Journal of

Oral Rehabilitation

Journal of Oral Rehabilitation 2012 39; 489501

Review Article

Are bruxism and the bite causally related?

F . L O B B E Z O O * , J . A H L B E R G , D . M A N F R E D I N I & E . W I N O C U R
*Department of Oral Kinesiology, Academic Centre for Dentistry Amsterdam (ACTA), Research Institute MOVE, University of Amsterdam and VU University Amsterdam, The Netherlands, Department of Stomatognathic Physiology and Prosthetic Dentistry, Institute of Dentistry, University of Helsinki, Finland, Department of Maxillofacial Surgery, TMD Clinic, University of Padova, Italy and Department of Oral Rehabilitation, The Maurice and Gabriela Goldschleger School of Dentistry, University of Tel Aviv, Tel Aviv, Israel

SUMMARY In the dental profession, the belief that bruxism and dental (mal-)occlusion (the bite) are causally related is widespread. The aim of this review was to critically assess the available literature on this topic. A PubMed search of the Englishlanguage literature, using the query Bruxism [Majr] AND (Dental Occlusion [Majr] OR Malocclusion [Majr]), yielded 93 articles, of which 46 papers were nally included in the present review*. Part of the included publications dealt with the possible associations between bruxism and aspects of occlusion, from which it was concluded that neither for occlusal interferences nor for factors related to the anatomy of the oro-facial skeleton, there is any evidence available that they are involved in the aetiology of bruxism. Instead, there is a growing awareness of other factors (viz. psychosocial and behavioural ones) being impor-

tant in the aetiology of bruxism. Another part of the included papers assessed the possible mediating role of occlusion between bruxism and its purported consequences (e.g. tooth wear, loss of periodontal tissues, and temporomandibular pain and dysfunction). Even though most dentists agree that bruxism may have several adverse effects on the masticatory system, for none of these purported adverse effects, evidence for a mediating role of occlusion and articulation has been found to date. Hence, based on this review, it should be concluded that to date, there is no evidence whatsoever for a causal relationship between bruxism and the bite. KEYWORDS: bruxism, aetiology, occlusion, articulation, review Accepted for publication 18 January 2012

Introduction
The relationship between bruxism and the bite is one of the topics in dentistry that has received much attention but has remained poorly understood. Bearing in mind, bruxism was commonly thought to be causally related to deviations in dental occlusion and articulation, and many generations of dentists have been educated on the ins and outs of the bite using textbooks such as Occlusion by Ramfjord and Ash (1). In the book of Ramfjord and Ash (1), a dual aetiology for bruxism is presented that includes both stress and occlusal interferences, but in which it is also stated that to eliminate
Based on a presentation at CORE China 2011. 2012 Blackwell Publishing Ltd

bruxism, the dentist should either lower the threshold for neuromuscular irritability so that the patients occlusal interference does not trigger bruxism, or remove enough occlusal interference so that the irritability may be tolerated by the patients neuromuscular system. As a consequence, for many decades, the treatment of bruxism was therefore focused on reshaping the bite as to achieving an occlusion and articulation that were free of deviations and interferences. Despite the large efforts to optimise occlusal treatments, however, the dental profession continued to struggle with the effective management of bruxism, thus opening up the minds of dentists for the possibility of other factors playing an important role in the aetiology of bruxism. For example, psychosocial factors like stress,
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depression, anxiety and certain personality traits received increasing attention, while more recently, pathophysiological factors such as alcohol abuse, heavy smoking, use of certain medicines and drugs, presence of certain pathologies, and genetic factors were suggested to be associated with bruxism. Nevertheless, in the dental profession especially, but also among bruxism patients, the belief that bruxism and dental occlusion are causally related is still widespread. Therefore, the aim of this literature review was to critically assess the available literature on this topic as to accepting or rejecting the hypothesis that bruxism and dental (mal)occlusion are causally related. It is hoped that this will contribute to more clarity in this largely controversial relationship. The review will be preceded by brief introductions to bruxism and the bite. published the American Academy of Orofacial Pain (4), bruxism is dened as a diurnal or nocturnal parafunctional activity including clenching, bracing, gnashing, and grinding of the teeth. While the sleepwake state of the condition is part of this denition, it should be noted that the use of sleep and awake is to be preferred over nocturnal and diurnal. Further, while clenching and grinding are commonly known phenomena, gnashing is not dened in the Guideline, while bracing is confusingly dened as clenching. For sleep bruxism, the ICSD-2 denition is to be preferred because of its unequivocal and operational nature, while for awake bruxism, such denition is still lacking. Below, whenever possible, it will be indicated specically whether sleep and or awake bruxism was the topic of the paper being discussed. When the sleep wake state while bruxing is unknown, the term bruxism will be used without a circadian adjective.

