International Journal of Pediatric Otorhinolaryngology (2008) 72, 299314

www.elsevier.com/locate/ijporl

REVIEW ARTICLE

Temporomandibular disorders and bruxism in

childhood and adolescence: Review of the
literature
Tas de Souza Barbosa a, Luana Sayuri Miyakoda b,
Rafael de Liz Pocztaruk c, Camila Pinhata Rocha d,
o a,*
Maria Beatriz Duarte Gavia
a

Department of Pediatric Dentistry, Piracicaba Dental School, State University of Campinas,

Avenida Limeira 901, CEP 13414-903, Piracicaba, SP, Brazil
b
Piracicaba Dental School, State University of Campinas, Avenida Limeira 901, CEP 13414-903,
Piracicaba, SP, Brazil
c
Department of Prosthetic Dentistry, Dental School of Lutheran University of Brazil,
o Luis, CEP 92420-280, Caixa-Postal 124, Canoas, RS, Brazil
Rua Miguel Tostes 101, Sa
d
Department of Morphology, Piracicaba Dental School, State University of Campinas,
Avenida Limeira 901, CEP 13414-903, Piracicaba, SP, Brazil
Received 13 July 2007; received in revised form 14 November 2007; accepted 14 November 2007
Available online 3 January 2008

KEYWORDS
Temporomadibular
disorders;
Bruxism;
Children;
Adolescent;
Review

Summary
Objective: The aim of this article was to review the literature about temporomandibular disorders and bruxism and their relationships in children and adolescents.
Methods: The literature was searched using Medline, ISI, Cochrane Library, Scielo and
the Internet, from March 1970 to the end of June 2007. The inclusion criteria were:
they evaluated a possible association between TMD and bruxism, and they dealt with
child and/or adolescent samples. Furthermore, interim reports, related Internet sites
and chapters in textbooks were considered. From 64 records found, 30 fulfilled the
inclusion criteria.
Results: The prevalence of temporomandibular disorders in children and adolescent
varies widely in the literature. Temporomandibular disorders are often defined on the
basis of signs and symptoms, of which the most common are: temporomandibular joint
sounds, impaired movement of the mandible, limitation in mouth opening, preauricular pain, facial pain, headaches and jaw tenderness on function, having mainly a
mild character, fluctuation and progression to severe pain and dysfunction is rare. One
of the possible causal factors suggested that temporomandibular disorders in children

rea de
* Corresponding author at: Faculdade de Odontologia de Piracicaba/UNICAMP, Departamento de Odontologia Infantil, A
Odontopediatria, Av. Limeira 901, CEP 13414-903, Piracicaba, SP, Brazil. Tel.: +55 19 2106 5200/5368; fax: +55 19 2106 5218.
E-mail address: mbgaviao@fop.unicamp.br (M.B.D. Gavia
o).
0165-5876/$ see front matter # 2007 Elsevier Ireland Ltd. All rights reserved.
doi:10.1016/j.ijporl.2007.11.006

300

T.S. Barbosa et al.

is a functional mandibular overload variable, mainly bruxism. Bruxism, defined as the
habitual nonfunctional forceful contact between occlusal tooth surfaces, is involuntary, excessive grinding, clenching or rubbing of teeth during nonfunctional movements of the masticatory system. Its etiology is still controversial but the
multifactorial cause has been attributed, including pathophysiologic, psychologic
and morphologic factors. Moreover, in younger children, bruxism may be a consequence of the masticatory neuromuscular system immaturity. Complications include
dental attrition, headaches, temporomandibular disorders and masticatory muscle
soreness. Some studies have linked oral parafunctional habits to disturbances and
diseases of the temporomandibular joint, mainly bruxism, suggesting its association
with temporomandibular disorders in the primary and mixed dentition, whereas other
authors did not observed respective relationship in primary dentition. The unreliability for the clinical assessment of bruxism also reduces confidence in conclusions
about the relationship with temporomandibular disorders.
Conclusions: Taken all evidence together, the relationship between bruxism and
temporomandibular disorders, if it exists, seems to be controversial and unclear.
# 2007 Elsevier Ireland Ltd. All rights reserved.

Contents
1.
2.
3.
4.
5.
6.

Introduction . . . . . . . . . . . .
Materials and methods . . . . .
Temporomandibular disorders .
Bruxism . . . . . . . . . . . . . . .
Relationship between TMD and
Conclusions . . . . . . . . . . . .
References . . . . . . . . . . . . .

.........................
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bruxism in childhood and adolescence
.........................
.........................

1. Introduction
Temporomandibular disorders (TMD) are a generic
term for a number of clinical signs and symptoms
involving the masticatory muscles, the temporomandibular joint (TMJ) and associated structures
[1].
TMD have generally been presumed to be conditions affecting only adults; however, epidemiological studies have reported signs and symptoms in
children and adolescents to be as frequent as in
adults [2]. The most prevalent clinical signs of TMD
are TMJ sounds (upon palpation), limitation of mandibular movements, TMJ and muscle tenderness
[2,3]. Symptoms, such as headache, TMJ sounds,
bruxism, difficulty in opening the mouth, jaw pain
and facial pain have been reported [2].
One of the most controversial issues in clinical
dentistry is the etiology of TMD, since these disorders are considered a heterogeneous group of psycho-physiological disturbers [47], but the relative
importance of individual factors is still controversial.
Parafunctional habits, which are common in children as bruxism, nail biting, nonnutritive sucking
and others, are considered contributory factors for

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300
300
304
309
311
311
312

TMD manifestation [8,9]. Those that persist may

have deep effects on orofacial structures [9]. Bruxism is classified as a parafunction, because it does
not have a functional objective, such as mastication, phonation, or swallowing [10]. However, the
relationship between oral parafunctional habits and
TMD, if it exists, seems to be controversial and
unclear.
The purpose of this paper is to review the literature about TMD and bruxism and their relationship in
children and adolescents.

