Bruxism: its multiple causes and its effects on dental implants – an updated review*

Journal of Oral Rehabilitation 2006 33; 293–300 Review ArticleBruxism: its multiple causes and its effects on dental implants– an updated review* F . L O B B E Z O O , J . V A N D E R Z A A G & M . N A E I J E Department of Oral Function, Academic Centre for DentistryAmsterdam (ACTA), Amsterdam, The Netherlands SUMMARY There is a growing interest in bruxism, as ism and implant failure reveals no new points of evidenced by the rapidly increasing number of papers view. Thus, there is no reason to assume otherwise about this subject during the past 5 years. The aim of than that bruxism is mainly regulated centrally, the present review was to provide an update of two not peripherally, and that there is still insufficient previous reviews from our department (one about evidence to support or refute a causal relationship the aetiology of bruxism and the other about the between bruxism and implant failure. This illustrates possible role of this movement disorder in the failure that there is a vast need for well-designed studies to of dental implants) and to describe the details of the study both the aetiology of bruxism and its purported literature search strategies used, thus enabling the readers to judge the completeness of the review. Most studies that were published about the etiology during implants, failure, overload, morphology, pathophys- the past 5 years corroborate the previously drawn conclusions. Similarly, the update of the review about the possible causal relationship between brux- sometimes difficult to unequivocally interpret the Bruxism is a movement disorder of the masticatory During the past decades, bruxism has been studied system that is characterized, among others, by teeth extensively, and many research papers and review grinding and clenching, during sleep as well as during articles have been published. To illustrate this, A wakefulness (1, 2). Bruxism has a prevalence in the MEDLINE search was performed on 28 April 2005, general adult population of about 10% and is usually using the National Library of Medicine’s (NLM) Medical regarded as one of the possible causative factors for, Subject Headings (MeSH) Database and PubMed. The among others, temporomandibular pain, tooth wear in search term ‘Bruxism’ [MeSH Terms] OR bruxism [Text the form of attrition, and loss of dental implants (3).
Word] yielded 1773 papers, 202 of which were reviews.
These possible musculoskeletal and dental conse- When using the truncated search term bruxi*, thereby quences of bruxism illustrate the clinical importance turning off automatic term mapping and the automatic of this disorder. Importantly, it should be borne in mind explosion of MeSH terms, 1791 papers were found, 206 that there is still a lack of agreement about, for of them being reviews. The overlap between these two example, the definition of bruxism, which makes it searches was 100%. A pure MeSH search on thissubject (viz. ‘bruxism’ [MeSH]) resulted in 1588 papers,including 172 reviews. About 20–30% of the papers, *Based on the Journal of Oral Rehabilitation Summer School 2005 in found with any of these three search strategies, were Bavagna, Italy. Kindly sponsored by Blackwell Munksgaard and NobelBiocare.
published during the past 5 years; the remaining papers, between 1966 and 2000. This shows, that there be involved in the aetiology of bruxism. Psychosocial factors like stress and personality are frequently Most of the reviews that were found with the above- mentioned in relation to bruxism as well. However, described search strategies have a broad nature, covering research to these factors comes to equivocal results and many aspects of bruxism, like its definitions, epidemiol- needs further attention. Taken all evidence together, ogy, diagnostic procedures, aetiology/pathophysiology, bruxism seems to be mainly regulated centrally, not concomitant disorders, clinical consequences, various therapeutic approaches and prognosis. Relatively fewof the review articles focus on specific aspects of bruxism. Recently, we published two ‘indepth’ focusedreviews: one about the aetiology of bruxism (4) and the To update the review by Lobbezoo and Naeije (4) about other about the possible role of bruxism in the failure of the aetiology of bruxism, a MEDLINE search was dental implants (5). Unfortunately, in these review performed on April 28, 2005, using the NLM’s MeSH articles, no controllable PubMed search was described, Database and PubMed. As search term, ‘Bruxism’ thus leaving the readers ignorant of the completeness [MeSH] was used. The term was exploded as to include of the review. Therefore, because of the above- ‘Sleep Bruxism’, a term which is found below ‘Bruxism’ substantiated growing interest in bruxism during the in the MeSH tree. The search was limited to the past past 5 years, the aim of the present review was to 5 years and yielded 330 papers, 48 of them being provide an update of both previous reviews and to reviews. On the basis of the titles, 68 research articles describe the details of the literature search strategies and 11 reviews were selected for their possible rele- vance to the subject of this review (viz. the aetiology ofbruxism), thereby avoiding overlap with the set ofreferences used by Lobbezoo and Naeije (4). As a next step, the abstracts (or, when not available, the full-length papers) of the 79 selected papers were read as to Summary of review by Lobbezoo and Naeije (4) establish the papers’ applicability to this review. Of The literature, which is so far published about the these papers, 17 were excluded because they turned out aetiology of bruxism, is often difficult to interpret. In to deal with subjects like tooth wear and myoclonus, part, this is because of the persisting disagreement that are outside of the main focus of this updated about the definition and diagnosis of this disorder.