Bruxism
During the past couple of years, several comprehensive reviews on bruxism-related topics have been published in the dental literature. In this paragraph, some important facts will be outlined that are relevant for a proper understanding of this review.

Epidemiology With rates varying between 6% and 91%, there is a great variability in the reported prevalence of bruxism (5, 6). These differences can be attributed to (i) the bruxism types studied (unspecied, sleep, awake); (ii) the applied diagnostic methodology (e.g. questionnaires, oral history, clinical examination); (iii) the presence or absence of comorbidities (e.g. anxiety, TMD oro-facial pain, cerebral palsy); and (iv) the characteristics of the study population (e.g. children, adults, general population, patient populations). There are only a few large-scale general population studies available on this topic. Lavigne and Montplaisir (7) and Ohayon et al. (8) report a prevalence of self-reported sleep bruxism of approximately 8% in the general adult population, in women and men alike. This prevalence is higher in teenagers, especially in girls (9), higher in young adults (18 29 years) (7, 10) and lower in the elderly (over 65 years) (7). The only available systematic review of epidemiological bruxism data obtained from adult populations (unpublished data) revealed a prevalence of 186% for bruxism, 159% for sleep bruxism and 238% for awake bruxism. Based on the above, it is clear that both sleep bruxism and awake bruxism are common conditions (11).

Denitions In the literature, several denitions for bruxism can be found. First, in The Glossary of Prosthodontic Terms (2), bruxism is dened as the parafunctional grinding of the teeth and as an oral habit consisting of involuntary rhythmic or spasmodic non-functional gnashing, grinding or clenching of the teeth, in other than chewing movements of the mandible, which may lead to occlusal trauma. This denition is commonly used by dental professionals. Its main drawback is the fact that there is no link to the sleepwake state of the condition. Second, in the second edition of the International Classication of Sleep Disorders (ICSD-2) (3), sleep bruxism is listed among the sleep-related movement disorders (previously, among the parasomnias). Sleep bruxism is dened as an oral parafunction characterized by grinding or clenching of the teeth during sleep that is associated with an excessive (intense) sleep arousal activity. This denition is used for research purposes and by sleep medicine clinicians. Its operationalisation requires polysomnography (ambulatory or sleep laboratory, including audio and or video). Third, in the fourth edition of the Orofacial Pain Guidelines,

Aetiology For the determination of risk factors, longitudinal studies are needed and for risk indicators, cross-sectional
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studies. Because as yet there are hardly any longitudinal studies available, the aetiological factors for bruxism in the current literature are mostly risk indicators. Two comprehensive reviews have been published on this topic during the past decade (12, 13). Therefore, only a brief summary will be given here. In the past, the focus was on peripheral factors, viz. morphologic factors such as anatomy and occlusion. This is the topic of the present review. Nowadays, the focus is mainly on central factors, like psychosocial factors (e.g. stress) (14, 15), physiological biological factors (e.g. neurochemicals (1618) and genetics (19)) and exogenous factors (e.g. smoking) (20). The general conclusion of both previous reviews is that bruxism is mainly regulated centrally, not peripherally. However, by means of PSG, one obtains the number of bruxism events per hour of sleep, while EMG only provides the researcher or clinician with the number of jaw-muscle activities per hour. It should be stressed that EMG and PSG are only indicated when the consequences of bruxism are severe and or its treatment fails.

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Consequences Bruxism has several purported consequences, which may be different for the different types of bruxism (viz. sleep and awake). Possible consequences include jawmuscle hypertrophy; tooth wear (especially attrition); fracture or failure of teeth, restorations or implants; sensitivity or pain of teeth, muscles or joints; and temporomandibular joint disc displacements (6). These purported consequences of bruxism should be differentiated from other pathologies, such as parotid gland pathologies from jaw-muscle hypertrophy; abrasion and erosion from attrition; dental or periodontal pathologies, material-related causes and iatrogenic causes from bruxism-related fractures or failures; dental or periodontal pathologies and non-musculoskeletalrelated oro-facial pain from bruxism-related sensitivity or pain; and symptomatic hypermobility from bruxismrelated disc displacements.

