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Sleep bruxism and vigil bruxism

Sleep bruxism and vigil bruxism: Should we consider a new therapeutic approach?

 

J Ferrer-Gallegos1, G Gómez-Moreno2

 

Joaquín Ferrer Gallegos1, Dentist, Loja/Montefrío Health Center (Granada, Spain), managed by the Andalucian Public Health System.

Gerardo Gómez-Moreno2, Department of Special Care in Dentistry, Pharmacological Research in Dentistry, Director of Master in Periodontology and Implant Dentistry, Faculty of Dentistry, University of Granada, Granada, Spain.

 

Running Title: SB and VB

 

Corresponding author:

 

Joaquín Ferrer Gallegos

 

C/Pedro Antonio de Alarcón 41-1d

18004 Granada, Spain.

Tel.: +34 958520496

Fax.: +34 958520496

E-mail: dentistagranada@gmail.com

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Abstract

Sleep bruxism (SB) and vigil bruxism (VB) are pathologies that remain among a group of diseasesput aside “for further research.” Much is known of their consequences and treatment but little of their etiology. Perhaps this is because these disorders have unusually limiting effects on daily life, but never place the sufferer’s life in danger. Maybe if their etiology was known approaches to treating SB and VB might be more effective and long-lasting. Today, it is clear that they are two separate pathologies, with different muscular activity and different etiologies, although both may co-exist in a single individual. Approaches to therapies for treating their consequences are undergoing a change. To datethe use of daytime occlusal splints has been recommended for both SB and VB. The splints are uncomfortable and patients often fail to use them regularly; for this reason, it would appear logical to improve their design, a project that represents an important line of research. Occlusal considerations (dental contact) are losing relevance in approaches to both pathologies, in fact occlusal splints represent an interference in the whole stomatognathic system, but remain the first choice for treating the consequnces of bruxism. Meanwhile, it has been observed that drastic changes in occlusal vertical dimension prevent bruxist episodes (orthodontic treatment).

 

 

 

Keywords: sleep bruxism, vigil bruxism, management, oral rehabilitation.

 

 

 

 

 

 

 

 

Introduction

According to the American Association of Orofacial Pain (AAOP), bruxism is defined as a diurnal or nocturnal parafunctional activity including clenching, bracing, gnashing, and grinding of the teeth that may be diurnal, known as vigil bruxism (VB), nocturnal sleep bruxism (SB), or mixed (1-2).

 

            SB and VB consist of a rhythmic muscular activity, which is considered phasic when muscular contractions have intervals of 0.2 - 5 seconds, tonic if the contractions are of more than two seconds. In some cases the SB and VB may combine tonic and phasic contractions. The most frequent form of SB is phasic, while diurnal/vigil SB and VB is commonly tonic. It can be considered a parafunctional habit (non-functional, with no purpose) or an orally self-destructive habit (1-4). Presser SB and VB, also called centric and eccentric SB and VB wiper (5-6).

 

            Vigil SB and VB are considered to be a twitch related to stress in daily life, while SB is induced by the central nervous system (CNS) associated with mechanisms of sleep lightening or with micro-awakenings (7).  Diagnosis must determine whether SB / VBis slight, moderate or severe, whether it is vigil or sleep SB and VB, and whether it consists of tooth grinding or teeth clenching. SB and VB present a challenge to any dental treatment, no matter how simple. The patient must be made aware of the problem, understand the complications arising from SB and VB, which may prevent treatment from achieving the expected outcomes both in terms of the duration of treatment and the aesthetic results (6). There are several questionnaires to identify SB and VB(7, 8).

 

Infantile SB and VB

SB and VB can sometimes appear at a young age and require treatment whenever one of the following symptoms occurs: dental attrition, dental fractures, muscular hypertrophy, breakage of dental prostheses, premature loss of teeth, cephalea, or TMJ pain. Currently, the consumption of fizzy drinks is claimed to be the most significant factor in dental wear, causing much erosion among youngsters. Children with SB and VB also have a greater tendency to suffer high levels of anxiety, and SB and VB often occurs in children with anxious personalities; hyperactivity and attention deficit disorder are also risk factors. No causal relation has been identified between infantile SB and VB and TMJ disorders. Parafunctional habits (nail biting and thumb sucking) have been associated with vigil SB and VB.  But children with respiratory problems show a greater tendency towards sleep SB and VB, which can be alleviated by sleeping without a pillow to improve air flow in the airway; this also alleviates the SB and VB.  Children with SB and VB should not chew gum; daytime naps are recommended, no television before going to bed, and parents should read their child a story before they go to sleep (8-10). The occurrence of SB and VB at a young age predisposes the individual to suffering SB and VB in adulthood (11). A child with a pattern of dental wear is a challenge but at the same time an opportunity to prevent risks to permanent teeth. Sometimes a change of lifestyle (diet: avoiding fizzy drinks, stimulants, soft diet, television, whatsapp) can correct the bruxist habit (12).For children with SB and VB, the most important service that dental professionals can provide in the clinic is early diagnosis and the prompt implementation of preventative measures. However, it should be remembered that SB and VB are not the only cause of dental wear (13). The first teeth to be affected by bruxist tooth grinding in children are the canines (canine guidance) and result in lateralization of group function (loss of canine guidance). In the adult population, this wear is physiological and leads to group function, whether SB and VB is present or not (14-15).