review. Hence, 62 papers remained for inclusion in the However, there is consensus about the multifactorial nature of the aetiology of bruxism. Besides peripheral(viz. morphological) factors, central (viz. pathophysio- logical and psychosocial) factors can be distinguished.
In the past, morphological factors, like occlusal discrep- As stated in the above-given summary of the review by ancies and deviations in the anatomy of the bony Lobbezoo and Naeije (4), the factors that may play a structures of the orofacial region, have been considered role in the aetiology of bruxism can be divided into the main causative factors for bruxism. Nowadays, three categories: morphological, pathophysiological and these factors are thought to play only a small role, if at psychosocial factors. Relatively few of the papers, all. Recent focus is more on the pathophysiological selected for inclusion in this updated review, deal with factors. For example, bruxism has been suggested to be morphological factors (approximately 10%), while only part of a sleep arousal response, the oral motor event slightly more papers have the role of psychosocial either preceding or following the arousal. In addition, factors in the aetiology of bruxism as their main focus bruxism appears to be modulated by various neuro- (approximately 20%). The vast majority of the selected transmitters in the central nervous system. More papers (approximately 70%) deal with possible aetio- specifically, disturbances in the central dopaminergic logical factors that can be classified among the patho- system have been described in relation to bruxism.
physiological ones. These percentages corroborate the Further, factors like medication, (illicit) drugs, genetics, commonly observed trend in bruxism research, away trauma, and neurological and psychiatric diseases may from a main focus on occlusion and towards a more ª 2006 Blackwell Publishing Ltd, Journal of Oral Rehabilitation 33; 293–300 B R U X I S M : A E T I O L O G Y A N D E F F E C T S O N D E N T A L I M P L A N T S biomedical/biopsychosocial point of view [see, e.g. the animal studies are in line with many observations in reviews by Kato et al. (6–8); De Laat and Macaluso (9); humans that there may be a causal relationship Lavigne et al. (10); and Lobbezoo et al., (3)]. Below, the between psychosocial factors like stress on the one possible role of occlusal factors will be discussed first, hand and bruxism on the other, as reviewed by followed by that of various psychosocial factors. Finally, Lobbezoo and Naeije (4). Importantly, these authors several pathophysiological factors will be described in state that the role of psychosocial factors in the relation to their purported role in the aetiology of aetiology of bruxism is far from clear, and that there bruxism. As in the review by Lobbezoo and Naeije (4), is a need for more controlled studies to this subject.
in the present update, unless otherwise specified, Since the publication of Lobbezoo and Naeije (4), bruxism will be considered the combination of all several studies to this subject have been published.
parafunctional clenching and grinding activities, exer- Unfortunately, none of them has a conclusive nature ted both during sleep and while awake, because these because of the absence of prospective, large-scale different phenomena are still not, or only inadequately, distinguished in most of the selected papers.
Taking into account these limitations of the evidence published during the past 5 years, the following view on Occlusal factors. Several occlusal factors (e.g., large and/ the role of stress and other psychosocial factors in the or inverse overjets and overbites) were suggested to be aetiology of bruxism emerges from the selected papers.
related to self-reported bruxism in a study with children Following from cross-sectional (case–control) studies, (11). In contrast to the recent insights as reviewed by bruxers differ from healthy controls in, among others, Lobbezoo and Naeije (4), Griffin (12) still state that for an the presence of increased levels of hostility (20) as well as effective management of bruxism, establishment of in the presence of depression and stress sensitivity (13, harmony between maximum intercuspation and centric 17). Bruxing children are apparently more anxious than relation is required. However, most studies to this subject non-bruxers (21), while 50-year-old bruxers more fre- now agree that there is no, or hardly any relationship quently report, among others, being single and having a between self-reported and/or clinically established brux- higher educational level (22). A series of papers about the ism on the one hand and occlusal factors on the other presence of bruxism and psychosocial factors among the hand, neither in adult samples (13–15) nor in children employees of the Finnish Broadcasting Company des- samples (16). Importantly, Manfredini et al. (17) state, cribes that self-reports of bruxism may reveal, among on the basis of a review of the literature, that there is still others, ongoing stress in normal work life (23) and a lack of methodologically sound studies to definitively dissatisfaction with one’s work shift schedule (24).
