Journal of Oral Rehabilitation

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

Journal: Journal of Oral Rehabilitation

Manuscript ID: Draft ManuscriptFor Type: Review Peer Review Date Submitted by the Author: n/a

Complete List of Authors: Ferrer-Gallegos, Joaquín; Servicio Andaluz de Salud, Dentistry Gómez-Moreno, Gerardo; University of Granada, School of Dentistry

Patient: adult, paediatric

Condition: bruxism

Co-morbidity: stress, smoking, depression / mood disorder

Content method: prosthodontics, restorative dentistry, therapeutics

Study method: literature review

N/A Page 1 of 40 Journal of Oral Rehabilitation

1 2 3 Sleep bruxism and vigil bruxism: Should we consider a new 4 5 6 therapeutic approach? 7 8 9 10 11 J. FERRER-GALLEGOS *, G. GÓMEZ-MORENO 12 13 14 15 *Dentist, Loja/Montefrío Health Center (Granada, Spain), managed by the Andalusian 16 17 18 Public Health System.For Peer Review 19 20 †Full Professor Department of Special Care in Dentistry, Pharmacological Research in 21 22 Dentistry, Director of Master in Periodontology and Implant Dentistry, Faculty of 23 24 Dentistry, University of Granada, Granada, Spain. 25 26 27 28 29 30 31 32 33 Running Title: Sleep bruxism and vigil bruxism 34 35 36 37 38 39 40 41 Correspondence: 42 43 Joaquín Ferrer Gallegos. C/ Pedro Antonio de Alarcón 411d,18004 Granada (Spain) 44 Tel.: +34 958520496, Fax: +34 958520496 45 Email: [email protected] 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 N/A1 Journal of Oral Rehabilitation Page 2 of 40

1 2 3 SUMMARY 4 5 Sleep bruxism (SB) and vigil bruxism (VB) are pathologies that remain among a group of 6 7 diseases put aside “for further research.” Much is known of their consequences and 8 9 10 treatment but little of their etiology. Perhaps this is because these disorders have unusually 11 12 limiting effects on daily life, but never place the sufferer’s life in danger. Maybe if their 13 14 etiology was known approaches to treating SB and VB might be more effective and long 15 16 lasting. Today, it is clear that they are two separate pathologies, with different muscular 17 18 activity and differentFor etiologies, Peer although Review both may coexist in a single individual. 19 20 21 Approaches to therapies for treating their consequences are undergoing a change. To date 22 23 the use of daytime occlusal splints has been recommended for both SB and VB. The splints 24 25 are uncomfortable and patients often fail to use them regularly; for this reason, it would 26 27 appear logical to improve their design, a project that represents an important line of 28 29 30 research. Occlusal considerations (dental contact) are losing relevance in approaches to 31 32 both pathologies. In fact, occlusal splints represent interference in the whole 33 34 stomatognathic system and yet remain the first choice for treating the consequences of 35 36 bruxism. Meanwhile, it has been observed that drastic changes in occlusal vertical 37 38 dimension prevent bruxist episodes (orthodontic treatment). 39 40 41 42 43 44 KEYWORDS: sleep bruxism, vigil bruxism, management, oral rehabilitation. 45 46 47 48

