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

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1 International Journal of Pediatric Otorhinolaryngology (2008) 72, REVIEW ARTICLE Temporomandibular disorders and bruxism in childhood and adolescence: Review of the literature Taís de Souza Barbosa a, Luana Sayuri Miyakoda b, Rafael de Liz Pocztaruk c, Camila Pinhata Rocha d, Maria Beatriz Duarte Gavião a, * a Department of Pediatric Dentistry, Piracicaba Dental School, State University of Campinas, Avenida Limeira 901, CEP , Piracicaba, SP, Brazil b Piracicaba Dental School, State University of Campinas, Avenida Limeira 901, CEP , Piracicaba, SP, Brazil c Department of Prosthetic Dentistry, Dental School of Lutheran University of Brazil, Rua Miguel Tostes 101, São Luis, CEP , Caixa-Postal 124, Canoas, RS, Brazil d Department of Morphology, Piracicaba Dental School, State University of Campinas, Avenida Limeira 901, CEP , 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 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 * Corresponding author at: Faculdade de Odontologia de Piracicaba/UNICAMP, Departamento de Odontologia Infantil, Área de Odontopediatria, Av. Limeira 901, CEP , Piracicaba, SP, Brazil. Tel.: /5368; fax: address: mbgaviao@fop.unicamp.br (M.B.D. Gavião) /$ see front matter # 2007 Elsevier Ireland Ltd. All rights reserved. doi: /j.ijporl

2 300 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. Introduction Materials and methods Temporomandibular disorders Bruxism Relationship between TMD and bruxism in childhood and adolescence Conclusions References 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 [4 7], 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 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

3 Table 1 Prevalence (%) of signs and symptoms of temporomandibular disorders in children and adolescents in different ethnic groups Reference First author Sample size Age (years) Country Symptoms (%) Signs (%) [1] Thilander (2002) 2371 boys; 2353 girls 5 17 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 6 8 Greece Headache 7.01 TMJ sounds 5.10 Opening difficulty 4.46 TMJ tenderness 5.10 Opening pain Muscle tenderness Reported clicking 4.14 Dysfunctional opening Deviation [8] Sari (2002) Mixed dentition; 80 girls; 102 boys Permanent dentition; 114 girls; 98 boys 9 14 Turkey Mixed dentition Overall Overall TMJ pain Clicking Restricted on opening 9.89 Popping 1.09 TMJ sound TMJ tenderness Muscle tenderness Permanent Dentition TMJ pain Clicking Restricted on opening 9.90 Popping 0.94 TMJ sound TMJ tenderness Muscle tenderness [11] Egermark (2001) 201 boys; 201 girls 7 15 Sweden TMJ joint sounds 0 Jaw fatigue 0 Opening difficulty 0 Chewing pain or fatigue 6 in the jaws or face 167 women; 153 men TMJ sounds 5 Jaw fatigue 0 Opening difficulty 1 Chewing pain or fatigue in the jaws or face 7 [14,15] Alamoudi (1998, 2001) 235 boys; 267 girls 3 7 Saudi Arabia TMJ sounds 7.8 Temporomandibular disorders and bruxism 301

4 Table 1 (Continued ) Reference First author Sample size Age (years) Country Symptoms (%) Signs (%) Muscle tenderness 6.77 TMJ pain during movement 2.6 Opening deviation 3.99 Restricted opening 1.79 [16] Widmalm (1995) 113 boys; 90 girls Caucasian TMJ pain 8.4 Clicking 21.4 Headache 16.7 Crepitation African American Earache 2.5 TMJ pain lateral 16.3 Neck pain 4.9 TMJ pain posterior 24.6 USA Chewing pain or tiredness 25.4 Masseter tenderness 10.8 Problems in jaw opening 12.9 Temporalis tenderness 10.3 Ear noise 19.6 Opening deviation 17.2 Restricted opening 2.0 [17] Castelo (2005) 58 boys; 41 girls 3 5 Brazil Headache 7.07 Mandibular deviation on opening Earache 3.03 Occlusal interference 5.05 Preauricular pain 4.04 Asymmetric condylar 5.05 movement TMJ sounds on opening and closing 3.03 [18] Feteih (2006) 230 girls; 155 boys Saudi Arabia Headache 22 TMJ sounds 13.5 TMJ noise 8.7 TMJ pain 2.6 Chewing pain 14 Muscle tenderness 0.5 Opening difficulty 2.5 Restricted opening 4.7 Jaw locking 2.1 Opening deviation 3.9 [19] Motegi (1992) 3219 boys; 4118 girls 6 18 Japan Overall TMD symptoms 12.2 Sound 89.3 Pain (from opening and 2.2 closing the mouth, chewing food, pain in TMJ Abnormal jaw movement (restricted opening, difficulty opening and closing the mouth) 0.9 [20] Bonjardim (2005) 120 Female; 97Male Brazil Facial/jaw pain 12.9 Opening click Opening difficulty 3.22 Closing click TMJ sounds Condyle superior region tenderness T.S. Barbosa et al.