refute the importance of occlusal factors in the aetiology Therefore, Ahlberg et al. (25) state that factors like of bruxism. Therefore, future research to this subject perceived stress should be taken into account when should include more objective techniques to establish treating bruxism-related temporomandibular pain. A the presence or absence of bruxism (e.g. electromyog- multi-national, large-scale population study to sleep raphy or polysomnography), using the proper design for bruxism revealed ‘highly stressful life’ as a significant risk studies to cause-and-effect relationships, viz. prospect- factor (26). Finally, in a longitudinal case study by Van Selms et al. (27), it was demonstrated that daytimeclenching could significantly be explained by experi- Psychosocial factors. Rosales et al. (18) evoked emotional enced stress, although both experienced and anticipated stress in rats by letting them observe other rats that stress were unrelated to sleep-related bruxism as recor- underwent electrical foot shocks in a neighbouring ded with ambulatory devices (27, 28). Taken the findings cage. Compared with rats that did not observe the foot- of all these studies together, the body of evidence for a shocked rats, the ‘observing’ rats had high levels of possible causal relationship between bruxism and var- brux-like masseter muscle activity. Although it is ious psychosocial factors is growing, though not yet unknown whether this brux-like behaviour in rats is conclusive. Hence, there remains a need for more, well- in any way related to bruxism in man, Slavicek and Sato (19) consider such behaviour in experimentalanimals as an emergency exit during periods of psychic Pathophysiological factors. As mentioned above, the vast overloading. The findings and suggestions of these majority of the selected papers for this updated review ª 2006 Blackwell Publishing Ltd, Journal of Oral Rehabilitation 33; 293–300 deal with possible pathophysiological factors. Many of Certain neurochemical factors, medications and (illi- these are sleep-related. While Nagels et al. (29) report a cit) drugs were described in detail in relation to bruxism significantly lower percentage slow wave sleep in by Lobbezoo and Naeije (4). During the past 5 years, the bruxers than in healthy controls, other authors report body of evidence of their role has been growing macrostructural sleep quality and architecture to be gradually, although its conclusive nature is still contro- normal in bruxism patients (28, 30). Interestingly, and versial (40). Several papers that were selected for this in contrast to one’s expectations, experimental depri- updated review deal with the influence of selective vation of slow wave sleep (this sleep stage being the one serotonine reuptake inhibitors (SSRIs) on bruxism.
during which the least bruxism activity reportedly SSRIs have an indirect influence on the central dopam- occurs) did not significantly influence sleep bruxism inergic system, which is the system that is thought to be (31). In contrast to these macrostructural sleep studies, involved in the genesis of bruxism (4). Lobbezoo et al.
in a study to sleep microstructure, the sleep of bruxers (41) state, that SSRIs may cause bruxism after long-term was found to be characterized by a low incidence of usage. The case reports of Jaffee and Bostwick (42), Wise K-complexes and K-alphas (30). This illustrates the (43) and Miyaoka et al. (44) corroborate this statement importance to include microstructural analyses of sleep for the use of venlafaxine, citalopram and fluvoxamine, respectively. Another case report describes severe brux- In relation to sleep quality and architecture, bruxism ism in relation to an addiction to amphetamine, which and habitual snoring were found to be closely related can be explained through amphetamine’s disturbing (32). Ohayon et al. (26) even report an increased risk of influence on the dopaminergic system (45). In line with reported sleep bruxism in the presence of loud snoring this report, the amphetamine-like medications that are and obstructive sleep apnoea syndrome (OSAS). Accord- used in the management of attention deficit hyperac- ing to Sjoholm et al. (33), these relationships are because tivity disorder (ADHD), like methylphenidate, have of the disturbed sleep of habitual snorers and OSAS bruxism as a possible side effect, as shown in a case– patients. However, if these relationships indicate a true control study by Malki et al. (46). Also, the amphetam- physiological association is still unknown.