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1 2 3 Introduction 4 5 Bruxism is defined as a diurnal or nocturnal parafunctional activity including tooth 6 7 clenching, bracing, gnashing, and grinding of the teeth that may be diurnal, known as vigil 8 9 10 bruxism (VB), nocturnal sleep bruxism (SB), or mixed (12). SB and VB consist of a 11 12 rhythmic muscular activity, which is considered phasic when muscular contractions have 13 14 intervals of 0.2 5 seconds, tonic if the contractions are of more than two seconds. In some 15 16 cases the SB and VB may combine tonic and phasic contractions. The most frequent form 17 18 of SB is phasic,For while VB isPeer commonly tonic. Review It can be considered a parafunctional habit 19 20 21 (nonfunctional, with no purpose) or an orally selfdestructive habit (14). SB and VB can 22 23 also be classified as centric consisting of clenching the teeth without sidetoside 24 25 movements, or excentric consisting of grinding the teeth by moving the jawbone (5, 6). 26 27 VB is considered to be a ‘tic’ related to stress in daily life, while SB is induced by 28 29 30 the central nervous system (CNS) associated with mechanisms of sleep lightening or with 31 32 microawakenings (7). In this way, they are separate pathologies with different etiologies. 33 34 Diagnosis must determine between the two and whether the SB/VB is slight, moderate or 35 36 severe, whether it consists of tooth grinding or teeth clenching. SB and VB present a 37 38 challenge to any dental treatment, no matter how simple. 39 40 41 The patient must be made aware of the problem, understand the complications 42 43 arising from the pathologies, which may prevent treatment from achieving the expected 44 45 outcomes both in terms of the duration of treatment and the aesthetic results (6). There are 46 47 several questionnaires designed to identify SB and VB (7, 8). 48 49 50 51 52 Infantile SB and VB 53 54 SB and VB can sometimes appear at a young age and require treatment whenever one of 55 56 the following symptoms occurs: dental , dental fractures, muscular hypertrophy, 57 58 59 60 N/A3 Journal of Oral Rehabilitation Page 4 of 40

1 2 3 breakage of dental prostheses, premature loss of teeth, headache, or TMJ pain. Currently, 4 5 the consumption of fizzy drinks is claimed to be the most significant factor in dental wear, 6 7 causing much erosion among youngsters. Children with SB and VB also have a greater 8 9 10 tendency to suffer high levels of anxiety, and SB and VB often occur in children with 11 12 anxious personalities; hyperactivity and attention deficit disorder are also risk factors. No 13 14 causal relation has been identified between infantile SB/VB and TMJ disorders. 15 16 Parafunctional habits (nail biting and thumb sucking) have been associated with VB. But 17 18 children with respiratoryFor problemsPeer show a Review greater tendency towards SB, which can be 19 20 21 alleviated by sleeping without a pillow to improve air flow in the airway; this also 22 23 alleviates the SB. 24 25 Children with SB and VB should not chew gum; daytime naps are recommended, 26 27 no television before going to bed, and parents should read their child a story before they go 28 29 30 to sleep (810). The occurrence of SB/VB at a young age predisposes the individual to 31 32 suffering SB/VB in adulthood (11). A child with a pattern of dental wear is a challenge but 33 34 at the same time an opportunity to prevent risks to permanent teeth. Sometimes a change of 35 36 lifestyle (diet: avoiding fizzy drinks, stimulants, soft diet, television, whatsapp) can correct 37 38 the bruxist habit (12). For children with SB/VB, the most important service that dental 39 40 41 professionals can provide in the clinic is early diagnosis and the prompt implementation of 42 43 preventative measures. However, it should be remembered that SB and VB are not the only 44 45 causes of dental wear (13). The first teeth to be affected by bruxist tooth grinding in 46 47 children are the canines (canine guidance) and result in lateralization of group function 48 49 50 (loss of canine guidance). In the adult population, this wear is physiological and leads to 51 52 group function, whether SB and VB are present or not (1415). 53 54 55 56 57 58 59 60 N/A4 Page 5 of 40 Journal of Oral Rehabilitation

1 2 3 Etiology 4 5 The etiology of SB is uncertain and there is no consensus as to its treatment. It has a high 6 7 prevalence in the general population and affects general health. Treating SB is not the 8 9 10 same as treating its consequences (16). No agreement has been reached among the 11 12 scientific community as to the exact definition or diagnosis of SB and VB. More 13 14 information has been generated on SB as its study is more reliable and suited to scientific 15 16 methodology (by means of polysomnography, for example). A better understanding of its 17 18 etiology might For serve to determine Peer the most Review appropriate form of treatment (17). Most 19 20 21 authors suggest that the origin of SB is pathophysiological and unrelated to 22 23 (TMJ) anatomy, and even less so to dental (18). 24 25 For treating SB and VB, the drilling of selected teeth is neither indicated nor 26 27 justifiable. More recent scientific research, involving premature contact with artificial 28 29 30 crowns, with occlusal fillings, or other means, have made it clear that these occlusal 31 32 interferences reduce the bruxist habit. Artificial occlusal interferences reduce SB and VB 33 34 but natural occlusal interferences are a consequence of SB and VB rather than its cause. 35 36 The same scenario occurs regarding maxillary, mandibular and TMJ anatomy/architecture 37 38 – not one scientific study has been able to relate SB and VB to these anatomical structures 39 40 41 (19). 42 43 44 45 Clinical signs of SB and VB 46 47 Clinical signs of SB and VB are as follows: nonspecific dental wear, dental fractures or 48 49 50 fractured restorations; temporal/masseter hypertrophy; widening periodontal ligament 51 52 space (xray); dental mobility without or dental ; 53 54 ulceration in patients with removable prostheses; enlarged cheek line or lingual 55 56 indentations (although there is some controversy regarding the latter); bruxofacets on night 57 58 59 60 N/A5 Journal of Oral Rehabilitation Page 6 of 40

