ETIOLOGICAL CONSIDERATIONS IN BRUXISM
Cristiana Ileana Croitoru1, Iulia Roxana Marinescu1, Emma Cristina Drăghici2,
Sanda Mihaela Popescu3, Monica Scrieciu4, Veronica Mercut5
1PhD student, Faculty of Dental Medicine, University of Medicine and Pharmacy Craiova, 2-4 Petru Rares street, Craiova 200349, Dolj, Romania
2Asisstant Professor, PhD student, Oral Rehabilitation Department, Faculty of Dental Medicine, University of Medicine and Pharmacy Craiova, 2-4 Petru Rares street, Craiova 200349, Dolj, Romania
3Associate Professor, PhD, MDM, Oral Rehabilitation Department, Faculty of Dental Medicine, University of Medicine and Pharmacy Craiova, 2-4 Petru Rares street, Craiova 200349, Dolj, Romania
4Associate Professor PhD, MDM, Prosthetics Department, Faculty of Dental Medicine, University of Medicine and Pharmacy Craiova, 2-4 Petru Rares street, Craiova 200349, Dolj, Romania
5Professor PhD, MDM, Prosthetics Department, Faculty of Dental Medicine, University of Medicine and Pharmacy Craiova, 2-4 Petru Rares street, Craiova 200349, Dolj, Romania
Sanda Mihaela Popescu, Faculty of Dental Medicine, University of Medicine and Pharmacy Craiova, 2-4 Petru Rares street, Craiova 200349, Dolj, Romania, email: firstname.lastname@example.org
Introducere: Etiologia bruxismului este controversată, fiind incriminaţi mai mulţi factori, printre care cel ocluzal, comportamental şi genetic.
Obiectiv: Scopul articolului a fost de a evalua sistematic literatura de specialitate pentru a identifica principalele teorii referitoare la etiologia bruxismului.
Surse: Extragerea datelor a fost realizată conform metodologiei Cochrane de analiză sistematică. Au fost studiate bazale de date PubMed, Google Scholar Search, Medline Database şi Google library.
Selecţia datelor: Etiologia bruxismului a fost obiectivul urmărit.
Extracţia datelor: Analiza studiilor eligibile şi extracţia datelor a fost realizată independent şi în duplicat. Bibliografia a fost analizată de doi cercetători folosind aceeaşi strategie şi aceleaşi criterii de includere pentru studiile selectate. Termenii folosiţi la căutare au fost „bruxism”, „etiologie” şi „mecanism”. Din cele 95 de articole evaluate, 25 au fost incluse în analiza finală.
Sinteza datelor: Etiologia bruxismului este plurifactorială, fiind implicaţi factori locali, sistemici şi psiho-comportamentali.
Cuvinte cheie: etiologia bruxismului, factori psiho-comportamentali
Background: The etiology of bruxism is controversial, many factors being implicated, like occlusion, psycho-behavioral factors, and genetic factors.
Objective: the aim of the present review was to systematically assess the literature and identify main theories regarding etiology of bruxism.
Data Sources: Data extraction was carried out according to the standard Cochrane systematic review methodology. The following databases were searched: PubMed, Google Scholar Search, Medline Database and the Google library.
Data Selection: The primary outcome was bruxism etiology.
Data Extraction: Screening of eligible studies and data extraction were conducted independently and in duplicate. The references were analised by two reviewers using the same search strategy and the same inclusion criteria were applied to the selected studies. Query terms used were „bruxism”, „etiology”, „mechanism”. Among the 95 related articles that were critically assessed, 25 were included in the critical appraisal.
Data Synthesis: There is convincing evidence that the etiology of bruxism is various, involving local, systemic and psycho-behavioral factors.
Key words: bruxism etiology, psycho-behavioral factors
Bruxism is a term generally used to define daytime and night time parafunctional activities of masticatory system, which includes strained jaw and teeth grinding friction associated with tooth wear, myalgia of the masticatory muscles, temporomandibular joint disorders and morning fatigue.
Hippocrates, quoted by Rozencweig , pointed out that “dental wear is soul’s clutter.” This aphorism shows the dimension of this condition, which is outside the oro-dental sphere.
In 1907, Karolyi then Marie and Pietkiewicz, used the term “bruxomania”, considering that “dental wear brings together at the same time the damages of the central nervous system”.
Bruxism term was first used in the literature in 1931 by Frohman for “non-functional grinding and rubbing the teeth”. 