ine-like substance XTC reportedly has bruxism as a side As already summarized by Lobbezoo and Naeije (4), effect (47). Based on a study with rats, Arrue et al. (48) sleep bruxism may be considered part of an arousal give a possible explanation for this side effect of XTC, response. During the past 5 years, several papers were viz. the XTC-induced reduction of the jaw-opening published on this subject. First of all, Kato et al. (34), reflex. Finally, bruxism was found more frequently in using a case–control design, found evidence for the heavy drug addicts (49) as well as in smokers (25, 26).
suggestion that sleep bruxism is an oromotor manifes- According to Ohayon et al. (26), smokers are at higher tation secondary to the microstructural sleep event risk than non-smokers of reporting sleep bruxism, as are ‘micro-arousal’ (i.e. an abrupt change in the frequency drinkers of alcohol and caffeine. In short, all of the of cortical EEG that is occasionally associated with above-summarized papers corroborate the conclusion of motor activity). Similarly, experimentally induced Lobbezoo and Naeije (4), viz. that disturbances in the micro-arousals were followed by masticatory motor central dopaminergic system can be linked to bruxism.
events in all sleep bruxers in another study by Kato et al.
However, as stated by Winocur et al. (40), more (35). Based on a review of the literature, Kato et al. (8) controlled, evidence-based research on this under- suggest a sequence of events from autonomic (cardiac) explored subject is needed. Further, it should be noted changes and brain cortical activation (sleep arousal) to that information about dopaminergic substances in the genesis of sleep-related masticatory muscle activities relation to the aetiology of bruxism is more readily (bruxism). Interestingly, associations have also been available than that about other neurochemicals. Thus, observed between bruxism activities on the one hand although it may seem from the available evidence that and a supine sleeping position, gastroesophageal reflux, mainly the dopaminergic system plays a role in the episodes of decreased esophageal pH, and swallowing on aetiology of bruxism, the lack of focus on other the other (36–39). The exact temporal relationship of substances in the literature as well as the presence of these factors to bruxism is, as yet, unknown. Future many possible interactions between dopamine and studies should therefore aim at unravelling an all- other neurochemicals indicates the need for more ª 2006 Blackwell Publishing Ltd, Journal of Oral Rehabilitation 33; 293–300 B R U X I S M : A E T I O L O G Y A N D E F F E C T S O N D E N T A L I M P L A N T S As already reviewed by Lobbezoo and Naeije (4), it remains unclear whether or not bruxism is, to a greateror lesser extent, genetically determined. In their review, Hublin and Kaprio (50) take the stand thatgenetic effects have a significant role in the origin of Bruxism is generally considered a clinical problem, bruxism, although the exact mechanisms of transmis- which may have detrimental consequences for dental, sion are still unkown. Bruxism was also shown to share periodontal and musculoskeletal tissues. Bruxism has a common genetic background with sleeptalking, also been suggested to cause excessive (occlusal) load of another parasomnia (51). Recent publications thus dental implants and their suprastructures, which may favour the role of genetics in the aetiology of bruxism.
ultimately result in bone loss around the implants or As stated before, however, the exact genetic mecha- even in implant failure. Not surprisingly, bruxism is nisms still need to be unravelled in future studies.
therefore often considered a contraindication for Finally, many of the papers that were selected for implant treatment, although the evidence for this is possible use in this updated review deal with diseases usually based on clinical experience only. So far, studies and trauma in relation to bruxism. To start with trauma, to the possible cause-and-effect relationship between brain damage was described as a possible cause for bruxism and implant failure do not yield consistent and bruxism in the case series and case report by Millwood specific outcomes. This is partly because of the large and Fiske (52) and Pidcock et al. (53), respectively.
variation in the literature in terms of both the technical Further, a host of diseases of mainly neurological and aspects and the biological aspects of the study material.
psychiatric nature has been linked to the aetiology of Although there is still no proof for the suggestion that bruxism, viz. basal ganglia infarction (54), cerebral palsy bruxism may cause an overload of dental implants and (55, 56), Down syndrome (57), epilepsy (58), Hunting- of their suprastructures, Lobbezoo et al. (5) conclude ton’s disease (59, 60), Leigh disease (61), meningococcal that a careful approach is nevertheless recommended.
septicaemia (62), multiple system atrophy (63), Parkin- There are a few practical guidelines as to minimize the son’s disease (64), post-traumatic stress disorder (65, 66) chance of implant failure. Besides the recommendation and Rett syndrome (67). With the exception of the study to reduce or eliminate bruxism itself, these guidelines by Rodrigues dos Santos (55) on cerebral palsy, which concern the number and dimensions of the implants, has a case–control design, all other references in the the design of the occlusion and articulation patterns, afore-given list of diseases in relation to the aetiology of and the protection of the final result with a hard bruxism are case series or case reports. This indicates, that a lot of well-designed research still needs to beperformed to further evaluate the nature of the rela- tionships that were found between bruxism on the onehand and diseases and trauma on the other.