1 2 3 guards that follow a set pattern. SB and VB can be diagnosed using a Bruxcore plate: a bite 4 5 plate fabricated with various layers of thermoplastic material (polyvinyl chloride) of 6 7 different colors. It can also be diagnosed using a Bite force sensor: interplate or intrabuccal 8 9 10 biteforce sensor, by using electromyography (Bitestrip device, recommended due to its 11 12 low cost and ease of use: http://bitestrip.com), or polysomnography (for a complete sleep 13 14 study). However, both the Bruxcore plate and intraoral sensors can alter the SB and VB 15 16 pattern and their diagnostic value has been questioned (20, 21). 17 18 Recent polysomnographyFor Peer studies suggest Review that periodontal sensory stimulation or 19 20 21 dental occlusal contact is not necessary to activate masticatory muscles during sleep – 22 23 these contractions also occur among edentulous subjects (22). Patients diagnosed with SB, 24 25 who also suffer TMJ pathology, present higher numbers of SB episodes during sleep (23). 26 27 Patients with SB present 25 times more episodes of tooth grinding than patients without 28 29 30 SB. This suggests that SB is an aggravated form of transitory motor activity during sleep, 31 32 and most of the sufferers do not complain of sleep disorders (24). 33 34 SB episodes precede an increase in sympathetic nervous system activity 35 36 (tachycardia/peripheral vasoconstriction) and might be caused by stimulation arising from 37 38 sleep arousal; SB is triggered when sleep suddenly becomes superficial, as an integrant 39 40 41 part of an arousal reaction. SB episodes are more frequent during light sleep (with no 42 43 REM) and in microawakenings as responses to arousal rather than as a pathology of sleep 44 45 awakening. However, bruxists do not usually complain of sleep disorders (2527). 46 47 In accordance with the international classification of sleep disorders, there must be 48 49 50 three factors present for the diagnosis of SB (28): the patient reports – is aware of – tooth 51 52 grinding or jaw clenching during sleep. One or more symptoms are present: 1) abnormal 53 54 dental wear, 2) mandibular discomfort, mandibular fatigue, pain, lockjaw on awakening, 3) 55 56 masseter hypertrophy in response to voluntary tooth clenching. The third condition is 57 58 59 60 N/A6 Page 7 of 40 Journal of Oral Rehabilitation

1 2 3 masticatory muscle activity during sleep that cannot be explained by any other sleep 4 5 disorder, use of medical or neurological drug for sleep, or any other disorder resulting from 6 7 substance use. 8 9 10 Polysomnography (PSG) in bruxists registers values of 20% maximum voluntary 11 12 mandibular contraction. Patients with light SB (24 episodes per hour) may suffer facial 13 14 aching or pain. Those with moderate or severe SB present more than four episodes per 15 16 hour with a peak frequency of at least six peaks per episode, and 25 peaks per hour, and at 17 18 least two grindingFor noise episodes Peer per hour of Review sleep. 19 20 21 22 23 SB and VB psycho-social factors 24 25 Stress in animals and humans suggest causality between stress and SB and VB, although 26 27 this is difficult to establish as it has to do with psychological factors. Psychosocial factors 28 29 30 have been studied using questionnaires and have associated SB and VB with stressed 31 32 personality types, such as perfectionists, subjects with tendencies towards anger, 33 34 aggression and hostility, depressives, those sensitive to stress, single people, individuals 35 36 with high educational levels, and others who lack job satisfaction (29, 30). In any case, 37 38 psychosocial factors associated with SB and VB differ greatly from one population to 39 40 41 another and their relation would appear to be less significant than previously presumed. 42 43 Animal studies have observed a trigeminal sensory loss in nonREM sleep, which explains 44 45 the weak relation between SB and occlusal interferences (31). 46 47 48 49 50 Pathophysiological factors 51 52 Pathophysiological factors seem to be more important in the etiology of SB and VB, 53 54 including sleep disorders, smoking, drugs (cocaine, heroin), alcohol consumption, 55 56 57 58 59 60 N/A7 Journal of Oral Rehabilitation Page 8 of 40