2. Materials and methods

The authors searched Medline, ISI, Cochrane Library
and Scielo computerized literature databases from
March 1970 to the end of June 2007, supplemented
by manual searching of reference lists from each
relevant paper identified.
The main search terms were temporomandibular disorders, signs and symptoms of temporomandibular disorders, bruxism, tooth
wear, child and adolescent. A total of 64
records were originally identified. Two reviewers
selected and reviewed the articles. First, each one

Prevalence (%) of signs and symptoms of temporomandibular disorders in children and adolescents in different ethnic groups

Reference First author

Sample size

Age (years) Country

[1]

Thilander (2002)

2371 boys; 2353 girls

517

Colombia

Headache

11.4

TMJ pain on palpation

4.1
Clicking
10
Locking
1.3
Luxation
0.4
Muscle pain on palpation 12.9
Maximal opening reduced 2.64
Opening deflection
9.5

[7]

Vanderas (2002)

161 boys; 153 girls

68

Greece

Headache
Opening difficulty
Opening pain
Reported clicking

7.01
4.46
21.66
4.14

TMJ sounds
TMJ tenderness
Muscle tenderness
Dysfunctional opening
Deviation

5.10
5.10
24.20
22.79
11.15

[8]

Sari (2002)

Mixed dentition;
80 girls; 102 boys

914

Turkey

Mixed dentition
Overall
TMJ pain
Restricted on opening
TMJ sound

67.58
29.67
9.89
18.13

Overall
Clicking
Popping
TMJ tenderness
Muscle tenderness

58.01
34.61
1.09
24.17
15.93

Permanent Dentition
TMJ pain

24.05 Clicking

29.71

9.90 Popping
16.03 TMJ tenderness
Muscle tenderness

0.94
19.81
18.86

Permanent dentition;
114 girls; 98 boys

Symptoms (%)

Restricted on opening
TMJ sound
[11]

Egermark (2001)

201 boys; 201 girls

715

Sweden

167 women; 153 men 1120

[14,15]

235 boys; 267 girls

37

Saudi Arabia

TMJ sounds

0
0
0
6
5
0
1
7
7.8

301

Alamoudi
(1998, 2001)

TMJ joint sounds

Jaw fatigue
Opening difficulty
Chewing pain or fatigue
in the jaws or face
TMJ sounds
Jaw fatigue
Opening difficulty
Chewing pain or fatigue
in the jaws or face

Signs (%)

Temporomandibular disorders and bruxism

Table 1

302

Table 1 (Continued )

Reference First author

Sample size

Age (years) Country

Symptoms (%)

Signs (%)

Muscle tenderness
TMJ pain during movement
Opening deviation
Restricted opening
[16]

Widmalm (1995)

113 boys; 90 girls

46

153 Caucasian

TMJ pain
Headache
50 AfricanAmerican Earache
Neck pain
USA
Chewing pain or tiredness
Problems in jaw opening
Ear noise

[17]

Castelo (2005)

58 boys; 41 girls

35

Brazil

Headache
Earache
Preauricular pain

[18]

Feteih (2006)

230 girls; 155 boys

[19]

Motegi (1992)

3219 boys; 4118 girls

Bonjardim (2005) 120 Female; 97Male

618

1218

Saudi Arabia

Headache
TMJ noise
Chewing pain
Opening difficulty
Jaw locking

Japan

Overall TMD symptoms

Sound
Pain (from opening and
closing the mouth,
chewing food, pain in TMJ
Abnormal jaw movement
(restricted opening, difficulty
opening and closing the mouth)

Brazil

Facial/jaw pain
Opening difficulty
TMJ sounds

8.4
16.7
2.5
4.9
25.4
12.9
19.6

Clicking
Crepitation
TMJ pain lateral
TMJ pain posterior
Masseter tenderness
Temporalis tenderness
Opening deviation
Restricted opening

7.07 Mandibular deviation

on opening
3.03 Occlusal interference
4.04 Asymmetric condylar
movement
TMJ sounds on opening
and closing
22
8.7
14
2.5
2.1

TMJ sounds
TMJ pain
Muscle tenderness
Restricted opening
Opening deviation

21.4
30.6
16.3
24.6
10.8
10.3
17.2
2.0
18.18
5.05
5.05
3.03
13.5
2.6
0.5
4.7
3.9
12.2
89.3
2.2

0.9

12.9 Opening click

3.22 Closing click
26.72 Condyle superior
region tenderness

19.80
14.70
10.60

T.S. Barbosa et al.