5 Table 1 (Continued ) Reference First author Sample size Age (years) Country Symptoms (%) Signs (%) Teeth grinding Condyle lateral region tenderness i Headache Condyle dorsal region tenderness [39] Farsi (2003) 942 boys; 1034 girls 3 15 Saudi Arabia Overall 24.2 Overall 20.7 Chewing pain 11.1 TMJ sounds 11.8 Headache 13.6 Muscle tenderness 1.5 Opening difficulty 2.1 TMJ tenderness infrequently Hearing TMJ noises 4.5 Restricted opening 5.3 Jaw lock 2.5 Deviation 2.8 Reference First author Sample size Age (years) Country Symptoms (%) Baseline 5 years after [41] Kieser (1998) 150 bruxists; 126 after 5 years 6 9 South Africa Earache TMJ pain Muscle tenderness Restricted opening Clicking - opening/closing Pain in ear on chewing Reference First author Sample size Age (years) Country Age [52] Pahkala (2004) 48; 23 girls; 25 boys; 49 control 31 girls; 18 boys Finland Opening deviation Muscle tenderness TMJ tenderness Clicking Opening deviation Muscle tenderness TMJ tenderness Clicking Reference First author Sample size Age (years) Country Symptoms (%) RDC/TMD diagnosis [87] Hirsch (2004, 2006) 525 female; 486 male Germany TMD pain 15 Face; jaw; temple; in front of the ear; in the ear Overall 10 Disc displacement with reduction 7.9 Temporomandibular disorders and bruxism 303

6 304 T.S. Barbosa et al. Table 1 (Continued ) Reference First author Sample size Age (years) Country Symptoms (%) RDC/TMD diagnosis Pain diagnosis 2.3 Jaw clicking 13 [91] Cheifetz (2005) 422 male 432 female 3 16 Caucasian; African-American; Hispanic; Asian Jaw tenderness 12 Jaw pain 11 Limited opening 7 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 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 patient s 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]. Itisinterestingtonotethattheincidence of signs and symptoms generally increased with age [13]. TheprevalenceofTMDinchildren and adolescent varies widely in the literature from

7 Table 2 Prevalence (%) of bruxism in children and adolescents in different ethnic groups Reference First author Bruxism signs and symptoms (%) Association TMD/bruxism [1] Thilander (2002) Dental wear (facets) Primary Teeth < 25.3, 20.7 Yes Permanent Teeth < 36.1, 34.3 [7,56] Vanderas (2002) Bruxism informed by parents/guardians Clenching < 45.96, Yes Grinding Day or night < 55.28, [8] Sari (2002) Bruxism informed by parents/guardians Without TMD < 24.24, Yes, permanent dentition With TMD < 24.63, Without TMD < 9.09, With TMD < 12.96, [15] Alamoudi (2001) Grinding day or night informed by parents With TMD symptom 8.73 Yes With TMD signs 11.1 [16] Widmalm (1995) Interview with the child Bruxism + other parafunction 20 Yes Only bruxism 3.4 [17] Castelo (2005) Bruxism informed by parents/guardians Only TMD symptoms 4 No Only TMD signs 4 Signs and symptoms 5 [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) < 10.7, 7.3 Permanent (n = 528) < 12.5, 6.5 [41] Kieser (1998) 150 bruxists Grinding or clenching 126 bruxists reexamined after 5 years Wear facets or pathological abrasion [67] Laberge (2000) Sleep bruxism informed by parents/guardians <, 11.3 No 3 10 years old 19.2 Not evaluated 11 years old years old years old 9.3 [87] Hirsch (2004) Incisal tooth wear TMD < 36, 45 No Control < 36, 35 [91] Cheifetz (2005) Bruxism informed by parents/guardians Overall 38 No Temporomandibular disorders and bruxism 305

8 306 T.S. Barbosa et al. 16% in children with primary dentition to 90% in children with mixed dentition [11,14 17]. 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]. Itistemptingto 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 (1.5 2 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, immunological 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. Liljeström et al. [27] observed no association between children s and mother s 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

9 Temporomandibular disorders and bruxism 307 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 relative s 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]. 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

10 308 T.S. Barbosa et al. 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 adolescents, 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 adolescent s 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. Helkimo s 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

11 Temporomandibular disorders and bruxism 309 (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, Reißmann 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 evidenced 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

12 310 T.S. Barbosa et al. 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 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

13 Temporomandibular disorders and bruxism 311 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 dentist s 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], butitwas 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]. Anteriortoothwearwasnotassociatedwith 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 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.

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