1 2 3 medication (dopaminergic agonists and antagonists, tricyclic antidepressants and SRIs, 4 5 amphetamines), trauma, disease, and genetic factors (2,3). 6 7 8 9 10 Sleep-related factors 11 12 Sleep bruxists present a reduction in slow wave sleep (revealed in polysomnography). SB 13 14 occurs in response to awakening (microawakenings) in which electroencephalograms 15 16 (EEG) reveal an increase in cardiac rhythm, respiratory changes, sudden body movements, 17 18 peripheral vasoconstriction,For Peer and complete orReview incomplete awakening. Some 80% of SB 19 20 21 episodes are associated with involuntary leg movements. Generally, cerebral cortex 22 23 activity increases during these microawakening episodes. In patients with heavy snoring 24 25 and obstructive sleep apnea syndrome the risk of SB is considerably higher. These 26 27 phenomena have not been studied sufficiently to determine whether a physiological 28 29 30 relation to SB and VB really exists (32, 33). 31 32 33 34 Neurochemical factors 35 36 Recent research has speculated on the possible relation between disturbances to the 37 38 neurotransmitter system (in particular, the basal ganglia) and the etiology of SB and VB. 39 40 41 The acute use of Ldopa decreases SB and VB episodes, while chronic use increases 42 43 episodes. Neuroleptic drugs in psychiatric patients cause VB to increase. In this way, a 44 45 higher frequency of SB and VB has been observed in patients with heavy drug addiction 46 47 (amphetamines, cocaine, heroin….) (34, 36). Smokers present double the incidence of SB 48 49 50 and VB compared with nonsmokers (35). These scenarios indicate that SB and VB are 51 52 mediated by the CNS. But research into this phenomenon has only just begun and deeper 53 54 and more specific investigation will take time. 55 56 57 58 59 60 N/A8 Page 9 of 40 Journal of Oral Rehabilitation

1 2 3 Heredity 4 5 Heredity is a factor that has not been studied in depth, although it could prove an important 6 7 factor. The exact mechanism of transmission – if one exists – remains unknown (25, 37). 8 9 10 11 12 Trauma and disease 13 14 SB and VB are receptive to trauma (mandibular dislocation, Le Fort fractures) (5) and 15 16 diseases such as brain damage (postanoxic brain injury) (4), infection (18) (syphilis, 17 18 , typhoidFor fever), systemic Peer diseases (21)Review (tumors, psoriasis, arthritis), neurological 19 20 21 and psychiatric diseases (neurosis, emotional tension) (26). 22 23 Epidemiological studies have found that the rhythmic muscular activity associated 24 25 with SB occurs among almost 60% of the adult population, although the extent of the 26 27 activity is far below the threshold for SB diagnosis. For this reason, this rhythmic motor 28 29 30 activity during sleep can be considered normal (38). The origin of SB is multifactorial but 31 32 is mainly a response to awakening. Dopamine disturbances are also involved in its origin. 33 34 Factors such as smoking, alcohol consumption, heredity, trauma and disease play a role, 35 36 while stress and other psychosocial factors probably play lesser roles than previously 37 38 assumed (39, 40). 39 40 41 42 43 Emotional factors 44 45 That SB and VB are related to stress is a common opinion. Increased daily stress is often 46 47 associated with increases in SB. Responses to questionnaires have also associated stress 48 49 50 with SB. Other research has set out to establish that a highly stressful lifestyle is a risk 51 52 factor for SB and VB but this remains a field for further research with specific objectives. 53 54 The relation is much more complex than first thought and may involve a range of factors 55 56 such as psychosocial factors, anxiety and depression, TMJ and muscular pain, and 57 58 59 60 N/A9 Journal of Oral Rehabilitation Page 10 of 40