Diagnosis To diagnose bruxism, several approaches can be used, viz. questionnaires, an oral history, inspection, a functional examination and additional tools. Questionnaires can be used to collect information on bruxism, its possible causes and its possible consequences. In daily practice, it is useful when they are completed prior to the rst consultation, so that the dentist better knows what to expect and the patient has an improved awareness of the ins and outs of bruxism. An example of a questionnaire that deals with aspects of bruxism and that is useful for research as well as for clinical purposes can be found in the study of van der Meulen et al. (21). In the clinic, even when questionnaires were completed in advance, it is important to always ask the patient about bruxism, including its causes and consequences. Extra-oral inspection in relation to bruxism mainly concerns jaw-muscle hypertrophy, while intra-oral inspection focuses on hyperkeratosis of the oral mucosa [e.g. white lines (linea alba) in the cheeks, and impressions of the teeth in the tongue or lips], tooth wear (22, 23), and tooth or implant fracture (24, 25). The aim of performing a functional examination of the masticatory system is to determine the presence or absence of a temporomandibular pain. To conrm the presence of such pain, one should rely on positive dynamic static tests and for its absence, on negative palpation tests (26). Finally, as additional diagnostic tools for bruxism, electromyography (EMG) or polysomnography (PSG) may be used. While EMG is relatively cheap and has a more or less high availability, PSG is characterised by high costs and a low availability.
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Management The management of bruxism is only indicated when the disorder causes any one of the possible consequences. As reviewed extensively by Lobbezoo et al. (27), there is not yet enough evidence for a safe and effective behavioural, orthopaedic or pharmacological management of bruxism. Therefore, in the absence of denitive evidence, these authors recommended the use of the so-called triple-P approach: Pep talk (i.e. counselling), Plates (i.e. occlusal stabilisation splints, which, in the absence of evidence for their efcacy, are useful protectors against dental wear) and Pills (i.e. medication) the latter option to be used only when the other two strategies have failed.

The bite
In the following sections, many terms will be used describing various aspects of dental occlusion and articulation. As to avoid confusion about these terms

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denitions, all terms that appear in this review are explained in Table 1 in alphabetical order. Most denitions have been derived from The Glossary of Prosthodontic Terms (2); some have been derived from De Leeuw (4). were excluded from this review, because they dealt with various diagnostic techniques for (mostly sleeprelated) bruxism (six papers), with non-occlusal management strategies for bruxism (ve papers), with conscious jaw-muscle activities in bruxism patients (10 papers), with the restoration and its possible adverse effect of bruxism-related tooth wear (two papers), with the evolutionary aspects of bruxism-related tooth wear (one paper), with the role of occlusal factors (and of bruxism) in temporomandibular disorders (six papers) and with the effects of bruxism and tooth wear on the maximal voluntary bite force (three papers). Exclusion was based on four separate assessments of the 79 articles by each of this reviews authors. Consensus was reached on the minor discrepancies between these assessments via email discussions. The 46 remaining papers (indicated with an asterisk in the reference list) were supplemented with articles from the reference lists of the included papers and from the authors personal collections.

Methods
On 17 June 2010, a literature search was performed in the U.S. National Library of Medicines database PubMed, using the following query: Bruxism [Majr] AND (Dental Occlusion [Majr] OR Malocclusion [Majr]). The search, which was limited to the English language, yielded 93 papers, nine of which were reviews. The oldest paper among the 93 articles was published in 1965. Because of the relatively limited number of papers, it was decided to retrieve all of them as full texts. This was possible for 79 papers. The other 14 papers could not be traced and were thus not taken into further consideration. Of the 79 retrieved articles, 33

Table 1. Denitions of terms describing various aspects of dental occlusion and articulation Term Angle class I relationship (neutro-occlusion) Denition

The dental relationship in which there is normal anteroposterior relationship of the jaws, as indicated by correct interdigitation of maxillary and mandibular molars, but with crowding and rotation of teeth elsewhere, i.e. a dental dysplasia or arch length deciency (2) Angle class II relationship (disto-occlusion) The dental relationship in which the mandibular dental arch is posterior to the maxillary dental arch in one or both lateral segments; the mandibular rst molar is distal to the maxillary rst molar (2) Angle class III relationship (mesio-occlusion) The dental relationship in which the mandibular arch is anterior to the maxillary arch in one or both lateral segments; the mandibular rst molar is mesial to the maxillary rst molar (2) Anterior deep bite Excessive vertical overlap of the incisal edges of the maxillary incisors to the mandibular incisors when the teeth are in maximum intercuspation (2) Articulation The static and dynamic contact relationship between the occlusal surfaces of the teeth during function (2) Interference Any tooth contacts that interfere with, or hinder, harmonious mandibular movement (2) Laterotrusive (working) side The side towards which the mandible moves in a lateral excursion (2) Malocclusion Any deviation from a normal occlusion (2). Rather than malocclusion, De Leeuw (4) uses the term occlusal variation, i.e. unusual biological or functional relationship between the maxillary and mandibular teeth Maximal intercuspal position The complete intercuspation of the opposing teeth, independent of condylar position (2) Mediotrusive (non-working; balancing) side That side of the mandible that moves towards the median line in a lateral excursion (2) Occlusion The static relationship between the incising or masticating surfaces of the maxillary or mandibular teeth or tooth analogues (2) Premature contact (prematurity) A contact that displaces a tooth, diverts the mandible from its intended movement or displaces a removable denture from its basal seat (2) Retruded contact position Point of initial tooth contact when the condyles are guided along the posterior slope of the eminence into their most superior position on jaw closure (4)

