Archives of Oral Biology 81 (2017) 56–60

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Archives of Oral Biology

journal homepage: www.elsevier.com/locate/archoralbio

Nocturnal sleep architecture is altered by sleep bruxism MARK

a,⁎ a a b,c
Marcelo Palinkas , Marisa Semprini , João Espir Filho , Graziela de Luca Canto ,
Isabela Hallak Regaloa, César Batagliond, Laíse Angélica Mendes Rodriguesa, Selma Siésserea,
Simone Cecilio Hallak Regaloa
a
Department of Morphology, Physiology and Basic Pathology, Ribeirão Preto School of Dentistry, University of São Paulo, São Paulo, Brazil
b
Department of Dentistry, Federal University of Santa Catarina, Florianopolis, Brazil
c
Department of Dentistry, University of Alberta, Edmonton, Canada
d
Department of Restorative Dentistry, Ribeirão Preto School of Dentistry, University of São Paulo, São Paulo, Brazil

A R T I C L E I N F O A B S T R A C T

Keywords: Objective: Sleep is a complex behaviour phenomenon essential for physical and mental health and for the body to
Sleep bruxism restore itself. It can be affected by structural alterations caused by sleep bruxism. The aim of this study was to
Sleep architecture verify the effects of sleep bruxism on the sleep architecture parameters proposed by the American Academy of
Polysomnography Sleep Medicine.
Design: The sample comprised 90 individuals, between the ages of 18 and 45 years, divided into two groups:
with sleep bruxism (n = 45) and without sleep bruxism (n = 45). The individuals were paired by age, gender
and body mass index: a polysomnography was performed at night.
Results: Statistically significant differences were found between (P ≤ 0.05) individuals with sleep bruxism and
individuals without sleep bruxism during total sleep time (P = 0.00), non-rapid eye movement (NREM) total
sleep time (P = 0.03), NREM sleep time stage 3 (P = 0.03), NREM sleep latency (P = 0.05), sleep efficiency
(P = 0.05), and index of microarousals (P = 0.04).
Conclusions: Sleep bruxism impairs the architecture of nocturnal sleep, interfering with total sleep time, NREM
sleep latency, and sleep efficiency.

1. Introduction insomnia, narcolepsy, or obstructive sleep apnea (OSA) (AASM, 2014),

A normal night sleep is defined as a vital physiological process
(Harrington & Lee-Chiong, 2009). It is also described as a transient
reversible state (the person can be awakened) (Gemignani et al., 2015)
with the purpose to restore the sensory perception and the neuromus-
cular function and to regulate the hormonal rhythms (Consensus
Conference Panel, 2015). Sleep has a complex architecture divided
into stages. Each has unique characteristics, including physiological
variations, and a structure that regulates the sleep–awake cycle with the
circadian rhythm (Yoshida, Shinohara, & Kodama, 2015).
There are two types of sleep: non-rapid eye movement (NREM)
sleep, characterized by non-rapid eye movements and muscle relaxa-
tion, and rapid eye movement (REM) sleep, which is the most
restorative part of sleep, with the presence of desynchronized brain
wave activity, muscle tone, and bursts of rapid eye movements (Berry
et al., 2015).
When a quiet night sleep is disturbed by sleep bruxism, chronic
the consequences of the possible functional changes in sleep architec-
ture need to be investigated, as these disorders can negatively affect the
quality of life, causing public health problems (Rao, Orpana, & Krewski,
2016), with substantial increases in hospitalizations (Malish,
Arastu, & O’Brien, 2016) and health care costs.
Previous studies on sleep bruxism reported a prevalence rate of
about 8% in adult population (Carra, Huynh, Fleury, & Lavigne, 2015),
whose oral-motor movements of the stomatognathic system (AASM,
2005) are characterized by jaw clenching and tooth gnashing or
grinding (Lobbezoo et al., 2013), causing a physio-pathological imbal-
ance of the body (Minakuchi et al., 2016). Bibliographic reviews show
that, although there are publications on this topic, further research is
needed in the field of sleep medicine to help health professionals to
better understand the architecture of sleep in individuals affected by
sleep bruxism.
Therefore, the present study aimed to evaluate the sleep architec-
ture through the analysis of some standards set by the American