1 2 3 personality type, as well as stress (41). Research must distinguish between SB and VB, and 4 5 between jaw clenching and tooth grinding in order to identify the real pathogenic pathways 6 7 (42). 8 9 10 SB is characterized by tooth grinding and sometimes by jaw clenching, while VB is 11 12 mainly associated with jaw clenching and only rarely with tooth grinding. Each has 13 14 different etiology and is influenced by diverse local and systemic factors (43, 44). A 15 16 consensus has been reached that mandibular pain is associated with VB (jaw clenching) 17 18 even though theFor pain is experienced Peer on awakening. Review SB and VB diagnosis in questionnaires 19 20 21 is mainly based on patients’ perception of pain in the masticatory muscles on awakening 22 23 (45), which is more related to VB than SB. 24 25 Unfortunately, no studies have related emotional factors with CNS activity (given 26 27 that the CNS activates SB). VB seems to be a consequence of emotional tension or 28 29 30 psychosocial disorders that drive the subject to suffer prolonged contractions of the 31 32 masticatory muscles. Again, it might be that dopamine is closely related to VB (46). On the 33 34 basis of the literature published to date, jaw clenching while awake is associated with 35 36 emotional factors and psychopathological disorders, while there is no evidence to relate SB 37 38 with psychosocial disorders (47). It is remarkable that the PubMed Medical Subheadings 39 40 41 (MeSH) tree structure of movement disorders does not include SB and VB, even though 42 43 this are defined as “a stereotypical movement disorder characterized by jaw clenching and 44 45 tooth grinding” (48). 46 47 48 49 50 Consequences of SB and VB 51 52 Dental wear arising from SB and VB is a type of parafunctional (not physiological) 53 54 attrition and will be pathological if it becomes associated with loss of the teeth’s 55 56 masticatory function, if the teeth do not survive beyond their life expectancy, or if the 57 58 59 60 N/A10 Page 11 of 40 Journal of Oral Rehabilitation

1 2 3 patient suffers sensitivity or pain. Abfraction – cuneiform cervical lesion – is also 4 5 common in patients with SB and VB, in this case as a result of centric forces. Abraction 6 7 forces may be impossible for the dentist to remedy if the SB and VB coexist (4951). 8 9 10 Vertical, almost static, bruxist jaw clenching can also leave a characteristic 11 12 ‘footprint’ such as dents in plastic or amalgam restorations, porcelain fractures with 13 14 extrusion of the antagonist canine. This is harder to observe on and is not 15 16 always attributable to SB and VB (52, 53). Tooth grinding provokes a great deal of 17 18 attrition (canine,For molar, and Peerincisor), which isReview not suffered by jawclenchers. Considerable 19 20 21 levels of attrition can be provoked without major muscular forces (54, 55). 22 23 It is important for the dentist to understand and be able to distinguish between the 24 25 different processes responsible for dental wear (SB and VB, physiological/pathological 26 27 attrition, mastication, , abfraction, erosion, and resorption) as they often interact – 28 29 30 it is rare for a single factor to act alone – and produce irreversible lesions of the teeth. Once 31 32 more, precise diagnosis and prevention are fundamental (56). Dentists must distinguish 33 34 between attrition (flat wear with antagonist contact) and erosion (concave wear without 35 36 antagonist contact) (57). Bite guards should be inspected; if this device does not show any 37 38 wear while the teeth do, then the cause will be other than SB or VB. There are 39 40 41 questionnaires to discern different types and causes of (58, 59). 42 43 SB and VB produce fissures in the teeth (which can reach as far as the dental pulp), 44 45 attrition, abfraction, pulp stones, periodontal widening (tooth mobility), periapical 46 47 granulomas (pulp necrosis due to fissures or wear). The first step is to treat or manage the 48 49 50 SB/VB and the second to deal with the dental pathology. Special care must be taken with 51 52 these fissures and with their extent. Providing they do not present pulpar affectation – even 53 54 though they may appear to reach the pulp – then treatment will be conservative (simple 55 56 filling), but if the pulp is affected then endodontic treatment must be carried out and in 57 58 59 60 N/A11 Journal of Oral Rehabilitation Page 12 of 40