Etiology

The etiology of SB is uncertain and there is no consensus as to its treatment.  It has a high prevalence in the general population and affects general health. Treating SB is not the same as treating its consequences (16). No agreement has been reached among the scientific community as to the exact definition or diagnosis of SB and VB. More information has been generated on SB as its study is more reliable and suited to scientific methodology (by means of polysomnography, for example). A better understanding of its etiology might serve to determine the most appropriate form of treatment (17). Most authors suggest that the origin of SB is pathophysiological and unrelated to temporomandibular joint (TMJ) anatomy, and even less so to dental occlusion (18).

 

For treating SB and VB, the drilling of selected teeth is neither indicated nor justifiable. More recent scientific research, involving premature contact with artificial crowns, with occlusal fillings or other means, have made it clear that these occlusal interferences reduce the bruxist habit. Artificial occlusal interferences reduce SB and VB but natural occlusal interferences are a consequence of SB and VB rather than its cause. The same scenario occurs regarding maxillary, mandibular and TMJ anatomy/architecture – not one scientific study has been able to relate SB and VB to these anatomical structures (19).

 

Clinical signs of SB and VB

Non-specific dental wear, dental fractures or fractured restorations, temporal/masseter hypertrophy, widening periodontal ligament space (x-ray) dental mobility without periodontal disease or dental pulp necrosis, ulceration in patients with removable prostheses, enlarged cheek line or lingual indentations (although there is some controversy regarding the latter), bruxofacets on night guards that follow a set pattern. SB and VB can be diagnosed using a Bruxcore plate: a bite plate fabricated with various layers of thermoplastic material (polyvinyl chloride) of different colors. It can also be diagnosed using a Bite force sensor: interplate or intrabuccal bite-force sensor, by using electromyography (Bitestrip device, recommended due to its low cost and ease of use: http://bitestrip.com), or polysomnography (for a complete sleep study). However, both the Bruxcore plate and intraoral sensors can alter the SB and VB pattern and their diagnostic value has been questioned (20, 21).

 

            Recent polysomnography studies suggest that periodontal sensory stimulation or dental occlusal contact is not necessary to activate masticatory muscles during sleep – these contractions also occur among edentulous subjects (22). Patients diagnosed with SB and VB, who also suffer TMJ pathology, present higher numbers of SB and VB episodes during sleep (23). Patients with SB present 2-5 times more episodes of tooth grinding than patients without SB. This suggests that SB is an aggravated form of transitory motor activity during sleep, and most of the sufferers do not complain of sleep disorders (24).

 

            SB episodes precede an increase in sympathetic nervous system activity (tachycardia/peripheral vasoconstriction) and might be caused by stimulation arising from sleep arousal; SB and VB are triggered when sleep suddenly becomes superficial, as an integrant part of an arousal reaction. SB episodes are more frequent during light sleep (with no REM) and in micro-awakenings as responses to arousal rather than as a pathology of sleep awakening. However, bruxists do not usually complain of sleep disorders (25-27).

 

             In accordance with the international classification of sleep disorders for the diagnosis of SB and VB (28) must be three factors: the patient reports – is aware of – tooth grinding or jaw clenching during sleep. One or more symptoms are present: 1)abnormal dental wear, 2)mandibular discomfort, mandibular fatigue, pain, lockjaw on awakening, 3)masseter hypertrophy in response to voluntary tooth clenching. And the third condition is masticatory muscle activity during sleep cannot be explained by any other sleep disorder, use of medical or neurological drug for sleep, or any other disorder resulting from substance use.  

 

            Polysomnography (PSG) in bruxists registers values of 20% maximum voluntary mandibular contraction. Patients with light SB (2-4 episodes per hour) may suffer facial aching or pain. Those with moderate or severe SB present more than four episodes per hour with a peak frequency of at least six peaks per episode, and 25 peaks per hour, and at least two grinding noise episodes per hour of sleep. 

 

 

SB and VB psycho-social factors

Stress in animals and humans suggest causality between stress and SB and VB, although this is difficult to establish as it has to do with psychological factors. Psychosocial factors have been studied using questionnaires and have associated SB and VB with stressed personality types, such as perfectionists, subjects with tendencies towards anger, aggression and hostility, depressives, those sensitive to stress, single people, individuals with high educational levels, and others who lack job satisfaction (29, 30). In any case, psychosocial factors associated with SB and VB differs greatly from one population to another and their relation would appear to be less significant than previously presumed. Animal studies have observed a trigeminal sensory loss in non-REM sleep, which explains the weak relation between SB and occlusal interferences (31).