[20]

1216

6.77
2.6
3.99
1.79

Reference First author

Sample size

Age (years) Country

Symptoms (%)

Signs (%)

Teeth grinding

17.98 Condyle lateral

region tenderness i
21.65 Condyle dorsal
region tenderness

Headache
[39]

Farsi (2003)

942 boys; 1034 girls

315

Saudi Arabia

Overall
Chewing pain
Headache
Opening difficulty

24.2
11.1
13.6
2.1

Hearing TMJ noises

Jaw lock

4.5
2.5

Reference

First author

Sample size

Age (years)

Country

[41]

Kieser (1998)

150 bruxists;
126 after 5 years

69

South Africa

7.83
10.60

Overall
TMJ sounds
Muscle tenderness
TMJ tenderness
infrequently
Restricted opening
Deviation

20.7
11.8
1.5

5.3
2.8

Symptoms (%)

Baseline

5 years after

Earache
TMJ pain
Muscle tenderness
Restricted opening
Clicking - opening/closing
Pain in ear on chewing

32.12
60.3
55.5
37.9
33.3
33.2

12.7
38.0
41.1
19.0
51.3
12.7

Reference

First author

Sample size

Age (years)

Country

Age

10

15

19

[52]

Pahkala (2004)

48; 23 girls; 25 boys;

49 control 31 girls;
18 boys

719

Finland

Opening deviation

10

29

35

31

Muscle tenderness
TMJ tenderness
Clicking
Opening deviation
Muscle tenderness
TMJ tenderness
Clicking

15
2
8
16
14
2
8

29
10
19
31
25
10
14

17
0
6
27
16
0
6

21
0
13
31
14
0
16

First author

Sample size

Age (years)

Country

Symptoms (%)

[87]

Hirsch (2004, 2006)

525 female; 486 male

1018

Germany

TMD pain
Face; jaw; temple;
in front of the ear;
in the ear

RDC/TMD diagnosis
15
Overall

10

Disc displacement
with reduction

7.9

303

Reference

Temporomandibular disorders and bruxism

Table 1 (Continued )

T.S. Barbosa et al.

13

12
11
7

Jaw clicking

Jaw tenderness
Jaw pain
Limited opening

Caucasian;
African-American;
Hispanic; Asian
316
422 male 432 female
Cheifetz (2005)
[91]

Pain diagnosis

First author
Reference

Table 1 (Continued )

Sample size

Age (years)

Country

Symptoms (%)

RDC/TMD diagnosis

2.3

304

independently selected the articles from their abstracts and checked their contents. Next, they looked
for the articles without abstracts. A 100% of agreement was obtained between the two researchers.
The studies were eligible for review if they
matched the following inclusion criteria: (1) they
evaluated a possible association between TMD and
bruxism and (2) they dealt with child and/or adolescent samples. Furthermore, original papers,
interim reports, related Internet sites and chapters
in textbooks were also considered.
A consensus was reached regarding the articles
that actually fulfilled the inclusion criteria (30 articles), and were finally included in this review. A
summary of each selected article is presented in
Tables 1 and 2.

3. Temporomandibular disorders
TMD is a collective term embracing a number of
clinical problems that involve the masticatory musculature, the TMJ, or both [6]. Myofascial pain, disc
displacements, joint pain and degenerative and
inflammatory joint disease are the major subtypes.
In accordance with McNeill [6] some contributing
etiologic factors are only risk factors, others are
causal in nature and others result from, or are purely
coincidental to, the problem. These factors are
classified as predisposing, initiating or precipitating, and perpetuating to emphasize their role in the
progression of TMD. Structural, metabolic and/or
psychological conditions that adversely affect the
masticatory system sufficiently are considered predisposing factors since they can increase the risk of
developing TMD. Initiating factors that lead to the
onset of symptoms are primarily related to trauma
or repetitive adverse loading of the masticatory
system. Overt trauma producing injury to the head,
neck, or jaw can result from an impact injury,
possibly a flexion-extension injury, an injury while
eating, yawning, or even from prolonged mouth
opening during long dental appointments. A second
form of trauma is associated with the sustained and
repetitious adverse loading of the masticatory system as a result of parafunction [10]. Parafunction,
hormonal factors, or psychosocial factors are considered perpetuating factors since they can keep
going the patients disorder and may be associated
with any predisposing or initiating factor [5,6,10].
Epidemiologic studies have shown that signs and
symptoms of TMD can be found in all age groups
[1,11,12]. It is interesting to note that the incidence of signs and symptoms generally increased
with age [13]. The prevalence of TMD in children
and adolescent varies widely in the literature from

Reference First author

Bruxism signs and symptoms (%)

Association
TMD/bruxism

[1]

Thilander (2002) Dental wear (facets)

Primary Teeth
Permanent Teeth

< 25.3
< 36.1

, 20.7
, 34.3

Yes

[7,56]

Vanderas (2002)

Bruxism informed by parents/guardians

Clenching
Grinding Day or night

< 45.96
< 55.28

, 42.48
, 42.48

Yes

[8]

Sari (2002)

Bruxism informed by parents/guardians

Without TMD

< 24.24

, 26.92

Yes , permanent
dentition

With TMD
Without TMD
With TMD

< 24.63
< 9.09
< 12.96

, 25.92
, 11.11
, 23.18

[15]

Alamoudi (2001) Grinding day or night informed by parents With TMD symptom
With TMD signs

8.73
11.1

Yes

[16]

Widmalm (1995) Interview with the child

Bruxism + other parafunction

Only bruxism

20
3.4

Yes

[17]

Castelo (2005)

Bruxism informed by parents/guardians

Only TMD symptoms

Only TMD signs
Signs and symptoms

4
4
5

No

[18]

Feteih (2006)

Bruxism informed by parents/guardians

< 12,1

, 6,7

No

[39,43]

Farsi (2003)

Bruxism informed by parents/guardians

during the day and/or night

Primary (n = 268)

< 9.4

, 7.1

Not informed

Mixed (n = 317)
Permanent (n = 528)

< 10.7
< 12.5

, 7.3
, 6.5

Grinding or clenching

126 bruxists reexamined <, 11.3

after 5 years

[41]