⁎
Corresponding author: Faculdade de Odontologia de Ribeirão Preto, Universidade de São Paulo, Avenida do Café, s/n, 14040-904 Ribeirão Preto, São Paulo, Brazil. Tel.: +55 16
33150281.
E-mail address: palinkas@usp.br (M. Palinkas).

http://dx.doi.org/10.1016/j.archoralbio.2017.04.025
Received 18 September 2016; Received in revised form 9 March 2017; Accepted 20 April 2017
0003-9969/ © 2017 Elsevier Ltd. All rights reserved.
M. Palinkas et al. Archives of Oral Biology 81 (2017) 56–60

Academy of Sleep Medicine (Berry et al., 2015), which characterize the 2.2. Polysomnography (gold standard)
micro-structure of the night sleep such as: registration period and total
sleep time, NREM and REM sleep latency, total period of NREM and Polysomnography (Stuginski-Barbosa, Porporatti, Costa,
REM sleep, period of NREM sleep in stages N1, N2, and N3, sleep Svensson, & Conti, 2017) was analyzed using the Meditron-Sonolab
efficiency and index of NREM microarousals. 620 device with 26 A/C programmable channels, six DC constant
channels, low consumption and noise level, coupled to 5000 v, multi-
user software, Windows XP/2000/NT and 32-bit C++ compiler. To
2. Material and methods
obtain the bruxism-related variables, the basic polysomnographic
measures of sleep, electroencephalography, electrooculography (bilat-
2.1. Subjects’ recruitment
eral), electromyography (masseter muscle (right and left), temporal
muscle (right and left), mentalis muscle and tibialis anterior muscle),
All subjects were informed about the experiment and agreed to
plethysmographic signals (respiratory effort of the chest and abdomen),
participate by providing their free consent according to resolution 466/
body movements and legs, nasal airflow, electrocardiogram, broncho-
12 of the Brazilian Health National Council conducted by 1964
gram, and visual analysis by video camera, were recorded to confirm
Declaration of Helsinki and its later amendments. This cross-sectional,
sleep bruxism diagnosis and to characterize the sleep micro-structure
observational study whose sample was random selection for the group
based on standards set by the AASM, 2005: registration period and total
with sleep bruxism and the selection of the control group was a
sleep time (min), NREM and REM sleep latency (min), total period of
convenience sample paired subject to subject with the group if, as
non-REM and REM sleep (min), period of NREM sleep in stages N1, N2,
provided for in the methodology of the study was approved by the
and N3 (min), sleep efficiency (%), and index of NREM microarousals
Research Ethics Committee of the Ribeirão Preto School of Dentistry of
(number of events). The bruxism sleep disorder was established when
the University of São Paulo (process no. 02735812.9.0000.5419).
the registered polysomnography showed four or more episodes (phasic,
Among the 580 subjects, ages between 18 and 45 years and with
tonic, and mixed) during 8 h of sleep or 25 or more bursts during sleep
normal occlusion, 150 participants were submitted a one single-night
(Lavigne, Rompré, & Montplaisir, 1996).
polysomnographic (De Siqueira et al., 2017). The participants were
The subjects were informed that the polysomnography could be
excluded if they presented with a history of neurological or degenera-
interrupted at any time or ended in the morning of the next day to the
tive disorders, chronic orofacial pain, awake bruxism, temporomandib-
examination. Comfort and well-being of the patients during the test
ular joint dysfunction, and any objection to take the polysomnography
were carefully taken into account, such as: type of pillow and bed, room
test (Palinkas et al., 2015).
temperature, sounds and noises, and correct way to fix the electrodes on
Polysomnographic recordings were obtained from 150 patients.
the body without causing discomfort. These electrodes were embedded
Among these, 90 subjects were considered for the final sample. The
in electrolyte medium and placed on the scalp, the face, and leg, using a
subjects were divided into two groups paired by gender, age, and body
hypoallergenic tape (3 M Micropore™) to record sleep data.
mass index: with sleep bruxism (29 men and 16 women with a mean
Before starting the sleep recordings, the subjects performed calibra-
age of 30.58 ± 6.78 years and a mean body mass index of
tion tests to recognize the physiological signs such as jaw movements,
25.59 ± 0.57 kg/m2) and without sleep bruxism (29 men and 16
coughing, swallowing, maximum voluntary contraction (maximum
women with a mean age of 29.44 ± 7.88 years and a mean body mass
force which a human subject can produce in a specific isometric
index 25.18 ± 0.64 kg/m2). A flowchart describing the process of
exercise), and rhythmic contractions.
identification, inclusion, and exclusion of subjects is shown in Fig. 1.
The anamneses provided data regarding the participants’ medical and
dental history, any possible symptoms and signs of temporomandibular 2.3. Statistical analysis
dysfunction (DC/TMD) (Schiffman et al., 2014), muscle fatigue and
sleep–awake cycles. Data were tabulated, and it was found that they were normally