Over the time there had been an ongoing concern for establishing a complete and comprehensive definition, related to the clinical manifestations of bruxism to explain at the same time the etiopathogenic mechanisms involved in the production and maintenance of bruxism.
Lavigne et al.  performed several studies on bruxism and concluded that the definition has evolved from the first considerations which were mainly referring to dental contacts and muscle contractions to considerations that relate to behavioral aspects and in particular the knowledge of sleep problems.
The aim of the present review was to systematically assess the literature and identify main theories regarding etiology of bruxism.
In the literature more then 400 articles on bruxism are available.
Data Sources: Data extraction was carried out according to the standard Cochrane systematic review methodology. The following databases were searched: PubMed, Google Scholar Search, Medline Database and the Google library. Case reports, reports with review and systematic review articles written in English were included.
Data Selection: The primary outcome was bruxism etiology.
Data Extraction: Screening of eligible studies and data extraction were conducted independently and in duplicate. The references were analised by two reviewers using the same search strategy and the same inclusion criteria were applied to the selected studies. Query terms used were „bruxism”, „aetiology”, and „mechanism”. Among the 95 related articles that were critically assessed, 31 were included in the critical appraisal.
- DATA SYNTHESIS
Internationally, the recent data published in the literature, shows that there is a consensus regarding a various etiologic involvement  in the pathogenic mechanisms of bruxism.
The first opinions on the aetiology of bruxism were considered to be the dental bite and the pathology of muscle contractions. Behavioural factors and in particular, aspects related to sleep were also included as etiological factors .
Attanasio R. , Lobbezoo et al , and Nascimento et al. , showed that sleep bruxism aetiology involved local factors, systemic factors, psychological factors and hereditary factors.
3.1. THE HYPOTHESIS OF OCCLUSAL ETIOLOGY
Regarding local occlusal aetiology of bruxism there were different opinions over the time. If in 1966 Ramfjord et al.  believed that occlusal factors, particularly occlusal interference, would have an important role in determination of bruxism, in 1984 Rugh et al.  proved by creating experimental occlusal interference, that the role of occlusal disharmony is secondary to bruxism, since correcting occlusal interference did not lead to disappearance of bruxism. The same situation occurred in patients with complete edentulism, which in the dentate period had bruxism. After wearing dentures, the bruxism reappeared.
However, the first affirmation on the role of occlusal interference in the bruxism was based on the fact that occlusal interference suppression in patients with bruxism produced an improvement in symptoms. This is evident in current dental practice. Ramfjord  called centric bruxism the frequently jaw clenching. The author argued that when clenching teeth was accompanied by grinding, this occurred in the central occlusal area, in the absence of occlusal interference even in presence of a stable oclusion, with slight slip teeth, of the mandible from centric relation to maximum intercuspidation.
Occlusal contacts during sleep, specific to bruxism, could be interrupted by swallowing, and muscle forces that appear during bruxism might exceed those of mastication. During sleep grinding, electromyographic bursts of masseter muscle were observed mainly with mediotrusive mandibular movement from the canine edge-to-edge position. According to Minagi et al  muscular dynamics during sleep are unique compared to that during voluntary clenching, and exert a greater mechanical load to the balancing side temporomandibular joint.
In 2001, Rosales et al.  showed that the relationship between occlusal disorders and bruxism was not very consistent. Also, in a review in 2012, Lobezzo et al  concluded that to date, there is no evidence whatsoever for a causal relationship between bruxism and the bite.
3.2. MUSCLE ETIOLOGY HYPOTHESIS
There are authors who associated muscle pathology and bruxism. Hellmann et al  argued that anterior and posterior neck muscles co-contract during jaw clenching, their findings supporting the assumption of a relationship between jaw clenching and the activity of the neck muscles investigated.
3.3. THE HYPOTHESIS OF PSYCHO-BEHAVIORAL ETIOLOGY
The psycho-behavioural factors whose influence on bruxism etiopathology is accepted by the majority of the specialists are: stress, anger, fear, repressed aggressiveness, etc. During the evolution of research, having as goal establishing of bruxism etiopathology, an important moment was considered to be the one when stress was regarded as a decisive factor.
Rugh and Solberg [16, 17] demonstrated the increase in intensity of bruxism episodes together with the increase of stress level. Kato  took into consideration the cognitive – behavioural factors such as stress, personality and anxiety in bruxisnm aetiology and considered that patients with bruxism presented an anxious personality and that the dominant of their personality represents the reaching / fulfilment of personal goals.