Kieser (1998)

150 bruxists

Temporomandibular disorders and bruxism

Table 2 Prevalence (%) of bruxism in children and adolescents in different ethnic groups

No

Wear facets or
pathological abrasion
[67]

Laberge (2000)

Sleep bruxism informed by

parents/guardians

310 years old

19.2

11 years old
12 years old
13 years old

13.8
11.2
9.3

Not evaluated

Hirsch (2004)

Incisal tooth wear

TMD
Control

< 36
< 36

, 45
, 35

[91]

Cheifetz (2005)

Bruxism informed by parents/guardians

Overall

38

No

No

305

[87]

306
16% in children with primary dentition to 90% in
children with mixed dentition [11,1417]. The different prevalence could be partly related to the
fact that most signs and symptoms in young children
are characterized as mild and therefore harder to
detect, and severe dysfunction is rare [11]. Moreover, the large frequency ranges for signs and symptoms of TMD previously described in reviews and
meta-analysis are apparently based on very different samples (e.g., random vs. non-random, patient
vs. non-patient, different ages, age ranges, sample
size, ratio of gender distribution) and different
examination methods (e.g., category of variable,
method of data collection) [18]. It is tempting to
believe that the wide range of differences in the
prevalence of TMD is of racial origin [19]. However
other reports do not support this theory and differences in the prevalence of TMD do exist not only
between various populations but within samples of
the same population and of the same age [1]. The
found prevalence variability can be due to the
studies focusing largely on samples of patients
seeking treatment or because they were conducted
on convenience non-representative samples of the
population.
The role of gender in TMD is also extensively
discussed in literature. The gender difference in
signs and symptoms was small in childhood [12],
but from late adolescence, women have been
reported more symptoms and exhibited more clinical signs than men did (1.52 times more prevalent
in women than in men) [5]. Muscular disorders, as
lateral pterygoid muscle tenderness, showed
greater prevalence among girls [20], but this finding
must be interpreted carefully due to the low specificity of intra-oral muscle palpation, since the
discomfort or pain observed in response to palpation
of the lateral pterygoid area may be caused by
anatomical structures other than the lateral pterygoid muscle [21]. One contributing factor to this
gender difference might be that women have a
greater sensitivity to pain than men. This has been
shown in experiments both in animals and in humans
[22]. For Bonjardim et al. [20] the majority of the
symptoms in adolescents were mild, and girls were
more affected, probably due to the result of biologic
variables (e.g., hormonal characteristics), as
maturation in girls typically occurs earlier than in
boys.
At present, the etiology of TMD is considered
multifactorial, since there are many involved factors, as well as their influence, but the relative
importance of individual factors is still controversial. Possible causal factors include different structural parameters, psychosocial variables, acute
trauma, degenerative articular illness, immunolo-

T.S. Barbosa et al.

gical factors, occlusal interferences [12] and functional mandibular overload variables (e.g.,
parafunctional habits, grinding or bruxism, chewing
hyperactivity and muscular spasms) [23]. Furthermore, TMD patients exhibit a variety of psychological and behavioral characteristics, including
increased somatization, stress, anxiety and depression [4,6,24].
There is controversy as to the genetic contribution to the pathogenesis of TMD. Several reports
reveal a marked familial aggregation in the signs and
symptoms of TMD, while others do not. Michalowicz
et al. [25] tested the hypotheses that these signs
and symptoms, as well as oral parafunctional habits,
are substantially heritable evaluating 494 pairs of
reared-apart and reared-together monozygotic (MZ)
and dizygotic (DZ) twins. MZ were no more similar
than DZ for any outcome, suggesting that genetic
factors do not influence these traits in the population. Reared-together MZ twins were no more similar than reared-apart MZ twins, suggesting a
negligible effect of the family environment on these
outcomes. Matsuka et al. [26] demonstrated that
the MZ twins had a higher tendency of inter-twin
concordance than DZ twins in terms of jaw pain in
wide mouth opening, difficulty in mouth opening
and difficulty in mouth closing, while there was no
significant difference between the MZ and DZ concordance levels in other general health-related and
behavior-related items, except toothache. Liljestro
m et al. [27] observed no association between
childrens and mothers TMD signs, agreeing with
others [25,28]. Raphael et al. [28] strongly supported the conclusion that myofascial/TMD does
not run in families, nor do symptoms associated
with a broad range of TMDs. They observed also
that relatives of myofascial/TMD probands were not
at increased risk of other musculoskeletal disorders.
On the other hand, the screen of three 5-HTrelated genomic DNA polymorphisms in patients
diagnosed as TMD by chronic and localized myalgia
and tenderness to palpation allowed concluding that
the pathogenesis of TMD is thought to be significantly associated with serotonergic neuronal dysfunction, reporting a genetic linkage to TMD [29].
This result emphasizes the 5- HTsystem dysfunction
hypothesis when considering the etiology of the
disease, as found in other functional somatic syndromes [30].
In this way, considering the mentioned findings in
relation to genetic contribution to TMD, the possibility of a familial predisposition of occurrence of
TMD should not be excluded due to its multifactorial
etiology. For example, the co-occurrence of causative factors such as occlusal characteristics or psychological stress may not be present in children at