1 2 3 some cases the treatment will be extraction of the tooth (if the fissure involves furcation, 4 5 roots, or the tooth’s prognosis). The patient must be alerted to the weakness of the 6 7 endodontically treated tooth, further endangered by SB/VB (60). The consequences of 8 9 10 on healthy periodontia are reversible. This affects the toothsupporting 11 12 periodontium and aggravates the situation in cases of patients with periodontitis (61). 13 14 Occlusal Interference has little or nothing to do with the incidence of bruxist symptoms 15 16 (62, 63). 17 18 For Peer Review 19 20 21 Effects of SB/VB on musculature and muscular disorders (A) 22 23 The Effects of SB/VB on musculature and muscular disorders are as follows: protective 24 25 contraction, myofascial pain, myositis, myospasm (acute ), muscular contraction or 26 27 chronic trismus, hypertrophy, abnormal (nonpainful) muscle enlargement, occasionally 28 29 30 with limited mandibular range (64, 65). 31 32 33 34 Management of the etiology of SB and VB 35 36 There is no specific or definitive treatment for SB and VB. Dental contact in SB is a 37 38 consequence of jaw motor activation rather than a cause. Intraoral and occlusal peripheral 39 40 41 factors do not directly trigger SB and VB. For SB sufferers, the increased activity of jaw 42 43 elevator muscles and increased dental contact could be associated with increased 44 45 mechanical load on the teeth, muscles, TMJ, and dental prostheses. As we have seen, in SB 46 47 the teeth and TMJ are not directly involved, nor are esophagolaryngeal structures (6669). 48 49 50 51 52 Treating the consequences of SB and VB 53 54 Influence of occlusal splints on SB and VB activity 55 56 57 58 59 60 N/A12 Page 13 of 40 Journal of Oral Rehabilitation

1 2 3 Many different studies have observed no differences in bruxist activity as a result of the 4 5 use of occlusal splints with canine guidance compared with splints with group function. 6 7 One study established that a plate that only covered the upper incisors did manage to 8 9 10 reduce the frequency and intensity of bruxist episodes, while a normal occlusal splint did 11 12 not achieve anything (whether with canine guidance or group function). Another study 13 14 showed that a plate with moderate mandibular advancement also succeeded in lowering the 15 16 frequency and intensity of episodes (70). 17 18 In any case,For the scientific Peer community Review does not accept that a bite plate, or any other 19 20 21 type of plate, acts on the genesis of SB by eliminating occlusal contact. Its use is justified 22 23 only by its protection of the teeth or prosthetics under attack (71, 72). One interpretation 24 25 of the role of occlusal splints is that the teeth and mucosa in contact with the splint (cheek, 26 27 tongue, , , etc.) might generate unusual sensory information that alerts the 28 29 30 sleeping subject and stops him/her grinding the teeth so intensively (73). To sum up, 31 32 current knowledge and understanding of trigeminal physiology and research into SB and 33 34 VB indicate that dental contact is the result of activation of the elevating musculature in 35 36 vigil and in sleep (74). In repose, teeth are separated physiologically. It is the central 37 38 nervous system that activates SB and VB by means of the jaw elevating muscles, 39 40 41 indicating that peripheral factors are not primary in activating bruxist episodes. Current 42 43 research into the connections between peripheral factors, SB and VB and its consequences 44 45 remains insufficient (75). 46 47 Craniofacial pain and SB/VB should be treated as separate problems as there is no 48 49 50 linear relation between them and bruxists may or may not suffer from this type of pain 51 52 (76). SB and VB per se do not act as an etiological factor for TMJ disorders, but it does 53 54 prolong these pathologies and hinders recovery. The SB/VB/TMJ disturbance relation has 55 56 not yet been studied purposefully and in isolation (77). 57 58 59 60 N/A13 Journal of Oral Rehabilitation Page 14 of 40