 

Pathophysiological factors

Pathophysiological factors seem to be more important in the etiology of SB and VB, including sleep disorders, smoking, drugs (cocaine, heroine),alcohol consumption, medication(agonists y antagonists dopaminergics, tricycles antidepresives and ISRS, anfetaminics, trauma, disease, and genetic factors(2,3).

 

Sleep-related factors

Sleep bruxists present a reduction in slow wave sleep (revealed in polysomnography). SB and VB occur in response to awakening (microawakenings) in which electroencephalograms (EEG) reveal an increase in cardiac rhythm, respiratory changes, sudden body movements, peripheral vasoconstriction, and complete or incomplete awakening. Some 80% of SB and VB episodes are associated with involuntary leg movements. Generally, cerebral cortex activity increases during these microawakening episodes.  In patients with heavy snoring and obstructive sleep apnea syndrome the risk of SB and VB is considerably higher. These phenomena have not been studied sufficiently to determine whether a physiological relation to SB and VB really exists (32, 33).

 

Neurochemical factors

Recent research has speculated on the possible relation between disturbances to the neurotransmitter system (in particular, the basal ganglia) and the etiology of SB and VB. The acute use of L-dopa decreases SB and VB episodes, while chronic use increases episodes. Neuroleptic drugs in psychiatric patients cause vigil SB and VB to increase. In this way, a higher frequency of SB and VB has been observed in patients with heavy drug addiction (amphetamines, cocaine, heroin….) (34, 36). Smokers present double the incidence of SB and VB compared with non-smokers (35). These scenarios indicate that SB and VB is mediated by the CNS. But research into this phenomenon has only just begun and deeper and more specific research will take time.

 

Heredity

Heredity is a factor that has not been studied in depth, although it could prove an important factor. The exact mechanism of transmission – if one exists – remains unknown (25, 37).

 

Trauma and disease

SB and VB are receptive to trauma (mandibular dislocation, Le Fort fractures) (5) and diseases, such as brain damage (post-anoxic brain injury)(4), infection (18) (syphilis, parotitis, typhoid fever), systemic diseases (21) (tumors, psoriasis, arthritis), neurological and psychiatric diseases(neurosis, emotional tension)(26).

 

            Epidemiological studies have found that the rhythmic muscular activity associated with sleep SB and VB occurs among almost 60% of the adult population, although the extent of the activity is far below the threshold for SB diagnosis. For this reason, this rhythmic motor activity during sleep can be considered normal (38).The origin of SB and VB is multifactorial but is mainly a response to awakening. Dopamine disturbances are also involved in its origin. Factors such as smoking, alcohol consumption, heredity, trauma and disease play a role, while stress and other psychosocial factors probably play lesser roles than previously assumed (39, 40).

 

Emotional factors

That SB and VB are related to stress is a common opinion. Increased daily stress is often associated with increases in sleep SB and VB episodes. Responses to questionnaires have also associated stress with SB. Other research has set out to establish that a highly stressful lifestyle is a risk factor for SB and VB but this remains a field for further research with specific objectives. The relation is much more complex than first thought and may involve a range of factors such as psychosocial factors, anxiety and depression, TMJ and muscular pain, and personality type, as well as stress (41). Research must distinguish between sleep SB and VB (SB) and vigil SB and VB (VB), and between jaw clenching and tooth grinding in order to identify the real pathogenic pathways (42). SB is characterized by tooth grinding and sometimes by jaw clenching, while VB is mainly associated with jaw clenching and only rarely with tooth grinding. Each has different etiology and is influenced by diverse local and systemic factors (43, 44). A consensus has been reached that mandibular pain is associated with vigil SB and VB (jaw clenching) even though the pain is experienced on awakening. SB and VB diagnosis in questionnaires is mainly based on patients’ perception of pain in the masticatory muscles on awakening (45), which is more related to VB than SB.  Unfortunately, no studies have related emotional factors with CNS activity (given that the CNS activates SB). VB seems to be a consequence of emotional tension or psychosocial disorders that drive the subject to suffer prolonged contractions of the masticatory muscles. Again, it might be that dopamine is closely related to VB (46). On the basis of the literature published to date, jaw clenching while awake is associated with emotional factors and psychopathological disorders, while there is no evidence to relate SB with psychosocial disorders (47). It is remarkable that the PubMed Medical Sub-headings (MeSH) tree structure of movement disorders does not include SB and VB, even though this is defined as “a stereotypical movement disorder characterized by jaw clenching and tooth grinding” (48).

 

Consequences of SB and VB

 
Dental wear arising from SB and VB is a type of parafunctional (not physiological) attrition and will be pathological if it becomes associated with loss of the teeth’s masticatory function, if the teeth do not survive beyond their life expectancy, or if the patient suffers sensitivity or pain.  Abfraction – cuneiform cervical lesion – is also common in patients with SB and VB, in this case as a result of centric forces. Abraction forces could be impossible to repair for the dentist ifthe SB and VB coexist (49-51).

 

            Vertical, almost static, bruxist jaw clenching can also leave a characteristic ‘footprint’ such as dents in plastic or amalgam restorations, porcel

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