Temporomandibular disorders and bruxism

an early age in the same way as in mothers to form
an effective causal complex of TMD [27]. On the
other hand, environmental factors may be more
important than genetic factors regarding the occurrence of TMD, because pain experiences and behavior seem to aggregate in certain families [31]. In
this way there is a great tendency of the child to
learn the relatives behavior in relation to stress and
pain model.
TMD in children are also considered to have a
multifactorial etiology [7]. TMD are often defined on
the basis of following signs and symptoms: TMJ
sounds, impaired movement of the mandible, limitation in mouth opening, preauricular pain, facial
pain, headaches and jaw tenderness on function are
the signs and symptoms that have been most commonly reported [6,7,20,32]. Nonetheless, it is not
yet clear whether these represent normal variation,
preclinical features or manifestations of a disease
state [33]. Both signs and symptoms of TMD fluctuate. Despite the signs and symptoms of TMD can
lead to inflammatory disorders (painful), articular
disorders, as disk displacements (non-painful) and
muscular disorders, a small but clinically challenging population of children and adolescents become
chronic pain patients who report not only pain, but
also associated with emotional distress and disability [34].
The most frequent TMD sign is pain, usually localized in the muscles of mastication (muscular disorders), the preauricular area, and/or the TMJ
(inflammatory disorders). There was a tendency
for the occurrence of masticatory muscle tenderness in subjects with long face type of craniofacial
morphology [35,36]. In general, TMD signs and symptoms were seen in connection with an increasing
overjet and long face characteristic, but no particular trait can be considered predictive of dysfunction. Moreover, it is not possible to draw any firm
conclusions about the presence of any particular
craniofacial morphology in children with signs or
symptoms of TMD [35], as well in adolescents
[36]. In addition to pain, which is usually aggravated
by chewing and other jaw functions, patients with
TMD often have non-painful articular disorders, as
limited or asymmetric mandibular movements and
joint sounds that are commonly described as clicking, popping, grating, or crepitus [37].
The prevalence of TMJ sounds seems to be
increasing from primary to permanent dentition,
due to the longer duration of muscle tension among
older age groups, causing intracapsular changes and
consequently TMJ sounds [12,38,39]. The state of
development of the dentition in this series might
contribute to the relatively frequent occurrence of
TMJ sounds in mixed and permanent dentition [1].

307
The high frequencies of occlusal interferences and
occlusal instability during mixed and early permanent dentition support the previous assumption. On
the other hand, occlusal factors were only weakly
associated with TMD signs and symptoms, but a
lateral forced bite between the retruded contact
position and the intercuspal contact position and a
unilateral crossbite deserve further consideration as
possible local risk factors for development of TMD
[12]. Thus, non-painful articular disorders in children, such as clicking, can occur without disc displacement, due to a compression of articular fluids
during condyle translation, which results in pressure
and produces an audible clicking and a palpable shift
in the mandible, coincident with the sound, differing from adults. TMJ sounds in children can also be
due to the transitory incompatibility of the disc
contour originating from differential growth rates
and calcification. In this way, these factors could
explain the increased prevalence of TMJ sounds
found in several studies [19,32,40,65] (1992).
Nevertheless, certain authors do not necessarily
consider sound as a problem, but mostly as a risk
factor. On the other hand, the results of the different studies must be interpreted with caution, due to
the different methodologies applied. The methods
to diagnose TMJ sounds can determine overestimate
results, as the use of the stethoscope. Kritsineli and
Shim [42] reported high prevalence of TMJ sounds
using stethoscope, differing from others who diagnosed the sounds by digital palpation and by audibly
listening during opening and closure of the mouth
and by palpation [20,39,43]. Furthermore, the differences among studies could be due to the fact that
the incidence of signs and symptoms generally
increase and also fluctuate with age, as mentioned
above.
Reduced range of deviation movement can be
regarded as an important sign or symptom in the
diagnosis and treatment of TMD, despite it seems
that opening deviation movement appears rarely in
epidemiological studies [39,43]. Tuerlings and
Limme [40] found that mandibular deviation on
maximal opening presented a positive correlation
with TMJ sounds, which could be associated with a
lack of muscle co-ordination concerning the origin of
TMJ sounds in children. It is important to consider
that their sample was composed of subjects with
different types of malocclusion that could mislead
the result interpretation.
Diseased TMJ can lead to altered, mainly
decreased mandibular movement ranges [45,46].
Therefore, substantially reduced mandibular
motion can be a strong indicator of the presence
of TMD and helps to distinguish TMD patients from
non-TMD controls [47]. In a young male population

308
Celic et al. [48] found that there were statistically
significant differences in the range of mandibular
movements that separate asymptomatic subjects
from patients with muscle disorders and disc displacements with reduction. Conversely, Hirsch et al.
[49] showed that TMD have only a negligible influence on the jaw motion measurements, which was
supported by Szentpetery [50] et al. and Bonjardim
et al. [51]. The differences could be explained by
the sample characteristics, such as the population
not seeking for treatment, usually evaluated in
epidemiological studies, and sample with defined
TMD diagnosis. If it is not observed reduction in
mandibular movements, a non-painful TMD condition could be predominant. Furthermore, limitation
of jaw movement capacity can have other etiologic
factors, such as surgical procedures, inferring that
not all subjects who have limitations in their jaw
movement have TMD [49]. Age and gender influence
the normative values for jaw movement capacity,
but not by the presence of TMD, since it was
observed that a mouth opening was greater for girls
and increased with age [49].
Conversely, Vanderas [46] considered that, on an
individual basis, children with TMJ disorders could
have decrease in the size of mandibular movements;
thus, it is advisable, when recording a dysfunctional
movement, to measure the comfortable movement
that is not associated with pain and the maximal
movement that may be associated with pain.
Furthermore, if signs and symptoms of dysfunction
do not restrict the movements, the comfortable and
maximal movements can be the same and any difference between them should be considered dysfunctional. In accordance with Magnusson et al.
[12], intra-individual change in maximal mouth
opening is a valid parameter reflecting the functional status in the masticatory system, and even a
moderate reduction, on an individual basis, should
be noted, as this may indicate a need for intervention.
Since signs and symptoms of TMD obviously make
an early appearance, routine dental examination
should include their evaluation to identify patients
who should be observed more closely. Nevertheless,
signs and symptoms in growing individuals may be
due in part to growth changes [52]. In this phase
there are both local and central factors associated
from time to time with TMD development and the
prediction of single TMD signs for the development
of severe disorder later in life is unclear [52] and
rare, as already stated.
Psychosocial variables may play an important role
in adaptation to pain and eventual recovery. It has
been noted the association between anxiety/
depression and the number of symptoms in adoles-

