SLEEP BRUXISM IN CHILDREN

PRERNA PRIYADARSHNI
JR-1
DEPARTMENT OF PROSTHODONTICS AND CROWN & BRIDGE

GUIDED BY-
Dr. ARVIND TRIPAHI
Dr. RAVI DWIVEDI
 CONTENT
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1 2 3
INTODUCTION EPIDEMILOG
ETIOLOGY Pathophysiolo
Y
gy
CONTENT
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6 7
Symptoms and Clinical Risk factors
manifestations features
CONTENT
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9
Diagnostic

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evaluation Management CONCLUSION
INTRODUCTION

0
• Derived from the Greek word “brychein”
bruxism means tooth grinding.

• The term first introduced in 1931, to

describe involuntary, excessive grinding,
clenching, or rubbing of the teeth during
nonfunctional movements of the
masticatory system.

• It refers to movements of the jaws that are

outside of the normal functional activity of
the teeth and jaws (eg, speaking, chewing,
or swallowing).
 • In children, bruxing when awake, which manifests as clenching of
the teeth, often occurs without any cognitive awareness, especially
during stressful situations or intense concentration. When the child
is made aware of the activity, the bruxism can be stopped or
modified.

• On the other hand, sleep bruxism, which presents as grinding or

clenching of the teeth during sleep, cannot be consciously stopped
by the child.

• The International Classification of Sleep Disorders

reclassified bruxism in 2005 as a sleep-related
movement disorder, rather than its previous
classification as a parasomnia, which is an
undesirable movement occurring during sleep.
Barbosa Tdc S, Miyakoda LS. Ppocztarux Rde L, Rocha CP, Gaviao mb.Tempomandibular disorders and bruxism in
childhood and adolescence:Review of literature. Int J Pediatr Otorhinolaryngol2008;72:299-314.
 DEFINITION
The American Academy of Sleep Medicine (AASM) defines sleep
bruxism as a stereotyped movement disorder characterized by
clenching and grinding of the teeth during sleep .

 Bruxism is found in 14%-20% of children, 8% of adults <60 years old, and 3% of

adults >60 years old.

 The mandibular movements of bruxism can be confused with rhythmic mandibular

movements associated with other sleep disorders, such as arousals/microarousals,
limb movement disorder, and obstructive sleep apnea/hypopnea syndrome.

Lavinge Gj, Rompre PH, Poirier G, H uard H, Kato T, Montplaisir JY. Rhythmic masticatory muscle activity
during sleep in humans. J Dent Res 2001;80:443-448.
EPIDEMIOLOGY

0
The prevalence of bruxism in children is difficult to
determine because estimates are generally based
on parental reporting or clinical finding of tooth
wear.

The occurrence of bruxism may be variable over

time, so finding tooth wear is not necessarily
indicative of current tooth grinding.

• The prevalence of bruxism in children varies

greatly—from 7% to 88%.

Children younger than 11 years are most affected

with a reported prevalence of 14% to 20%. (

Prevalence of bruxism and associated correlates in children as reported by parents. J Dent Child (Chic). 2005;72:67-
73.)
 Bruxism may commence in infancy with the eruption of first primary
tooth.

 In healthy infants, sleep bruxism typically starts at about 1 year, soon

after the eruption of the primary incisors.

 Infants with no teeth to oppose the newly erupted teeth have been
seen to lacerate the opposing gum pad.

 Bruxism may occur throughout life; mostly seen to increase through

the mixed dentition period and then decreases later with age.

 Bruxism can occur at any stage of sleep; mostly during the transition
from a deeper stage to a lighter stage of sleep. It is also reported to
occur during the rapid eye movement stage, and is most damaging.

J.
 The research is not definitive on the role of gender and the
prevalence of bruxism.

 While some studies indicate there is no significant gender effect on

the prevalence of bruxism, others report that girls are more
frequently affected.

 The role of genetics in bruxism is also unclear, however, an

association appears to exist between child and parental bruxism.
Based on self-reports, 20% to 50% of sleep bruxism patients have
an immediate family member who experienced tooth grinding in
childhood .