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playing with a premature contact may initiate a grinding habit (31) and temporary bite-raising tends to interfere with the sensory stimuli involved in the habit and frequently leads to its cessation (31). Interestingly, aggressive occlusal approaches are discouraged in this latter paper: permanent bite-raising is rarely indicated and fraught with many difculties. Similarly, Levene (32), although an advocate of eliminating premature occlusal contacts in the presence of clear consequences of bruxism, states, such corrections must be made with an awareness of the involved dangers and only after palliative treatment and muscle therapy have been insufcient. In other words, occlusal therapy was already considered a secondary strategy in the management of bruxism in an era where the belief in a strong bruxismbite relationship was common. Not every author in the 60s and 70s of the past century promoted such careful approach. For example, Butler (33) describes a number of situations that call for occlusal adjustment, and bruxism is one of these situations. The only restriction in Butlers technical description of how to proceed with occlusal adjustment is that prophylactic adjustment is not indicated for all patients (but apparently for some, it is). This approach of occlusion in relation to bruxism was still advocated more recently, for example, by McCoy (34), who describes a three-phase occlusion-oriented technique (educationequilibrationocclusal guards) for the management of the so-called dental compression syndrome a term that includes a wide range of parafunctional activities, including bruxism. According to McCoy (34), one of the main problems in the discussions on the bruxismbite relationship is the fact that the dental profession does not thoroughly understand the difference between ideal occlusion and malocclusion. This lack of understanding would hamper an unequivocal assessment of the association between bruxism and the bite. Although this might indeed be true, most occlusal characteristics are well dened. Rather, as indicated before, controversies in relation to the various denitions and diagnostic approaches of bruxism prevent clear conclusions to be drawn from most studies. From the above paragraphs, it can be gathered that especially premature contacts (also indicated as prematurities) and interferences in articulation have been considered to be causally involved in bruxism. In his classical study, Ramfjord (35) reported that occlusal grinding procedures always led to a disappearance of

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Results
Main ndings The interaction between bruxism and the bite appears to be characterised and inuenced by several functional and morphological factors. Most importantly, however, occlusion is generally considered a mediating factor between bruxism and its purported consequences (see Bruxism and Consequences). In that respect, frequently mentioned effects of bruxism are tooth wear (especially attrition and abfraction); failure of dental restorations and implants; loss of periodontal tissues, teeth and alveolar bone; and temporomandibular pain and dysfunction. The review below will follow the abovesketched structure. Hence, separate sections will deal with the interaction between bruxism and the bite and with the bite mediating between bruxism and its purported consequences. To study the possible associations between bruxism and the bite, a wide variety of study designs, population samples and techniques for case denition have been used. The literature search yielded, among others, study types like experimental studies, casecontrol studies and cohort studies. Further, the studied patient samples were composed of children, adolescents and adults. Notably, some of the studied samples contained patients with temporomandibular disorders, the presence of pain being a possible confounder when studying the bruxismbite relationship (28, 29). Finally, the various study techniques used were, among others, self-report, clinical examination techniques, a combination of self-reports and clinical assessments, EMG, and PSG. In this review, it will be indicated for every topic which study types, samples and techniques were used in the papers that are included in the various sections.