T.S. Barbosa et al.

cents, suggesting that as the number of subjective
symptoms increases, the same happens with the
proportion of individuals presenting anxiety and
depression complaints [4,20]. TMD symptoms and
orofacial pain could have a psychosocial impact on
the adolescents quality of life, as is the case in
adult populations [53]. Although there is no consensus regarding the percentage of TMD patients in
who psychological factors play a role, it is clear that
such factors need to be taken into account, along
with structural indicators, to properly diagnose and
plan management strategies. The heterogeneity of
TMD disorders (pain diagnoses versus non-pain diagnoses, the presence/absence of structural changes
including degenerative changes in the temporomandibular joint) suggests that there may be associated
differences in patient-perceived impact [54].
The information regarding signs and symptoms of
TMD has been collected by a clinical examination
and a questionnaire in some studies [11,12,38],
while others have been used a clinical examination
and interview [16]. The advantage of the interview
method is the possibility to determine whether
subject understands a question or not, while the
advantage of the questionnaire is that the subject
can consider the question calmly or that parents can
help their children. On the other hand, the application of an anamnestic questionnaire for detecting
TMD symptoms has the advantage of to be easily
used by general practitioners or epidemiologists
[20].
Many papers point towards the need to have a
standardized classification for TMJ disorders signs
and symptoms, and the use of indices is an excellent
means to allow disease severity to be individually
classified in order to examine the incidence of such
problem in a specific population, measure the effectiveness of the therapies employed and study etiologic factors [3,24,35,55]. Moreover, specific indices
applied provide the possibility of objectively measuring the severity of TMD, using clearly defined
criteria, simple clinical methods and easy scoring.
Helkimos index [56] assess individually and in the
general population the prevalence and severity of
TMJ disorders in mandibular pain and occlusal
instability, thus providing an anamnestic and clinical
dysfunction index. This index can be appropriate to
really define subjects without any sign or symptom
of TMD, because signs of TMD must not be reported
by them, as well as clinical symptoms of TMD must
not be found in the clinical examination. Nowadays,
the research diagnostic criteria for temporomandibular disorders RDC/TMD [24] is the tool most used in
TMD researches and represents a multiaxial
approach, evaluating clinical aspects of TMD (Axis
I), as well as psychological and psychosocial factors

Temporomandibular disorders and bruxism

(Axis II). The RDC/TMD is an accepted and validated
diagnostic tool for epidemiological and clinical
research on TMD. Nonetheless, due to the case
definition in the RDC/TMD, Reimann et al. [54]
observed that not all subjects with signs and symptoms of TMD can be assigned a specific TMD diagnosis, and they suggested that the level of impaired
oral health-related quality of life (OHRQoL) could be
used to characterize the severity of TMD. The craniomandibular index (CMI) uses clearly defined criteria, simple clinical methods and easy scoring [57].
Recently, the operational definitions for CMI were
redesigned to conform precisely to those RDC/TMD
[24] resulting in a clinical evaluation protocol, the
temporomandibular index (TMI). Because the CMI/
TMI instruments include almost the same examination items as the RDC/TMD, the diagnostic outcomes
would be expected to be similar to those of RDC/
TMD [38]. To avoid using subjective and descriptive
reports in the assessment of the severity of TMD, CMI
is recommended as the clinical criteria.
Considering the literature reviewed, signs and
symptoms in childhood and adolescence have been
indicating mild disorders, but these findings do not
detract from the importance of early diagnosis to
provide proper growth and development of the
stomatognathic system [43]. Additionally the known
fluctuation in signs and symptoms of musculoskeletal disorders in a time-dependent context might
have been better addressed by carrying out
repeated clinical recordings.

4. Bruxism
Bruxism, defined as the habitual nonfunctional forceful contact between occlusal tooth surfaces [33],
is involuntary, excessive grinding, clenching or rubbing of teeth during nonfunctional movements of
the masticatory system [16].
Bruxism can occur during the day or night [58,59],
characterized in awake individuals, by voluntary or
semivoluntary jaw clenching (so-called awake bruxism) and, on rare occasions, by tooth gnashing and/
or grinding. During sleep bruxism, both clenching
and tooth grinding are observed [60]. Sleep bruxism
should be distinguished from the daytime-awake
bruxism that is mainly related to stress/anxiety
reactivity and expressed as a jaw muscle clenching
habit/tic [61]. Wake bruxism is very rare with
little or no sound during clenching rather than the
loud involuntary grinding that characterizes sleep
bruxism. Reported complications include dental
attrition, headaches, temporomandibular joint dysfunction and soreness of the masticatory muscles
[62]. Bruxism usually causes tooth wear as evi-