Temporomandibular disorders and bruxism in childhood and adolescence: Review of

the literature. Int J Pediatr Otorhinolaryngol. 2008;72:299-314 )
ETIOLOGY

0
 The etiology of bruxism is a
controversial phenomenon, but the
consensus is that it is multifactorial.

• Basically two groups of etiological

factors can be distinguished:
peripheral (morphological factors),
and central (pathophysiological and
psychological) factors.

• Morphological factors include

occlusal discrepancies and anomalies
of articulation of the orofacial region,
however, research shows the
elimination of interferences in
occlusion and articulation has no
influence on bruxism activities.

Bruxism physiology and pathology: an overview for clinicians. J Oral Rehabil.2008;35:476-494.

 Moreover, experimentally-placed deflective occlusal contacts do not seem to elicit
bruxism. Therefore, not every child with bruxism has occlusal interferences, and not
all children with such interferences have bruxism.

 It is often difficult to determine in children whether tooth attrition is due to bruxism

because the occlusal surfaces of primary teeth become ground physiologically.

 One theory about how bruxism starts in children is the occlusion instability created
during the replacement of the primary teeth by the permanent dentition.

 Studies, however, have failed to show a significant role of occlusal discrepancies in

the genesis of sleep bruxism with no evidence for a role of occlusion and articulation
in its etiology.

Lobbezoo F, Naeije M. Bruxism is mainly regulated centrally, not peripherally. J Oral Rehabil.
2001;28:1085-1091
PATHOPHYSIOLOGY

0
• Pathophysiological factors are believed to
play a role in the precipitation of bruxism. In
younger children, bruxism may be due to the
immaturity of the masticatory
neuromuscular system.

• Current thinking is that bruxism is part of

an arousal response.

• An arousal response is a sudden change in

the depth of sleep during which a person
either arrives at a stage of lighter sleep or
wakes up.

• In young adults, more than 80% of sleep

bruxism episodes occur during sleep stages
1 and 2 of nonREM (light sleep stages), and
5% to 10% in REM (deep stages).

• Many bruxism episodes lead to a shift in Bruxism physiology and pathology: an

sleep stage, usually toward awakening or overview for clinicians. J Oral Rehabil.
lighter sleep. 2008;35:476-494 c
 Hyperactivity is
There appears to be
associated with
a relationship with
bruxism and the
the autonomic 2 amphetamines
nervous system in
used for managing
that there is
attention deficit
increased cortical The involvement of hyperactivity
and autonomic
the dopaminergic disorder can also
cardiac activity
system may play a cause bruxism.
preceding bruxism
activity. role in sleep
1 bruxism, but this
3
idea remains
controversial.

Temporomandibular disorders and bruxism in childhood and adolescence: Review of the

literature. Int J Pediatr Otorhinolaryngol. 2008;72:299-314
STRESS AND PSYCHOSOCIAL INFLUENCES

 Stress and personality have been implicated in the etiology of bruxism.

 Bruxism, either clenching while awake or grinding during sleep, is associated with
stress and anxiety.

 The exact mechanism by which these and other psychological factors contribute to
the etiology of bruxism is still unknown.

 Emotionally stressful states are often manifested physiologically by an increase in

the endogenous release of catecholamines (epinephrine, norepinephrine, and
dopamine).

 Patients with bruxism have elevated levels of catecholamines in their urine in

comparison to patients without bruxism. But the majority of data about the
association between psychosocial disorders and bruxism come from studies that use
clinical or self-reporting to achieve their diagnosis as opposed to sleep laboratory
 One report studied bruxism as it relates A study by Restrepo et al.
to other factors such as aggression and
somatization (the process by which investigated the effectiveness of
psychological distress is expressed as
physical symptoms). The report psychological techniques in
indicated that an increased amount of children with bruxism. They used
aggression and somatization can already
be found in bruxing 5- and 6-year-olds different psychological techniques