1 2 3 The forces generated in normal mastication range between 20 and 120N but in SB 4 5 and VB episodes they can reach 1.500N (in extreme or exceptional cases), causing severe 6 7 wear and even dental fractures or restoration fractures as a result of fatigue (78, 79). 8 9 10 Patients with severe SB and VB have been treated with botulinum toxin injections into two 11 12 separate masseter muscles and it was observed that muscle relaxation has an ephemeral life 13 14 of between 16 and 24 weeks, causing further dysarthria and dysphagia. This does not cure 15 16 SB or VB but can be useful for dealing with severe episodes of tonic contraction (8083). 17 18 The objectiveFor of occlusal Peer splints is toReview protect dental structures. Their use does not 19 20 21 guarantee the avoidance of parafunction (as an umbrella will not stop rain). While they 22 23 may prevent muscular pain and fatigue when the patient wakes up, they will not prevent or 24 25 cure SB or VB (84). Recent research has suggested a null relation between dental 26 27 occlusion and SB. Occlusal splints with canine guidance or group function obtain similar 28 29 30 results and it is not clear which is the better option (85). The effects of occlusal splints on 31 32 SB and VB are unpredictable, can even exacerbate the problem, and may have no effect at 33 34 all. Soft occlusal splints exacerbate both SB and VB (86). Occlusal splints do not help 35 36 cases of intermittent or permanent TMJ lock, as they do not act on condylar disc position. 37 38 Such cases need a mandibular advancement device (which should not be used for more 39 40 41 than a year in the same position) that must cover all teeth in order to avoid extrusions, and 42 43 must maintain contact between all antagonist teeth (87). 44 45 SB is a parasomnia (88) and VB is a habit (89), the latter should be treated by 46 47 addressing emotional factors and by reducing stress. For treating VB, it is essential that the 48 49 50 condition shifts from the subconscious to the conscious, so that the patient is made fully 51 52 aware of his/her habit. To do this, a range of techniques can be applied that include 53 54 psychoanalysis and autosuggestion, aversion therapy, relaxation techniques, conscious 55 56 muscle relaxation training, biofeedback, massed practice therapy, and hypnosis (90). 57 58 59 60 N/A14 Page 15 of 40 Journal of Oral Rehabilitation

1 2 3 When making an occlusal splint, the minimum thickness of the acrylic should be 2 4 5 mm in molar regions, to provide sufficient strength and resistance to wear. To rehabilitate 6 7 lost vertical dimension (VD), no method indicates an exact position; this will be 8 9 10 determined by restoration needs. The lips must remain comfortably in contact without 11 12 incisor contact, and the patient should assess their own facial aesthetics in the mirror. In 13 14 order for procedures to be registered, repeatable, and unalterable, and to supply 15 16 information to the laboratory, an anterior bite plate should be used, which can also be used 17 18 to take a bite registerFor (91, 92).Peer Using the Reviewsemiadjustable articulator, the dentist works 19 20 21 with the jaw in therapeutic occlusion (the position in which muscles and TMJ would be 22 23 relaxed and stable in the future interdental relation), rather than centric relation (CR); in 24 25 this way, the bite key will be taken in therapeutic occlusion rather than CR (9396). 26 27 Patients’ use of occlusal splints is often irregular (for example when patients fall 28 29 30 asleep watching television without the splint in place, or forget to wear it, or find it 31 32 embarrassing…). The dentist usually supplies an occlusal splint (as a gift) after performing 33 34 rehabilitation in an attempt to prolong the survival of the treatment but this measure does 35 36 not ensure that the splint will be used, or appreciated. For this reason it is important to 37 38 stress the importance of splint use but even so, it might not be used regularly and it is for 39 40 41 this reason that implementing canine guidance is so important. The requirements of the 42 43 occlusal splint is that it be comfortable and avoid iatrogeny. It should be flat (so that it does 44 45 not trap the jaw), smooth, polished, stable, comfortable, and make contact with all 46 47 antagonists. It must seek a balance between weight and strength, as the thicker the splint, 48 49 50 the more uncomfortable it will be (97). 51 52 53 54 Restorative dentistry and SB/VB 55 56 57 58 59 60 N/A15 Journal of Oral Rehabilitation Page 16 of 40