Fig. 1. Diagram of selection CriteriaSB group.

57
M. Palinkas et al. Archives of Oral Biology 81 (2017) 56–60

Table 1 In our study, it was observed that the sleep parameters that included
Means, standard error ( ± ), and statistical significance (P ≤ 0.05)* of sleep macro- total monitoring time sleep latency sleep efficiency, and microarousal
structure: sleep time period (STP), total sleep time (TST), NREM sleep latency (NREMSL),
frequency presented significant differences between the study groups.
REM sleep latency (REMSL), NREM sleep time (NREMST), REM sleep time (REMST),
sleep efficiency (SE), and NREM microarousal index (MI) for individuals with sleep These results were not in agreement with those found by Lavigne et al.
bruxism (SBG) and individuals without sleep bruxism (CG). (2002), who reported that individuals with sleep bruxism display
normal sleep architecture in terms of total sleep time, sleep latency,
Varibles SBG CG P value and percentage of the sleep stage distribution. Although our methodol-
STP (min) 455.22 ± 4.55 464.02 ± 4.79 0.18 ogy is similar to the study of Lavigne et al. (2002), the number of
TST (min) 400.54 ± 5.51 420.52 ± 4.50 0.00* individuals who participated in this study was four times larger and
NREMSL (min) 35.23 ± 3.18 26.57 ± 3.27 0.05* exclusion criteria were different, which may have influenced the
REMSL (min) 156.81 ± 14.19 149.37 ± 14.66 0.71 difference of results.
NREMST (min) 390.20 ± 6.19 372.70 ± 5.09 0.03*
Sleep is essential for the maintenance of adaptive emotion regula-
TREM (min) 27.84 ± 3.08 30.33 ± 3.65 0.60
SE (%) 90.80 ± 0.75 88.38 ± 0.99 0.05* tion and reactivity. Sleep deprivation or shorter sleep periods may
MI (no. of events TST) 67.76 ± 4.48 54.49 ± 4.89 0.04* produce adverse changes in cognitive and physical performance
(Palmer & Alfano, 2016). This statement corroborates the results ob-
tained in the present study, i.e. the total sleep period in individuals with
distributed (Kolmogorov–Smirnov). A descriptive analysis was carried sleep bruxism showed shorter duration when compared with indivi-
out for each variable. A Student's t-test was used for group comparison duals without sleep bruxism. Sleep bruxism in children causes sig-
(significance level of 5%, 95% CI). The statistical analysis was nificant problems of attention and behaviour (Herrera et al., 2006).
performed using the SPSS software, version 22.0 for Windows (SPSS This study has not evaluated the cognitive performance of individuals.
Inc., Chicago, IL, USA). The NREM sleep cycle starts with stage N1, which corresponds to
5–10% of the total sleep time. After 1–10 min, a deep sleep stage starts
3. Results (stage N2) with 45–55% of the total duration. Stage N3 typically starts
35–45 min after falling asleep; the brain waves slow down and become
Table 1 shows the sleep macro-structure patterns for individuals larger. This stage corresponds to 15–25% of the total sleep time. After
with sleep bruxism and individuals without sleep bruxism. Comparisons 90 min, a standard NREM–REM sleep cycle (25% of the total sleep time)
of the two groups showed that individuals with sleep bruxism presented is complete with a total of 4–6 different sleep stages (Consensus
a shorter total sleep period when compared with individuals without Conference Panel, 2015).
sleep bruxism. The level of statistical significance was set at P ≤ 0.05. The results obtained in our study showed that there were no
SBG revealed increased non-REM latency compared to individuals significant differences in NREM stage N3. However, the mean percen-
without sleep bruxism, with statistical significance level of P ≤ 0.05. tage in individuals with sleep bruxism was higher compared to control
The NREM and REM sleep periods lasted longer in individuals with (8.87 and 6.34%, respectively).