including directed muscle

relaxation for 6 months in children

age 3 years to 6 years who had a

history of bruxism. They found that

Lobbezoo F, Naeije M. Bruxism is mainly regulated
centrally, not peripherally. J Oral Rehabil. 2001;28:1085- the psychological techniques used
1091)..
were effective in the reduction of
Effects of psychological techniques on bruxism in
children with primary teeth. JOralRehabil.2001;28:354- signs of bruxism in children with
360.
primary teeth.
 Bruxism is found in those who suffer from
post-traumatic stress disorder, further
suggesting that a psychological etiology
may be involved. A recent systematic
review by Manfredini et al (Role of
psychosocial factors in the etiology of
bruxism. J Orofac Pain. 2009;23:153-166). A case report by Antonio et al
concluded that while wake clenching
seems to be associated with psychological described two cases of children who
factors and a number of
had tooth wear attributed to bruxism.
psychopathological symptoms, there was
no evidence to support that these factors In both cases, the condition was
were implicated in sleep bruxism.
believed to be triggered by
psychological disturbances resulting
from harrowing experiences. Based
on the emotional problems of the
children, they were referred for
psychological monitoring.
RESPIRATORY FACTORS
 Bruxism and habitual snoring are closely related.

 Sleep bruxism is also a frequent complaint of parents of children who are mouth
breathers.

 One theory suggests there is a correlation between bruxism and upper airway
obstruction, with obstructive sleep apnea causing sleep bruxism. Bruxism does
appear to be more prevalent when sleeping in a supine position, which correlates
with a greater possibility of airway obstruction.

 A link has also been made between bruxism and tonsillar hypertrophy, which is
strongly correlated to upper airway obstruction. Adenotonsillectomy surgery has
been shown to improve bruxism in some children. Bruxism may also be caused by
allergic processes such as asthma and respiratory airway infection.

G J Lavinge et al.Bruxism physiology and pathology: an overview for clinicians. J Oral Rehabil.
2008;35:476-494.
 Other Pathophysiological
Factors

Pathophysiological factors implicated in bruxism among

adolescents include smoking, alcohol, illicit drugs, trauma,
disease, and medication. In addition, a host of diseases among
children have been linked to bruxism such as basal ganglia
infarction, cerebral palsy, Down syndrome, epilepsy,
Leigh disease, meningococcal septicemia, multiple
system atrophy, gastroesophageal reflux, and Rett
syndrome.
Tais de Souza Barbosa et al.Temporomandibular disorders and bruxism in childhood and
adolescence: Review of the literature. Int J Pediatr Otorhinolaryngol. 2008;72:299-314.)
Findings in sleep

In children between 5 and 18 years of age, 66% of SB episodes are associated with
electroencephalographics arousals; these occurs more than in stage 2 of non rapid eye
movement and rapid eye movement sleep.

A sequence of events preceding onset of an sleep bruxism episode has been defined in
adults but needs confirmation in children.

Incresed Incresed respiratory

Incresed sympathetic
electrocephalographi amplitude associated
activity 1 minute
c activity 4 seconds withtachycardia 1
before
before second before

Incresed
electromyographic Finally RMMA with or
activity of suprahyoid without tooth
muscles 0.8 secs grinding
before
Pharmacology and neurochemistry

Dopamine and norepineherine may play a role in pathophysiology

of adult Sb, but there role in children is unknown.

Children with attention-deficit-hyperactivity disorder(ADHD)who

are treated pharmacologically with central nervous system
stimulatants have a higher prevelance of bruxism(consider to be
secondary SB)than do children with untreated ADHD and control
children without SB.

C.C.Restrepo et al.Effects of psychological techniques on bruxism in children with primary

teeth. JOralRehabil.2001;28:354-360.)
Genetics and familial predisposition

 SB is a persistent trait: more than 86%of adults with SB report having been bruxuers
as children.

 No clear pattern f genetic transmission has been found.

 A study of twins showed that monozygotic twins(r=0.58) were more likely to be tooth
grinders than hetrozygotic twins(r=0.20).

 Another study showed that a child with one parent who exhibits bruxism is 1.8 times
more likely to be a bruxuer.

 Environmental factors are also critical in the development of SB, as shown in twin
study.

 Polymorphism is most likely genetic heritability pattern.