For an update of Lobbezoo et al. (5) about the possible Taken all the above evidence together, it can be role of bruxism in the failure of dental implants, a concluded that most papers that were published during MeSH search strategy was performed, using the follow- the past 5 years about the aetiology of bruxism have a ing query: ‘Bruxism’ [MeSH] AND (‘Dental Implants’ corroborative nature in relation to the review by [MeSH] OR ‘Dental Abutments’ [MeSH] OR ‘Dental Pros- Lobbezoo and Naeije (4). The most promising develop- thesis, Implant-Supported’ [MeSH] OR ‘Dental Implantation’ ments that yield new points of view on this subject can [MeSH]). This query yielded 41 papers, four of them be found in the research on sleep-related aetiological being reviews. Of these 41 papers, 16 were already factors, especially sleep arousal. This factor has been included in the paper by Lobbezoo et al. (5). Another 13 studied in well-designed experiments and yielded an papers were judged as non-applicable for use in the interesting model for the genesis of sleep bruxism.
current review. Of the remaining 12 papers, the titles Future research should try to further elaborate, test suggested a possible relevance to the subject of this and validate this model. Preferably, this should be review (viz. the role of bruxism in implant failure). In performed by taking into account other promising addition to this search, the titles of the papers from the aetiological mechanisms, like psychosocial and neuro- above-described MeSH search (‘Bruxism’ [MeSH]) over the past 5 years (see Aetiology of bruxism – Search ª 2006 Blackwell Publishing Ltd, Journal of Oral Rehabilitation 33; 293–300 strategy) were judged, which yielded another two (sets of) expert opinions of Schneider et al. (70) and papers of which the titles suggested their possible relevance to the subject of the current review. Hence, Despite the apparent lack of evidence, it may be good 14 papers were selected on top of the papers that were clinical practice to adopt the conclusions and practical already included in the review by Lobbezoo et al. (5). As guidelines of Lobbezoo et al. (5). The recommendation a next step, the abstracts of these 14 papers were read as for future research to specifically address the possible to establish the papers’ applicability to this review.
relationship between bruxism and dental implant fail- Three papers turned out not to deal with dental ure, using high-quality study designs, still holds out implants after all, while two other papers mainly dealt firmly against time, the more so because most of the with prevalence rates of biomechanical problems and of above-included papers have a low strength of evidence bruxism itself in dental implant patients. These five according to the grading system of the Oxford Centre papers were further disregarded. The remaining nine papers were included in the below-given updatedreview, regardless of them being research papers, case The aim of this review was to provide an update ofthe reviews by Lobbezoo and Naeije (4) and by Lobbezoo et al. (5). From both updates, it followed The nine papers that were selected for this update using that the conclusions of these previous reviews are left the above-described search strategy could be classified unchanged. In other words: there is no reason to as follows: one editorial (68); three (sets of) expert assume otherwise than that bruxism is mainly regu- opinions (69–71); two case reports (72, 73); one lated centrally, not peripherally, and that there is still (prospective) case series (74) and two non-systematic insufficient evidence to support or refute a causal relationship between bruxism and implant failure.
Without exception, these publications’ conclusions This illustrates that there is a vast need for well- regarding causality and their practical guidelines for the designed studies to both the aetiology of bruxism and use of dental implants in bruxism patients fit into the to its purported relationship with implant failure.
picture as sketched by Lobbezoo et al. (5). For example, on the basis of a (non-systematic) review of the would be welcomed in the dental clinic, where the literature, Jacobs and De Laat (75) also conclude that causes and consequences of bruxism still frustrate there is no direct causal relation between bruxism and implant failure. Further, Engel and Weber (74) corro-borate the recommendation of Lobbezoo et al. (5) to proceed carefully when planning implant procedures inbruxists. In line with this recommendation, Tagger- 1. Thorpy MJ. Parasomnias. In: Thorpy MJ ed. International Green et al. (76) state that good clinical examinations classification of sleep disorders: diagnostic and coding manual.
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