sleep bruxism than in individuals without sleep bruxism, with statistical The percentage values found in this stage are not in agreement with
significance level of P ≤ 0.05 in NREM. Data on sleep efficiency those presented in the literature, which correspond to 15–25% of the
showed that individuals with sleep bruxism had significantly higher total sleep (Consensus Conference Panel, 2015). These values are also
sleep efficiency (P ≤ 0.05) compared to controls. The results showed inconsistent with those of Silva et al. (2012), who reported that sleep
that the index of NREM microarousals, during the total sleep period, disorders reduced the time spent in stage N3.
was significantly higher (P ≤ 0.05) in individuals with sleep bruxism NREM stage N3 is called “slow wave sleep” and is characterized by
when compared with individuals without sleep bruxism. the presence of slow brain waves called “delta waves”. Growth
Table 2 shows values during NREM sleep stages N1, N2, and N3 in hormones are secreted during this stage (Sprecher et al., 2016).
both groups. The duration of stage 3 was statistically longer (P ≤ 0.05) Moreover, muscles are relaxed and energy is restored (De Gennaro
in individuals with sleep bruxism compared with individuals without et al., 2002). We believe that individuals with sleep bruxism require
sleep bruxism. Although there were significant differences for the other longer stage N3 to recover their muscle functions from a non-physio-
stages when the groups were compared, those differences were not logical rhythmic masticatory muscle activity (RMMA) (Kato,
statistically significant. Masuda, & Morimoto, 2007), which occurs more frequently and with
a wide variation in masseter muscle activity.
4. Discussion There is evidence in the literature that normal sleep efficiency is at
least 85% (asleep 85% of the night) represented by the proportion of
It is known that there is a direct relationship between a normal sleep in the episode potentially filled by sleep (i.e. the ratio of total
night's sleep and a peaceful and productive day. A normal sleep follows sleep time to time in bed) (Silva et al., 2012). Our findings revealed that
predictable sleep architecture patterns that are used to recover energy both groups showed normal sleep efficiency, even individuals with
that was recruited during sleep–awake cycles and to maintain func- sleep bruxism which presented higher percentage value when com-
tional and emotional balance (Louca & Short, 2014). In contrast, the pared to individuals without sleep bruxism.
regular sleep stages may be disturbed by some disorders, including However, this result does not mean that the night's sleep has
sleep bruxism, with great impact on the sleep dynamics (Boutros, affected the repair of neural functions (Raschke, 2004), in view of the
Montgomery, Nishioka, & Hatch, 1993). shorter duration of the REM stage when compared to individuals
without sleep bruxism.
Table 2 The NREM sleep latency is defined as the length of time that it takes
Means, standard error ( ± ), and statistical significance (P ≤ 0.05)* of NREM sleep (min) to accomplish the transition from full wakefulness to sleep. The results
stage N1, stage N2, and stage N3 for individuals with sleep bruxism (SBG) and individuals
of this study showed that the mean values found for the latency period
without sleep bruxism (CG).
in individuals with sleep bruxism were higher when compared to
Stages SBG CG P value individuals without sleep bruxism. This finding is in agreement with
that described in the literature with regard to the increased latency,
N1 91.35 ± 4.19 96.79 ± 5.58 0.43
except the time, which was less than 30 min (Correa, Bittencourt,
N2 265.73 ± 4.70 250.35 ± 8.54 0.11
N3 35.64 ± 3.29 25.40 ± 3.31 0.03* Tufik, & Hachul, 2014) for the normal sleep of the individual in contrast
to our individuals without sleep bruxism, in which the time was