Symptoms and manifestations

0
Symptoms of bruxism.
•Anxiety, stress, and tension

•Depression

•Earache

•Eating disorders

•Headache

•Hot, cold, or sweet sensitivity in the teeth

•Insomnia

•Sore or painful jaw

MANIFESTATION
•The signs and symptoms of bruxism depend on:

• Frequency of bruxing

• Intensity

• Age of patient associated with duration of habit.

Clinical features

0
 Occlusal trauma: Resulting in mobility (more in the mornings).
Tooth structure: Results in nonfunctional occlusal wear; sensitivity; atypical
shiny wear facet with sharp edges; Pulpal exposure; # crown, restoration.

Muscular tenderness: Lateral pterygoid, masseter on palpation; fatigue on

waking, hypertrophy of masseter.

TMJ disturbances: Crepitation, clicking, restriction of mandible movement;

deviation of chin; pain ( dull , unilateral).

Headache : Muscular contraction type.

Other signs and symptoms: Sounds-(grinding and tapping);soft tissue
trauma ; small ulceration or ridging on buccal mucosa opposite the molar teeth.
Risk factors

0
 In a pilot sleep study with 10 children, 40% of the subjects scored high on attention
and behavioral problem checklists.

 Other studies have also reported that children with persistant bruxism presentd
with a trend toward a higher prevelance of ADHD.

 Children with other psychologic disorders are also at increased risk of bruxism.

AIRWAY PATENCY
 A significant increase in breathing amplitude occurs just prior to an SB episode,
suggesting that SB may help to reinstate airway patency in some patients.

 A relationship between SB and sleep disordered breathing has been reported

previously.

 In one study, 16 of 17 pediatric patients with SB were also snorers, according to

parental reports.

 children with nasal obstruction had a 65.2% prevalence of bruxism.

 In two pediatric studies in patients with sleep disorderd breathing, the pre4valance
of bruxism and tooth grinding decreased after tonsillectomy or adenotonsillectomy,
from 45.5% to 11.8%and from 25.7% to 7.1% respectively
various risk factors for SB have been
listed below

+++ solid
evidence
++ modest
evidence
+ low evidence
Diagnostic evaluation

0
• The diagnosis of SB is based on clinical interview, clinical
evaluation, and objective polysomnographic testing.

• The interview investigates the history of clenching and tooth

grinding . This history of SB is usually corroborated by a sibling or
by parents, who have heard grinding noise while patient is
sleeping.

• Parents who keep their bedroom door open report bruxism 1.7
times more often than who do not.

• The interview should include questions about medications used,

such as anti depressants or antipsychotic and recreational drug.

• Reported tooth fracture or increased tooth sensitivity can also be

associated with jaw clenching while awake and SB.

• Drooling during sleep and sleep talking are 1.7 and 1.6 times
respectively more likely to be associated with bruxism.
 The clinician must enquire about
concomitant jaw muscle pain,
temporomandibular dysfunction and
headaches.

The prevalence of bruxism is higher in

children with headaches(23.3%) than in
children without headaches(16.%).

Andrew T Cheifetz et al.Prevalence of bruxism and associated correlates in children as reported by

. parents. J Dent Child (Chic). 2005;72:67-73.)
The evaluation should include palpation of the
head and neck to rule out pain from either tmj
disorders or other joint pains, examination of the
buccal mucosa(tooth grooving or ridging inside
the cheek or on side of the toungue).

Assesment of salivary secretion( increased risk

for tooyh wear in the absence of saliva or when
salivation is low).
Examination of severity of tooth wear.

The presence of hypertrophied

masseteric muscles can be an indirect
sign of tooth clenching or grinding.
  To investigate and to confirm the presence of unusual oromandibular motor

Ambulatory activity during sleep, ambulatory recording or in- laboratory polysomnography

and sleep is helpful.
laboratory  Ambulatory recordings are made with portable EMG recording devices that can
monitoring be used while the patients sleeps at home.
 These ambulatory recordings are not SB specific and cannot confirm diagnosis
of SB in the absence of audio-video recording, because approximately 30% of
oromotor activities during sleep are not SB specific.