Interactions between bruxism and the bite Over the past 45 years, a number of reviews and opinion papers have paid attention to the possible association between bruxism and aspects of occlusion. In the older works, usually without making a distinction between sleep bruxism and awake bruxism and without providing any scientic evidence, statements can be found like bruxing patterns can be set up in an effort to rid the teeth of () so-called high spots so that the muscle can go back to a rest position (30),
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bruxism. Based on EMG recordings, Ramfjord held discrepancies between the retruded contact position and maximal intercuspal position as well as the presence of mediotrusive (balancing side) contacts during articulation responsible for the initiation of bruxism. Interestingly, bruxism was determined during an approximately 1-h EMG protocol that included the conscious performance of several movement tasks. Such conscious tasks, however, cannot be compared with unconscious bruxism behaviour. For that reason, papers dealing with conscious jaw-muscle activities in bruxism patients were excluded from this review (see Methods). Nevertheless, even though no controls were included and the use of conscious tasks for bruxism renders Ramfjords results impossible to interpret according to more recent insights into study design, the conclusions of this study have had a major impact on clinical dentistry and have led to many heated debates. Also, letters to Editors of dental journals have been used for these debates. For example, in the Journal of the American Dental Association, Hoopingarner (36) states that if occlusal prematurities are the cause of bruxism, then we should be able to create bruxism in non-bruxists by introducing them. This letter was a reaction on a letter written by Gilligan, whose response to Hoopingarners letter includes a summary of the above-described classical work of Ramfjord, and is thus not very convincing. Budtz-Jrgensen (37, 38) successfully induced bruxism in monkeys by creating a dysfunctional occlusal relationship that contained prematurities. This was accomplished by inserting gold splints in the premolar and molar areas of the upper jaw that raised the bite by approximately 34 mm and caused vertical and horizontal overloading of the mandibular teeth by means of occlusal interferences. The author used the observed increase in tooth mobility, gingival inammation and radiographic evidence of alveolar bone breakdown as oral signs of bruxism. Because during the initial, 3-week phase of the 12-week observation period, urinary and plasma cortisol levels were elevated, the author concluded that emotional stress plays a role in the periodontal reactions to experimentally induced bruxism. Bruxism was thus considered a tensionrelieving mechanism as well as an attempt to convert the occlusal abnormality to the normal situation. Gomez et al. (39) conrmed the inuence of occlusal disharmonies (i.e. an acrylic cap placed on the lower incisors) on experimental, apomorphine-induced bruxism in the rat. Also using a rat model, Areso et al. (40) concluded that such occlusal disharmonies modulate the central catecholaminergic neurotransmission and thus non-functional jaw-muscle activities (1618). However, for the above-cited animal studies, it is questionable whether acute, articial prematurities have the same effects on oro-motor activities as naturally existing premature contacts, these latter possibly being the effect of bruxism rather than its cause. Further, extrapolating evidence from animal studies to the human situation should always be carried out carefully. In that respect, the study by Rugh et al. (41) is worth mentioning. These authors studied the effects of articial occlusal interferences, incorporated in crowns in the molar region, on masticatory muscle activity during sleep in humans. Bruxism was quantied by means of EMG recordings from the sleeping patient. In contrast to the ndings of Ramfjord (35), the experimental prematurities caused a signicant decrease in sleep-related bruxism in 90% of the cases. At least partly in line with these ndings, Shiau and Syu (42) observed that articial workingside interferences in articulation led to a self-reported reduction in bruxism in almost half of the participating bruxers. The results of the studies of Rugh et al. (41) and Shiau and Syu (42) thus shed some serious doubts on the role of occlusion and articulation in the aetiology of bruxism, although as for the studies by Budtz-Jrgensen (37, 38) articial prematurities and interferences cannot be directly compared with natural ones. More convincingly, in better-controlled studies, the elimination of naturally existing premature contacts was shown to have no inuence on bruxism activities (43, 44). Rieder (45) observed a higher prevalence of parafunctional habits (including self-reported bruxism) in patients with more complex mandibular displacements (i.e. with asymmetries in the slide from retruded contact position to maximal intercuspal position). However, as indicated by the author, the study sample was not representative for the population from which the participants were recruited, thus rendering the outcomes of this study inconclusive. Moreover, Greene and Marbach (46) argue that not every bruxer has occlusal interferences and not every person with such interferences is a bruxer. Therefore, the conclusion seems justied that even though occlusal schemes are relevant for the distribution of bruxism-related forces (47), there is no evidence for a role of premature
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contacts or interferences in articulation in the aetiology of bruxism (48). Apart from prematurities and interferences, another frequently blamed occlusal factor in association with bruxism in the older literature is the anterior deep bite, for which clinical experience rather than scientic proof is put forward (49). Also in the more recent literature, as reviewed by Vanderas and Manetas (50), a deep bite (along with occlusal variables such as occlusal interferences and Angle class II and III molar relationships) was described in cross-sectional studies as being signicantly associated with tooth wear as a measure for bruxism in children and adolescents. However, no signicant causal relationships between malocclusion and bruxism could be inferred from the few longitudinal studies that these authors included in their review. Vanderas and Manetas (50) therefore concluded that malocclusion does not increase the probability of bruxism. In line with this conclusion, Tsolka et al. (51) observed no differences in occlusal variables (e.g. prematurities and balancing-side interferences) between self-reported bruxing and non-bruxing adult patients with temporomandibular disorders. In contrast, self-reported bruxism was found to be associated with occlusal factors like a large overjet and overbite in mixed and permanent dentitions in a group of 9- to 14year-old children (52). However, because Sari and Sonmez (52) used a cross-sectional study design along with self-reports of bruxism, the ndings of their study cannot be interpreted unequivocally. In a large-scale study in 7- to 19-year-olds, employing a self-report and clinical assessment of bruxism, none of the examined occlusal variables seemed to play a role in the aetiology of bruxism (53). As a consequence of such contrasting and difcult-to-interpret ndings, and in line with the recommendation by Vanderas and Manetas (50), treatment for occlusal conditions to prevent bruxism is not scientically justied. Besides the role of morphological factors related to dental occlusion and articulation in the aetiology of bruxism, several studies assessed the possible relationship between bruxism and the oro-facial regions anatomy. Miller et al. (54) found a more pronounced asymmetry in condylar height in bruxers than in nonbruxers, while Young et al. (55) observed larger bizygomatic and cranial widths in bruxers. In both studies, however, the presence or absence of bruxism was assessed by means of self-report and a clinical examination. The lack of conrmation of the bruxer status by
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means of PSG or EMG hampers the interpretation of these results. Such lack also hampers the interpretation of the study by Menapace et al. (56), although these authors found no differences between bruxers and nonbruxers in the dentofacial morphology. In another study that primarily focused on bruxism-related tooth wear in relation to the morphology of the craniofacial structures (57), a more rectangular form of the maxillary dental arch and face, in combination with an more anteriorly rotated mandible, a smaller anterior facial height and a larger bimaxillary interincisal angle, were found in severe attrition patients as compared to control subjects. Again, unfortunately, Waltimo et al. (57) did not use PSG to classify their patients. Also employing self-reported bruxism rather than a PSG conrmation of bruxism status, two studies reported that Angle class II and III relationships were associated with bruxism (58, 59). In the study by Gadotti et al. (58), even an EMG assessment of conscious jaw-muscle activities was included in the study design. However, for the reasons outlined above, neither of these studies can be interpreted unequivocally in terms of a possible causal association between bruxism and the bite. To date, only the study by Lobbezoo et al. (60) has employed polysomnography to study the relationship between bruxism and morphological factors. In that study, the authors compared 26 occlusal variables and 25 cephalometric variables between bruxers and nonbruxers. No differences were found between both groups. Over the years, the attention for the possible multicausal nature of bruxism is growing steadily. Initially, the rst steps towards this still valid insight were unsteady. Authors clearly struggled with the need to let go of a fully occlusion-based aetiology of bruxism, as evidenced by this citation from Suzuki (61): From the available literature, one must accept a multiple aetiology involving occlusal disharmonies compounded by mental stress and tension. Suzuki comes to this conclusion based on studies like the one by Robinson et al. (62), who reported that not all bruxists have malocclusions and not all individuals with malocclusions brux. Studies like this one opened the way for other possible aetiological factors of bruxism to be examined. Nevertheless, even in the past decade, dentists are suggested to approach bruxism not only as a psychologist or behavioural expert but also as an engineer. According to McCoy (63), the engineering point of view is important in recognising and managing