Okeson  showed that patients with bruxism had a greater emotional stability, were more meticulous and got better learning results. Lavigne  showed that bruxism was connected to anxiety and was secondary to micro excitations during sleep (the increase of the cortical activity and cardiac frequency) followed by the grinding of the teeth. Lavigne  pointed out that nocturnal bruxism must be differentiated from the diurnal one, the latter being linked to the organism reaction to stress or anxiety and being manifested like a contraction tic of the mobilising muscles of the mandible.
3.3.1. BRUXISM AS A SLEEP DISORDER
Sleep is an active state which takes 30% of our time, and makes part of our vital behaviour being essential to the survival and life quality of any individual. Sleep is made up of a succession of repeated stages which can be pointed out through EEG, EKG, EMG, and eye movements. Specialists described two types of sleep REM (Rapid Eye Movement) and NREM (Non Rapid Eye Movement). There are several stages described: in NREM there are stages 1 and 2 corresponding to light sleep as well as stages 3 and 4 corresponding to deep sleep, and in REM there is the paradoxical sleep which includes the dreaming period.
These stages of sleep alternate during a period of approximately 90 minutes on the average and repeat themselves four or five times.
There has been anticipated the idea that bruxism was produced during paradoxical sleep, but it seems that there might also be present during stages 1 and 2 of the NREM sleep. These periods were associated with episodes of micro wakening, body movements and temporary acceleration of cardiac rhythm .
Nascimento LL underlined the fact that nocturnal bruxism was found in all the stages of sleep but more often in stages 1 and 2 .
Kato  did polysomnographic recordings in which he specified the events which took place in stage 2 of sleep in normal subjects with bruxism. In the second stage it has been noticed the increase of cardiac frequency through the intensification of the autonomous cardiac system, and during the last stage it has been observed the apparition of some rhythmic activity of the masticatory muscles (ARMM). The authors have ascertained that in normal subjects the endogenous micro excitations appear approximately four seconds before ARMM while in bruxer they appear 10-60 seconds before. The increase of cardiac frequency, in normal subjects, appears at the beginning of ARMM episode, while in patients with bruxism a gradual increase of cardiac frequency appears before the beginning of ARMM and an acceleration of the cardiac frequency at the beginning of the bruxism episode.
It is still unclear why the ARMM is three times more frequent and 30% more ample in bruxers than in patients without bruxism . Hence the hypothesis that bruxism is a parasomnia.
In 2005, American Academy of Sleep Medicine achieved the International Classification of Sleep Disorders 2nd ed. Westchester, showing that „nocturnal bruxism is defined as a disorder of the stereotypical movements during sleep and is characterised by the grinding of the teeth or/and the clenching of the teeth.” According to this classification nocturnal bruxism is a sleep disorder, being included in the parasomnias .
3.3.2. THE ROLE OF THE CHEMICAL MEDIATORS IN BRUXISM
During recent years, at Lavigne insistences, the research paths have lead towards neuropsychology in order to explain the mechanisms involved in the apparition and maintenance of bruxism, by invoking the role of some neuromediators such as dopamine and serotonin.
Dopamine and serotonin are neurotransmitters which ensure the communication between neurons. The dopamine is involved in lust, pleasure and movement. Its deficit is met in Parkinson disease which is accompanied by a deficit of movement and in schizophrenia. The serotonin has a role in adjusting sleep, appetite and humour. Its deficit is met in case of anxious states and depressions [24, 4].
The role of dopamine, as causing factor of bruxism, is that of dopaminergic psycho stimulus (the same as amphetamines), worsening the bruxism episodes. The dopaminergic system has been placed in an important position in the regulation of stereotypical movements and in the control of motion problems during sleep [24, 4].
Yet, the voices announcing that dopamine plays a key role in bruxism aetiology, are today more temperate. The selective inhibitors for the reuptake of serotonin have a direct influence on the dopaminergic system. Lobezzo et al. [25, 26] stated that dopamine did not have an essential role in producing bruxism, as the selective inhibitors for the serotonin reuptake receptors had a direct influence on the dopaminergic system. These serotonin inhibitors are represented by antidepressives currently prescribed and which, used for a long time, can maintain or induce bruxism. In spite of these, the authors consider that bruxism can be adjusted at the central nervous system level and not at the peripherical one.