309
denced by wear facets that can range from mild
to severe and can be localized or found throughout
the dentition [63]. Other trauma to the dentition
and supporting tissues include thermal hypersensitivity, tooth hypermobility, injury to the periodontal
ligament and periodontium, hypercementosis, fractured cusps and pulpitis and pulpal necrosis [16].
Preliminary evidence suggests that juvenile bruxism
is a self-limiting condition that does not progress to
adult bruxism [41]. According to American Academy
of Sleep [64], dental damage with abnormal wear to
the teeth is the most frequent sign of the disorders.
Other complication is damage to the structures
surrounding the teeth can include recession and
inflammation of the gums and resorption of the
alveolar bone. Hypertrophy of the muscles of mastication can occur, and bruxism can be lead to
temporomandibular joint disorders, often associated with facial pain.
The prevalence of awake bruxism in the general
population is approximately 20%, while the prevalence of sleep bruxism is about 8% [64,65]. Complaints of tooth grinding occurring during sleep
decline over time, from 14% in children to 8% in
adults to 3% in patients over 60 years of age [65]. In
healthy infants, the age of onset of sleep bruxism is
about 1 year of age, soon after the eruption of the
primary incisors [64].
Reported prevalence in children ranges from 7%
to 15.1% [69] with girls apparently more frequently
affected [68]. Generally, patients clench their teeth
throughout the day and gnash and clench them
during sleep [68]. However, nocturnal bruxism is
more frequent; it varies with the individual and
has been related to emotional or physical stress
[63].
The etiology of bruxism is still controversial.
Many authors claim a multifactorial cause [69].
Three groups of etiologic factors can be distinguished. First, pathophysiologic factors may be
involved in the precipitation of bruxism. For example, it has been claimed that bruxism is part of an
arousal response, thus linking sleep-related bruxism
to the field of sleep disorders [70]. There is also
evidence that, in younger children, bruxism may be
a consequence of the immaturity of the masticatory
neuromuscular system [71]. Altered brain chemistry
(e.g., an asymmetric nigrostriatal dopaminergic
function) has been associated with bruxism as well
[69]. Other pathophysiologic factors that have been
implicated in bruxism in adolescents and adults are
the effects of cigarette smoking [72], alcohol, illicit
drugs, trauma, disease and medication [73]. Second, psychologic factors, such as stress and personality, have influence upon the pathophysiology of
bruxism. Lobbezoo et al. [69] considered that the

310
level of stress and personality type have been
included in the etiology of bruxism for many years.
However, the exact contribution of psychological
factors remains debatable, and they consider that
bruxism is mainly centrally, not peripherally
mediated. These findings have been previously
observed by Kampe et al. [66] who also demonstrated the presence of a higher level of anxiety
in a group of people with bruxism. Vanderas et al.
[7,74] have demonstrated that stress and anxiety
may be directly related to bruxism, as patients
showed a higher catecholamine level, generally
ascribed to emotional stress. Third, morphologic
factors (e.g., dental occlusion and anatomy of the
orofacial skeleton) are thought to be involved in the
etiology of bruxism. Occlusal discrepancies (e.g., a
slide between retruded contact position and intercuspal position), were historically considered the
most common cause of bruxism [75]. More recently,
the role of occlusion has been debated and contested [10,75] in part because it has been demonstrated that experimentally placed deflective
occlusal contacts do not elicit bruxism [77].
The involvement of the dopaminergic system has
also been reported to explain sleep bruxism, but
remains controversial since in most randomised
experimental trials with dopaminergic medications
the onset of sleep bruxism episodes is only slightly
reduced [61]. During wakefulness, dopamine has a
role in the execution of movement and in maintaining vigilance; during sleep the dopaminergic system
is probably minimally active at the exception of
brief period of arousal-related movements such as
periodic limb movements [78].
Since bruxism is common in the general population, it can be considered almost as normal behavior. It is when the patient has severe tooth damage,
the noise is sufficient to disturb the parents or bed
partners, sleep is disturbed or pain reported that it
becomes a pathological condition [73].
Several studies have indicated different techniques to record bruxism. One of them is the evaluation of the dental attrition, either from direct visual
observations in the mouth using ordinal scale [79],
from occlusal appliances [80] from dental study
casts [81], by digital image analyzer [82]. However,
it is very difficult to be sure if it is a consequence of a
parafunctional or a functional habit [69]. This is
especially so in the primary teeth as the occlusal
surfaces become ground physiologically the reliability of this technique is controversial. Therefore,
there is considerable controversy about the correlation between bruxism and tooth wear. Some authors
questioned the role of bruxism as a causal agent of
tooth wear [83] while others suggested that
increased tooth wear is related to parafunctional

T.S. Barbosa et al.