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oral parafunctions, including bruxism. Similar to the literature on the aetiology of temporomandibular disorders, where a comparable paradigm shift is ongoing from a mechanical point of view to a biopsychosocial one (64), the occlusion-oriented engineers approach of bruxism is still supported in parts of the literature. In contrast to the literature cited in the previous paragraph, some authors take another point of view. For example, Lavigne and Kato (65) describe the aetiology of bruxism as being mainly determined by psychosocial factors and or medical or drug-related conditions, while they state that bruxism may be concomitant with intra-oral conditions such as, among others, occlusal variations. Koyano et al. (66, 67) support this point of view, thereby stating that evidence has been reported to counter the historic concept of occlusal interferences being regarded as a cause of bruxism. Also, Luther (68) concludes in her review of the literature that the available evidence fails to support the assumption that occlusal interferences cause bruxism. Finally, Al-Ani (69) states that occlusalmorphological factors play only a minor role if any in the aetiology of bruxism. Hence, the recent literature moves with increasingly steady steps towards the acceptance of a multicausal, non-occlusionoriented aetiology of bruxism. Several studies have contributed to the abovesketched paradigm shift. Seligman et al. (70) found no clinically relevant associations in a non-patient population between dental attrition, discernible on dental study casts, as a proxy for bruxism on the one hand and several occlusal factors (e.g. premature contacts) on the other. The authors conclude that their ndings point to bruxism as a centrally induced phenomenon that is unrelated to local (i.e. morphological) factors. Employing a self-report and clinical assessment of bruxism, also Manfredini et al. (71, 72) conclude that the role of occlusal factors in the aetiology of bruxism is very small, if at all present, and accounts for only about 5% of the variance of bruxism. Rather, self-reported bruxism and clinical bruxism seem to be associated with psychological factors such as anxiety, depression and manic symptoms (72). Similarly, in a 20-year follow-up study, Carlsson et al. (73) found that self-reported bruxism was not associated with any of the assessed occlusal factors. Interestingly, and seemingly in contrast to their ndings related to self-reported bruxism, a post-normal occlusion (i.e. an Angle class II relationship) in childhood predicted increased tooth wear in adulthood (73). This apparent deviation in ndings between self-reported bruxism and tooth wear as a proxy for bruxism actually corroborates the fact that indirect measures for bruxism lack validity; see also Abe et al. (74). Carlsson et al. (73) discuss their ndings among others in relation to the possible psychological modulation of bruxism, even though in their study, psychological tension only explained a small proportion of the variance of bruxism. In summary, there is no evidence available that occlusal interferences or factors related to the anatomy of the oro-facial skeleton play a role in the aetiology of bruxism. Instead, there is a growing awareness of other factors (viz. psychosocial and behavioural ones) being important in the aetiology of bruxism.