58
M. Palinkas et al.
149.37 ± 14.66. When some studies in the literature describe that the
latency is high, the researchers are suggesting that individuals may
have difficulties falling asleep, indicating initial or middle insomnia
(Schutte-Rodin, Broch, Buysse, Dorsey, & Sateia, 2008). Sleep disorders
such as OSA in adults and children are characterized by prolonged sleep
latency and decrease in sleep time (Gurbani, Verhulst,
Tan, & Simakajornboon, 2017).
Previous studies on normal sleep stages showed that microarousals
are frequent and in NREM sleep may occur without a rise in muscle tone
(Ramirez et al., 2013); with that in mind, we decided to verify the
relationship between the number of microarousals during nocturnal
sleep in sleep bruxism patients. It was observed that individuals with
sleep bruxism presented a mean microarousal index of 67.76, with
statistical significance, compared to 54.49 in individuals without sleep
bruxism. Sleep fragmentation is associated with poor mood, muscle
fatigue, sleepiness, and negative effects on mental processes, hormone
imbalance, reduced lung capacity, and changes in metabolic rate
(Ogawa, Nittono, & Hori, 2005). Huynh et al. (2006) reported that the
microarousals in individuals with sleep bruxism were higher during the
N2 and N3 with statistically significant results.
In this study, 83% of the individuals with sleep bruxism who
responded to the anamnesis questionnaire reported tiredness, sleepiness
during the day, and muscle discomfort upon awakening, which
probably suggest that such manifestations are associated with rhythmic
masticatory muscle activity involving the masticatory muscles.
These results corroborate with those by Mayer, Heinzer, & Lavigne
(2016) and in contrast, Dumais et al. (2015) observed that those
manifestations were related to microarousals during the total period
of sleep. The association between the incidence of microarousals,
muscle fatigue, and initial sleepiness was not included in the present
study.
The changes found in the sleep architecture of individuals with
bruxism may be attributed to the interaction of innumerous situations
and should be justified separately to demonstrate a single and total
effect. For example, sleep efficiency in individuals with sleep bruxism
could reflect on a normal sleep period; in contrast, the microarousals,
the latency, and the period of non-REM sleep showed the opposite,
considering that the incidence and the percentage remained higher.
The results obtained encourage us to continue exploring this topic
and to verify other parameters, namely, the behaviour and the social
interaction of the individual with sleep bruxism, muscle fatigue and
emotional changes caused by stress, irritability, anxiety, and depres-
sion. The assessment of sleep architecture requires detailed observation
of those external or internal stimuli that can affect the sleep dynamics.
Despite the great interest of the healthcare community in Sleep
Medicine that seek to understand what happens to sleep architecture
associated with several disorders, there is lack of information regarding
the effects of sleep bruxism.
The results described in the present study aimed to provide health
professionals with parameters to obtain a better understanding of the
sleep structure in bruxers and to prescribe adequate treatment for this
sleep-related movement disorder.
Limitation of this study includes the fact that the participants were
observed only during a single night at the sleep laboratory. Probably,
more time would be needed for the adaptation to the equipment,
sleeping environment, or both. However, according to Hasegawa et al.
(2013), one-night sleep recording may be sufficient for moderate-high
frequency sleep bruxism individuals.
5. Conclusions
Sleep bruxism impairs the night sleep architecture evidenced by the
different parameters related to the total sleep time (TST), the NREM
sleep latency (NREMSL), and the sleep efficiency (SE), which char-
acterize adverse changes in the sleep macrostructure, affecting its
quality. Based on the results obtained, it can be concluded that
59
Archives of Oral Biology 81 (2017) 56–60
additional studies should focus on this topic.
Funding
Fundação de Amparo a Pesquisa do Estado de São Paulo (FAPESP),
Brazil provided financial support (012/10228-6). The sponsor had no
role in the design or conduct of this research.
Competing interests
None declared.
Ethical approval
All procedures performed in studies involving human participants
were in accordance with the ethical standards of the Institutional and/
or National Research Committee and with the 1964 Helsinki declara-
tion and its later amendments or comparable ethical standards. This
research was approved by the Research Ethics Committee of the
Ribeirão Preto School of Dentistry of the University of São Paulo (case
no. 02735812.9.0000.5419).
Informed consent
Informed consent was obtained from all individual participants
included in the study.
Acknowledgments
We gratefully acknowledge the support of Fundação de Amparo a
Pesquisa do Estado de São Paulo (FAPESP), Brazil.
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