²³ shows that some sleep instability can be related to the bruxism event per se. Phasic and tonic bruxism showed similar changes, such as arousal, tachycardia, and leg movements. With regard to the descriptive values, the 3 phenomena mostly occurred before the bruxism episodes, as shown in Table 3. This situation is in line with the knowledge that SB occurs most often in the arousal phase, which indicates superficialization of sleep and activation of sympathetic pathways, as reflected in increased heart rate and leg movements.²⁴

In addition, it can be observed that central apnea occurred more frequently in the window of tonic bruxism, as observed in research carried out with adults that found a correlation between oxygen desaturation, increased carbon dioxide levels, and tonic episodes.²⁵ Tonic contraction may occur in response to central apnea, as sustained muscle contraction may be related to adverse situations.²⁶

The common event in the control windows for both phasic activity and tonic activity was bradycardia (P < .001). One of the functions of sleep is to reduce blood pressure during the night to maintain adequate physiological function of the cardiovascular tissues, and bradycardia reflects a stable sleep window. Thus, the control window fulfils the appropriate role for the initial analysis, temporally prior to sympathetic activation. In the control window of phasic activity, there was also a significant increase in the frequency of OSA events (P = .003).

Cardiovascular changes accompany OSA events when a decrease in the heart rate can be observed. When breathing recovers, relative tachycardia is observed only at the end of the apneic event.²⁷ The OSA observed in the control window of phasic bruxism does not seem to establish a direct causal association with muscular events. In the hypothesis of causality, mandibular movement, which increases airway permeability, occurs at the moment of desaturation to immediately restore oxygenation.⁹

In the window preceding the SB episode, whether phasic or tonic, the most frequent physiological phenomenon is arousal. This phase, which is the superficialization of sleep where transient intrusion from wakefulness to sleep can be observed, is related to sympathetic nervous system activity, which corroborates previous studies carried out in adults.¹³

Previous studies have observed that patients with OSA, even if mild, have a lower threshold for sleep interruptions and are ultimately more susceptible to interference in sleep.²⁸ Sleep instability is common among children with apnea. Some children present an increased motor response, shown in patients with bruxism by chewing movements, while others do not. This response, more than a physiological mechanism of protection or aggression, probably indicates the presence of a motor response pattern to the individual’s own event. Analyzing only the characteristics of apnea in this group of patients, OSA events established a higher frequency pattern during the REM sleep phase. In the non-REM phase, breathing can be within the ideal parameters of regularity, which prevents apnea events, as has been reported in previous studies.^29,30 The association between OSA and phasic SB has been found in research, mainly in adults,³¹ and the hypothesis that mandibular movement is immediately secondary to the apneic episode, as a form of protection of the organism, has also been reported.³² In the present study, the OSA events that preceded phasic SB episodes, which were statistically significant, were not in the same window. At this point, we cannot establish comparisons of results because no research has established a comparison with the control window.

With regard to the findings in the event window, immediately before or after the SB, although not statistically significant, a greater number of OSA events before phasic SB was observed. These data agree with those of other studies that also evaluated SB in relation to apneic events.^31,33 In contrast, this temporal sequence is not repeated in all OSA phenotypes, and other authors have not found the same findings, reporting episodes of SB occurring before, concomitantly, and after the onset of OSA.³⁴

One of the limitations of the regression analysis evaluating associated OSA factors is the nature of data collection. Only physiological phenomena that happened during the event and control windows were included. Further investigation is necessary to evaluate the associated factors during the full sleep study (total duration of the PSG).

In situations such as that observed in the present study it can be conjectured that SB may be a physiological response to OSA desaturation. In addition, this condition did not occur in relation to central apnea. One of the differences between central apnea and OSA is the muscular effort required to restore adequate breathing. Thus, 1 possibility is the usefulness of SB as a terminal event in an episode of OSA to restore patency of the upper airways. However, in central apnea, SB does not have a physiological function to maintain the airway patency as it seems to occurs in obstructive apnea events.

One of the limitations of the study is the first night effect, since the conditions allowed 1 night of PSG. There are reports that the first night effect would decrease the quality of sleep in children,³⁵ but other authors suggest that, in children, a single night is adequate and effective.³⁶ In addition, although the first night effect is comparable in adults and children, adaptation seems to be more necessary in studies of sleep architecture that exhibit parameter variability from 1 night to the next, which does not happen with respiratory parameters in children with OSA.³⁷ Considering that this study presents laboratory data on the physiopathology of SB, these cannot be readily extrapolated to clinical practice, and there is a clear need for studies that provide information that associate PSG recordings with clinical outcomes. This study, therefore, paves the way on the understanding the physiological mechanisms of SB and associated events.

CONCLUSIONS

This is the first study to evaluate the use of a control window (where no mandibular activity was detected) in comparison with SB events in a PSG study. It was shown to be representative since no activation of the sympathetic nervous system was noticed. There was a difference in the physiological parameters evaluated in children with mild sleep apnea when comparing the 2 windows (SB and control). Sleep bruxism was associated with other physiological phenomena such as leg movements, tachycardia, and microarousal.

DISCLOSURE STATEMENT

All authors have reviewed the final paper prior to its submission. Work for this study was performed in the Children’s Institute of the Clinical Hospital at University of Sao Paulo Medical School (HCFMUSP). The authors report no conflicts of interest.

ABBREVIATIONS

OSA

obstructive sleep apnea

PSG

polysomnography

REM

rapid eye movement

SB

sleep bruxism