The bite mediating between bruxism and its purported consequences While the validity of the purported causal association between bruxism and the bite is still a matter of debate, dentists do agree that bruxism may have several adverse effects on the masticatory system. Below, some examples of such possible consequences of bruxism will be given, including tooth material loss (wear), loss of periodontal tissues, and temporomandibular pain and dysfunction. Especially, it will be illustrated that occlusion and articulation play a mediating role in these adverse processes. Ricketts (75) considers tooth wear the most detrimental bruxism-related condition. Most likely for that reason, tooth wear has been described in relation to bruxism for many years. Especially, attrition has been mentioned in this context. In The Glossary of Prosthodontic Terms (2), attrition is dened as the mechanical wear resulting from mastication or parafunction, which is limited to contacting surfaces of the teeth. During tooth grinding, this is exactly what happens: opposing teeth are being rubbed against each other forcefully. It should be noted, however, that also tooth clenching may cause localised, attrition-like tooth wear: when biting down in maximal intercuspal position during clenching, small tooth movements may still occur owing to a tooths mobility in its socket. This phenomenon is called fremitus and may cause small wear facets in the area of the cusp-fossa contact points (76). Besides the small movements of the tooth in the socket during clenching, bruxism may even result in deformation of the crown, as shown by nite element modelling (77). It
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can be hypothesised that such deformations contribute to the localised attrition owing to clenching. Another type of tooth wear that has been described in relation to bruxism is abfraction (i.e. cervical tooth wear owing to occlusal, bruxism-related forces that create stresses in enamel and dentine, thus causing v-shaped cervical lesions). It has been suggested that the larger the occlusal contact area (which is actually the case when bruxism has caused considerable attrition), the stronger the association between occlusion and abfraction (78). However, there is controversy as to whether this type of tooth wear actually exists or whether it is merely an expression of toothbrushing-related abrasion. According to The Glossary of Prosthodontic Terms (2), abfraction is nothing but a hypothetical phenomenon. Nevertheless, abfraction is still being described and discussed in the literature. Regardless of such controversies, tooth wear is the clearest example of how occlusion mediates between bruxism and one of its purported consequences. Without occlusal contacts, bruxism would not lead to the mechanical loss of dental tissues. Lytle (79, 80) refers to this occlusion-mediated phenomenon as occlusal disease; a rather provocative term that attracted much attention from other oral healthcare professionals like dental hygienists (81). Carlson-Mann (81) even compares occlusal disease to periodontitis, both being irreversible but maintainable. She considers observing occlusal wear and appropriately referring patients suffering from occlusal disease as one of the dental hygienists professional duties. Another possible consequence of bruxism that is mediated by occlusal contacts is periodontal breakdown. This possibility has already received the attention of dentists, including periodontists, for many decades. In 1969, Yardeni (82) discussed this topic without coming to a clear conclusion. He simply states that there is a certain antagonism between periodontal diseases and natural attrition. It should be noted, however, that if a causal relationship between bruxism and periodontal breakdown via occlusal contacts (also known as trauma from occlusion) actually exists, this would have a major impact on periodontal treatments, of which occlusal adjustment would then constitute an important part. So, is there evidence for such causality? As also described in the previous section, BudtzJrgensen (83) successfully developed an animal (monkey) model for trauma from occlusion owing to occlusally induced bruxism. The articial occlusal interferences did not only yield increased tooth
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mobility but also marginal and inter-radicular alveolar bone loss. However, the author concludes that there was no evidence that bruxism had caused a progression of gingivitis to destructive, chronic, marginal periodontitis. Again, this is an animal study, and extrapolation of the ndings to the human situation is difcult. A case report of a patient with severe tooth mobility with root and alveolar bone resorption describes the successful use of a hard occlusal stabilisation splint and occlusal adjustments, yielding a cessation of the resorption processes and a reduction in the tooth mobility (84). The outcome in this case is discussed in terms of a reduction in bruxism that in turn causes the elimination of trauma from occlusion. The level of evidence of this single case is of course low. Consequently, as for the studies by Budtz-Jrgensen (83), this case report does not contribute to nding an answer to the question whether a causal relationship between bruxism and periodontal breakdown via occlusal contacts actually exists. In this context, also the study by Calderon et al. (85) is worth mentioning. These authors hypothesised that excessive occlusal loads applied to the teeth for prolonged periods of time, such as in sleep and awake bruxism, would lead to differences in periodontal sensation as compared to non-bruxing conditions. Using the participants ability to discriminate between foils of various thicknesses, no such differences could be detected. In other words, even though it cannot be excluded that muscle spindles or TMJ mechanoreceptors are responsible for this negative outcome, the sensory capacities of the periodontal tissues seem to be unaffected by bruxism. Hence, unfortunately, no unequivocal evidence is available to support the presumed causal relationship between bruxism and periodontal problems. In this context, Stephens (86) rightfully states that, given the lack of evidence underlying trauma from occlusion, it is disturbing that many occlusions continue to be adjusted for reason of treating (or even preventing) periodontal breakdown. As the role of bruxism in the aetiology of temporomandibular pain and dysfunction remains unclear (28, 29), an unequivocal mediating role of occlusal factors in this relationship is also difcult to establish. Manfredini et al. (87) nevertheless tried to test the hypothesis that occlusion acts as a modulator through which bruxism activities may cause damage to the masticatory system. None of the occlusal variables that these authors included in their model turned out to contribute