Scoring
 Methods and criteria for SB scoring have been develoved for and
adults but have severity
scale of
not been validated for children.
SB

It may be possible to revise adult criteria to make them applicable to

Management

0
 Management of primary
complaints of pediatric SB

Tooth
grinding noise
or tooth damage
and wear

Behavioral Dental
modification appliances
Behavioral modification
The parents and patients should be educated
about relaxation techniques and sleep hygiene.
This is also applicable in case of separation
anxiety( for eg. Gradual separation and a reward
system
Dental
appliance Dental appliances have only been studied in
adults, and lack of evidence prevents firm
and safe conclusions about their use in
children.
If oral appliances are worn, they should not
interfere with growth and development.
In adults, it was shown that with 4 weeks of
use the SB index returned to the baseline
level after the initial drop.
In the pediatric population, burden would
fall on the parents to maintain a higher
level of compliance by and oral hygine of
their child.
Occlusal splints and occlusal adjustments are usually sufficient
to correct habit.

Occlusal splints are indicated to reprogramme the existing

muscular pattern.

Soft splints are advisable with flat occlusal surfaces so that

mandibular movements will be free in all planes which breaks
the reflex response of muscles established during habit.
 Jaw muscle pain or headaches on
awakening

Refferal to a sleep specialist:

patient should be sent to specialist to
investigate the possibility of upper Medication history: the history
airway resistance syndrome or sleep should include a list of all medications
apnea. being used because some may
Children with migraine headaches exacerbate movements during sleep.
reportedly experience more sleep
disturbances, such as bruxism(29%)
and snoring(23%)

Medication: In adult population, Head posture: it has been

various muscle relaxants and reported that bruxuers have a more
botulinum toxins have been used in anterior and downward head tilt.
SB treatment management. The effect Another study suggest that cervical
and safety of these medications have spine muscle- joint dysfunction could
not been studied in children. be an etiology of pediatric SB.
CONCLUSION

1
 Pediatric SB is underdiagnosed in
The condition is also poorly managed
sleep medicine because of ‘parents
and clinicians’ limited knowledge of its 01 because of the lack of knowledge and
evidence about its risk factors,
characteristics and because of poor pathophysiology, and consequences.
interdisciplinary communication
among health care professionals.
02
At the present time,because of the
It is hoped that future research will paucity of studies supporting
determine that not all children with
SB and tooth grinding required
03 preventive or management
approaches, only children with
intervention. severe tooth malocclusion or damage
and those presenting with
04 concomitant medical problems are
actually directed to care.
 REFERENCES
1. Barbosa Tdc S, Miyakoda LS. Ppocztarux Rde L, Rocha CP, Gaviao mb.Tempomandibular disorders and bruxism in
childhood and adolescence:Review of literature. Int J Pediatr Otorhinolaryngol2008;72:299-314.

2. Lavinge Gj, Rompre PH, Poirier G, H uard H, Kato T, Montplaisir JY. Rhythmic masticatory muscle activity during sleep in
humans. J Dent Res 2001;80:443-448.
3. Prevalence of bruxism and associated correlates in children as reported by parents. J Dent Child (Chic). 2005;72:67-73.

4. Temporomandibular disorders and bruxism in childhood and adolescence: Review of the literature. Int J Pediatr
Otorhinolaryngol. 2008;72:299-314.

5. Bruxism physiology and pathology: an overview for clinicians. J Oral Rehabil.2008;35:476-494.

6. Lobbezoo F, Naeije M. Bruxism is mainly regulated centrally, not peripherally. J Oral Rehabil. 2001;28:1085-1091.

7. Bruxism physiology and pathology: an overview for clinicians. J Oral Rehabil. 2008;35:476-494 c
8.t emporomandibular disorders and bruxism in childhood and adolescence: Review of the
literature. Int J Pediatr Otorhinolaryngol. 2008;72:299-314.

9. Effects of psychological techniques on bruxism in children with primary teeth.

JOralRehabil.2001;28:354-360.)

10. Prevalence of bruxism and associated correlates in children as reported by parents. J

Dent Child (Chic). 2005;72:67-73.

11. Therapies most frequently used for the management of bruxism by a sample of
German dentists: Journal of Prosthet Dent (2011)105:194-202.

12.
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THANKYOU.