3.4. GENETIC ETIOLOGY HYPOTHESIS
Genetic aetiology hypothesis  was advanced, but the transmission mechanism could not be demonstrated. Clinically, bruxism occurrences have been observed in patients belonging to the same families, parents, children or brothers. Original hypothesis about the fact that nocturnal bruxism may be associated with a familial predisposition was supported by studies on twins . Obviously, these observations can not be considered as the results of a research process.
In a case-control study, Abe et al  investigated the association of genetic, psychological and behavioural factors with sleep bruxism in a Japanese population. Their analysis revealed that only the C allele carrier of HTR2A single nucleotide polymorphism rs6313 (102C>T) was associated significantly with an increased risk of sleep bruxism (odds ratio = 4.250, 95% confidence interval: 1.599-11.297, P = 0.004), suggesting a possible genetic contribution to the aetiology of sleep bruxism.
3.5. OTHER POSSIBLY INVOLVED FACTORS IN BRUXISM’S ETIOLOGY
In 2003, Winocur et al.  published a study showing the correlations between the consumption of alcohol, tobacco, drugs and pills and bruxism occurrences. In 2006, Lobezzo et al  showed that bruxism might be a brain injury consequence and might be associated with some psychiatric or neurological diseases. Also, bruxism was linked to the use of amphetamines, levodopa, phenothiazines and alcohol. Lavigne et al.  stated that the ARMM and nocturnal bruxism episodes were influenced by the brain electrical activity increase and by the ascending reticular system stimulation, which increased the motor neuronal network activity and cardiac autonomic system.
According to Behr et al , theories on factors causing bruxism are a matter of controversy in current literature, two main etiological models being most important. The first one was peripheral local morphological disorders, such as malocclusion. This etiological model is based on the theory that occlusal maladjustment results in reduced masticatory muscle tone. In the absence of occlusal equilibration, motor neuron activity of masticatory muscles is triggered by periodontal receptors. The second theory assumes that central disturbances in the area of the basal ganglia are the main cause of bruxism. An imbalance in the circuit processing of the basal ganglia is supposed to be responsible for muscle hyperactivity during nocturnal dyskinesia such as bruxism.
In Romania, the recent most important views on bruxism considered particularly the stress and occlusal interferences in the aetiology of bruxism, but affirmed that until now, there could not clearly be establish a direct causal link between a specific etiologic factor and bruxism . Just like the occlusal trauma, it is sure that only one etiologic factor can not be incriminated in bruxism aetiology. The evidence of this finding is that, to date, there is not a single therapeutic method to obtain the removal or improvement of bruxism, there are always used more associated therapeutic procedures .
* Bruxism is a dental disorder that deeply alters the dento-maxillary system normal functionality.
* Bruxism aetiology is various, involving local, systemic and psycho-behavioural factors.
1.Rozencweig D. Algies et dysfonctionnements de l’appareil manducateur. Paris:CdP;1994;
- Marie MM, Pietkiewicz M. La bruxomanie. Rev de Stomat.1907;14:107-116;
- Graf H. Bruxism. Dent Clin North Am. 1969;13(3):659-665;
- Lavigne GI, Montplaisir JY. Bruxism: epidemiology, diagnosis, pathophysiology, and pharmacology. In: Fricton JR, Dubner R, editors. Orofacial pain and temporomandibular disorders. New York: Raven Press;1995; 387-404;
- Lobbezoo F, Naeije M. Bruxism is mainly regulated centrally, not peripherally. J Oral Rehabil. 2001; 28(12): 1085-1091;
- Brocard D, Laluque JF, Knellesen C. La gestion de bruxisme. Paris: Quintessence International; 2007:15-18;
- Attanasio R. Nocturnal bruxism and its clinical management. Dent Clin North Am. 1991; 35(1),:245-252;
- Lobbezoo F, Van Der Zaag J, Naeije M. Bruxism: its multiple causes and its effects on dental implants-an updated review. J Oral Rehabil. 2006;3(4):293-300;
- Nascimento LL, Amorim CF, Giannasi LC, Oliveira CS, Nacif SR, Silva Ade M, Nascimento DF, Marchini L, de Oliveira LV. Occlusal splint for sleep bruxism: an electromyographic associated to Helkimo Index evaluation. Sleep Breath. 2008; 12(3):275-280;
- Ramfjord SP, Ash MM. Occlusion. Philadelphia: WB Saunders Company;1996;
- Rugh JD, Barghi N, Drago CJ. Experimental occlusal discrepancies and nocturnal bruxism. J Prosthet Dent.1984; 51(4):548-553;
- Minagi S, Akamatsu Y, Matsunaga T, Sato T. Relationship between mandibular position and the coordination of masseter muscle activity during sleep in humans. J Oral Rehabil. 1998 Dec;25(12):902-7.