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signicantly to the bruxismTMD associations. Only nite element models seem to suggest that prolonged clenching in situations where the condylar disc is anteriorly displaced may lead to cartilage breakdown on the condylar articular surface (88). However, such models, while useful for hypothesis formulation, have limited value and the outcomes cannot be extrapolated to the clinical situation. Closer to the clinic, but still based on an experimental design is the nding of Takenami et al. (89), who reported that sustained clenching with the incisors (and thus with no molar support) reduces the intra-articular space as established on serial tomograms. Similar to the study by Nishio et al. (88), this study is not conclusive either, because of its two-dimensional nature which only yields limited insight. In other words: the small number of papers that have tried to assess the mediating role of occlusion in the purported causal relationship between bruxism and temporomandibular disorders has yielded negative or difcult-to-interpret outcomes. In short, even though most dentists agree that bruxism may have several adverse effects on the masticatory system, for none of these purported adverse effects, evidence for a mediating role of occlusion and articulation has been found to date. the present search strategy, it is the opinion of the authors of the present review that it is rather unlikely that papers that would have changed our conclusions have been missed. The fact that the papers that were added from the reference lists of the included papers and from the authors personal collections did not modify this reviews conclusions either strengthens our opinion. It remains surprising that occlusal and morphological factors are still commonly blamed for causing and maintaining bruxism, both by dental professionals and by bruxism patients. Possibly, this strong-held belief is related to the fact that dentists can modify dental occlusion and articulation relatively easily, while at the same time for patients, morphological causes for their condition are relatively safe and out of their own control. If this possibility is actually true, we may never live the day of the denitive farewell to occlusion in bruxism, unless dental professionals start educating each other and subsequently their patients in a nonocclusal paradigm.

Conclusion
Based on this review, it should be concluded that to date, there is no evidence whatsoever for a causal relationship between bruxism and the bite.

Discussion
This review focused on the role of occlusal factors in the aetiology of bruxism. Further, attention was paid to the presumed mediating role of the bite in bruxisms purported adverse effects. Neither for the causal relationship under study nor for the mediating role of occlusion was strong and convincing evidence found in the literature. Instead, there is growing agreement that it is not important how someones occlusion looks like, but rather how one copes with a certain type of occlusion. Dentists should prevent the creation of so-called occlusal neurotics, which might already happen when occlusal adjustment procedures are only discussed with the patient (90). The search method used in this study was limited to English-language publications that appeared in PubMed. Thus, it may be possible that some publications on this topic have been left out, because they were published in another language or would only have been found in other databases. However, given the absolute absence of an evidence base for any role of the bite in bruxism in the papers that were found using

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*Papers included in this review. Correspondence: Prof. Frank Lobbezoo, Department of Oral Kinesiology, Academic Centre for Dentistry Amsterdam (ACTA), Gustav Mahlerlaan 3004, 1081 LA, Amsterdam, The Netherlands. E-mail: f.lobbezoo@acta.nl

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