habits [84]. Pergamalian et al. [85] considered that
bruxism causes attrition but others have not found
this association [41,86]. The association between
severity of bruxism and tooth damage is not yet
established.
Another important point is the time needed for
the attrition of the teeth surface, so there is a
question of recording bruxism while the subjects
have only recently begun and bruxism may not show
signs of attrition. The same risk exists if bruxism has
disappeared but attrition is present [87]. Further,
dental wear can be caused by many factors other
than bruxism, such as acid regurgitation and salivary
and dietary factors, apart from occlusal parafunctions [88]. Some authors do not consider tooth wear
a reliable indicator of bruxism [89]. In addition, the
assessment of worn teeth cannot differentiate
between the different forms of bruxism (sleeprelated or daytime bruxism, recent or past bruxism)
[90].
Other method to record bruxism is the use of
questionnaires to obtain information by interviewing the children and evaluating the questionnaires
answered by the parents. As bruxism can appear
during sleep, the children are not aware of this habit
[59]. As a result, the occurrence of parafunction can
be under-reported [59]. Thus, obtaining data from
the parents is very important for the validity of the
studies in children and adolescents [91].
The measurements of masticatory muscle activity, by means of EMG in a sleep laboratory or in the
patients in their home, are another commonly used
technique to evaluate bruxism [10,65,92]. However,
this holds true only if audio and video recordings are
obtained in parallel with all-night polygraphic
recordings [92]. Such an experimental setup is
almost impossible using an ambulatory (home)
recording system, leaving the sleep laboratory as
an expensive and time-consuming alternative and
not appropriate for children.
The spectrum of bruxism management ranges
from patient/parent education, occlusal splints
and psychological techniques to medications [63].
For Cheifetz et al. [91] a child with a psychological
disorder had a 3.6 times greater likelihood of bruxism. If either parent had a history of bruxism, their
child was 1.8 times more likely to brux. Therapeutic
approaches can include occlusal adjustment of dentition, use of interocclusal appliances [93] behavior
modification [94] and pharmaceuticals [95]. A biteplate covering the occlusal surfaces of all teeth
should be used by patients suffering from bruxism
to prevent continuous abrasion [93]. Nonetheless,
there is controversy among clinicians over the treatment of children with bruxism, as considered by
Restrepo et al. [94], who demonstrated that several

Temporomandibular disorders and bruxism

psychological techniques have been efficacious in
reducing signs of bruxism when they were applied to
preschool children.
From this, it is a pressing need for the development of reliable standards for the clinical assessment of bruxism. Current levels of unreliability limit
the correct identification of those who may need
preventive treatment to preserve tooth structure
[83].
Considering the problems intrinsic in modern
society, bruxism is becoming an increasingly common condition in children. In treating this parafunctional habit, clinicians play a leading role in
determining possible etiological factors. In many
situations, it is the dentists task to warn parents
and institute multidisciplinary treatment [71].
Nonetheless, it should be borne in mind that there
is still a lack of agreement about the definition of
bruxism, which makes it sometimes difficult to
unequivocally interpret the available evidence,
agreeing with Lobezzo et al. [69].

5. Relationship between TMD and

bruxism in childhood and adolescence
The relationship between TMD and bruxism in
childhood and adolescence is controversial. Bruxism was not considered related to signs and symptoms of TMD in young children [17,42], but it was
suggested that the prevention of parafunctions in
early childhood could help to decrease TMD problems related to parafunctional habits [42,43].
Juvenile bruxing was also considered a self-limiting
condition that does not progress to adult bruxism
and appeared to be unrelated to TMJ symptoms
[41]. Anterior tooth wear was not associated with
self-reported TMD pain in 10- to 18-year-old subjects as well [86].
Conversely, Alamoudi [15] verified in preschool
children significant relationship between attrition,
symptoms of TMD and deviation on opening. Widmalm et al. [16] reported a significant association
between bruxism and most of the TMD signs and
symptoms in same age children, but clinical examination and interview were carried out without the
parents. If information is obtained by interviewing
the children and evaluating the questionnaires
answered by the parents the validity of the study
can be more reliable [17].
Vanderas [59], using other methodology, found
also statistically significant correlation between
TMD and oral parafunction, such as grinding, clenching and lip/cheek biting in children classified as calm
who did not experience unpleasant life events.
Moreover, Magnusson et al. [96] stated that the

311
positive correlation found in their study, which
included up to three evaluations during a 10-year
period in children and adolescents, indicates the
existence of a causal relationship between parafunctions and signs of TMD.
According to Widmalm et al. [16] of the 10 pain
variables experienced by preschool children, eight
were significantly associated with bruxism, three
with thumb sucking and two with nail biting. Association does not, however, tell if a parafunction is
the cause or the consequence of pain or if a third
factor is causing both pain and increased prevalence
of oral parafunctions.
As bruxism may occur during sleep a careful
interpretation about the findings of many studies
should be considered, which might overestimate the
relationship between bruxism and TMD in children.
The unreliability for the clinical assessment of bruxism also reduces confidence in conclusions about its
relationship with TMD, to the extent that such conclusions are based on clinical assessments of bruxism, such as tooth wear, which can be a chronic
problem. The parafunctional activity that caused
tooth wear could have occurred several months or
years previously [86]. Thus, it is possible to infer
that no association between chronic parafunctional
activity and TMD pain could occur, but is possible to
consider an association between recent grinding and
TMD pain which has probably not yet led to detectable tooth wear [86].

6. Conclusions
Based on the evidences reviewed above, it seems
that TMD etiology is considered multifactorial and
still controversial. Many studies have demonstrated
an association between bruxism and symptoms and
signs of TMD in children and adolescents, whereas
other authors did not. Moreover, the unreliability for
the clinical assessment of bruxism also reduces
confidence in conclusions about their relationship.
In agreement with the findings found in the literature bruxism in children and adolescent could be
associated with muscular disorders, but it was perceived little evidence about the respective association with non-painful articular disorders, as disk
displacements and joint pathologies. Different diagnosis criteria for both TMD signs and symptoms and
bruxism have been factors of influence on result
comparison that it is difficult to reach reliable
evidences. Further, the studies should be interpreted with caution, because causality is extremely
difficult to establish. In short, the relationship
between bruxism and TMD seems to be controversial
and unclear, at least until nowadays.

312

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