- Rosales VP, Ikeda K, Hizaki K, NaruoT, Nozoe S, Ito G. Emotional stress and brux-like activity of the masseter muscle in rats. Eur J Orthod. 2002; 24(1):107-117;
- Lobbezoo F, Ahlberg J, Manfredini D, Winocur E. Are bruxism and the bite causally related? J Oral Rehabil. 2012 Jul;39(7):489-501.
- Hellmann D, Giannakopoulos NN, Schmitter M, Lenz J, Schindler HJ. Anterior and posterior neck muscle activation during a variety of biting tasks. Eur J Oral Sci. 2012 Aug;120(4):326-34.
- Rugh JD, Solberg WK. Psychological implications in temporomandibular pain and dysfunction. Oral Sci Rev.1976;7:3-30;
- Solberg WK, Clark GT, Rugh JD. Nocturnal electromyographic evaluation of bruxism patients undergoing short term splin therapy. J Oral Rehabil. 1975; 2(3):215-223;
- Kato T, Thie NM; Huynh N, Miyawaki S, Lavigne GJ. Topical review: sleep bruxism and the role of peripheral sensory influence. J Orofac Pain 2003 Summer; 17(3):191-213.
- Okeson JP. A simplified technique for biteguard fabrication in bruxism. J Ky Dent Assoc. 1977 Oct; 29(4)11-16;
- Lavigne GJ, Kato T, Kolta A, Sessle BJ. Neurobiological mechanisms involved in sleep bruxism. Crit Rev Oral Biol Med. 2003; 14(1): 30-46;
- Lavigne GJ, Huynh N, Kato T, Okura K, Adachi K, Yao D, Sessle B. Genesis of sleep bruxism. Motor and autonomic-cardiac interactions. Arch Oral Biol. 2007 Apr; 52(4):381-384. Epub 2007 Feb 20;
- Kato T, Rompre P, Montplaisir JY, Sessle BJ, Lavigne GJ. Sleep bruxism: an oromotor activity secondary to micro-arousal. J Dent Res. 2001; 80 (10): 1940-1944;
- American Academy of Sleep Medicine. International classification of sleep disorders, 2nd ed. Diagnostic and coding manual. American Academy of Sleep Medicine. Westchester: IL; 2005;
- Chapotat B, Lin JS, Robin O, Jouvet M. Bruxism du sommeil: aspects fondamentaux et cliniques. J Parodontol Implant Orale.1999; 18(3): 277-289;
- Lobbezoo F, Naeije M. Bruxism is mainly regulated centrally, not peripherally. J Oral Rehabil. 2001; 28(12):1085-1091;
- Lobbezoo F, Van Der ZaagJ, Naeije M. Bruxism: its multiple causes and its effects on dental implants- un updated review. J Oral Rehabil. 2006;33(4):293-300;
- Hublin C, Kaprio J, Partinen M, Koskenvuo M. Sleep bruxism based on self- report in a nationwide twin cohort. J Sleep Res.1998;7(1):61-67;
- Abe Y, Suganuma T, Ishii M, Yamamoto G, Gunji T, Clark GT, Tachikawa T, Kiuchi Y, Igarashi Y, Baba K. Association of genetic, psychological and behavioral factors with sleep bruxism in a Japanese population. J Sleep Res. 2012 Jun;21(3):289-96.
- Winocur E, Gavish A, Vokovitch M, Emodi-Perlman A, Eli I. Drugs and bruxism: a critical review. J Orofac Pain.2003;17(2):99-111;
- Behr M, Hahnel S, Faltermeier A, Bürgers R, Kolbeck C, Handel G, Proff P. The two main theories on dental bruxism. Ann Anat. 2012 Mar 20;194(2):216-9.
- Mercuţ V, Scrieciu M, Popescu SM, Craitoiu M, Marasescu P, Marinescu R, Extended Case report. Bruxism with a history of early onset in a 25-year-old male. OHDM. 2011;10(4):209-214.