1 2 3 Silver amalgam should be considered for restorations in bruxist patients due to its high 4 5 strength and good performance in extensive restorations, although no material to date has 6 7 produced satisfactory longterm results (98). When performing , the 8 9 10 principal of minimum invasiveness, minimizing dental tissue loss, should be applied in all 11 12 restoration dentistry including the treatment of bruxist patients (99). Metal materials 13 14 undergo wear in similar ways to dental tissue, through their characteristic nonelastic 15 16 deformation. Porcelains are fragile and rigid and also cause wear to the antagonist tooth. 17 18 Resins suffer wearFor but do notPeer exert wear onReview the antagonist; they are easily handled and 19 20 21 combining resins with porcelain materials improves their properties. Ceromers (resin plus 22 23 porcelain filling crystals) improve the individual properties of their components, handle 24 25 well in the clinic and in the laboratory (metal/ceromer crowns), but lack adhesion between 26 27 the two phases which leads to loss of filling material (ceramic) when the matrix (resin) 28 29 30 suffers wear (100102). Fragile materials such as porcelain have different wear 31 32 mechanisms from those observed in ductile materials such as metal (103). 33 34 Patients with xerostomy not only have less saliva, but the saliva they do have is 35 36 more acidic, which increases corrosion and wear on restoration materials and teeth (104). 37 38 The ideal material is that which accompanies normal wear without affecting (exerting wear 39 40 41 on) the antagonist. The success of composite fillings in posterior teeth depends on the size 42 43 of the restoration, and so these materials are counterindicated for patients with SB and VB 44 45 whenever the filling required is large and functional. In such cases, amalgam or 46 47 incrustations are preferable. Porcelain restorations tend to suffer microfissures in bruxist 48 49 50 patients, and so it is better to use metal/porcelain crowns rather than porcelain alone. 51 52 Zirconia is more liable to fracture. When aesthetics permit, it is better to use amalgam or 53 54 metal alloys. Gold alloys present the most similar wear levels to dental enamel but are not 55 56 well received by patients for reasons of aesthetics (105, 106). 57 58 59 60 N/A16 Page 17 of 40 Journal of Oral Rehabilitation

1 2 3 In the case of SB, the first course of action is to recommend to patients that they 4 5 avoid all stimulating factors for at least two hours before they go to sleep (smoking, 6 7 alcohol, coffee, television) (107). It is important to distinguish between SB, VB and TMJ 8 9 10 disorders; they are not the same thing and although they can coexist they have different 11 12 etiologies and are treated differently (108, 109). 13 14 15 16 Prosthetic rehabilitation in SB and VB patients 17 18 When rehabilitatingFor a bruxist Peer (B), it is important Review to be aware that the centric relation (CR) 19 20 21 is a forced position, limited by ligaments, retruded, and if rehabilitation takes place with 22 23 the jaw in this jaw position, the TMJ may be affected generating pathology and discomfort. 24 25 This retruded position can only be maintained by the patient for very short periods (no 26 27 more than a moment). After any excursion, the will always return to the 28 29 30 intercuspal position (IP, one of comfort, without interference, although it may differ from 31 32 the ideal occlusion). All masticatory muscles possess force vectors upwards and forwards, 33 34 and so firstly, it is not anatomically possible for the jaw to be kept in a retruded position 35 36 for long and secondly, any clinical maneuver to retrude the jaw effectively will depend on 37 38 prior relaxation of the masticatory muscles. 39 40 41 Working in the CR means working with ligaments and articulations in tension 42 43 (110). Maximum intercuspation (MI) is the only stable occlusal relation (111115). CR is a 44 45 point that is used to locate a therapeutic position or a stable, painless and comfortable 46 47 occlusion in MI. In CR, only two antagonist teeth are in contact and in the past it was 48 49 50 proposed that the selective wear of these teeth could be considered as interference, 51 52 although nowadays this is considered to be iatrogenic, and in any case, a new ‘interference’ 53 54 in CR will always occur. Sometimes, the discrepancy between CR and MI is greater than 55 56 the accepted measurement (in mm). In these cases the cause must be established, which 57 58 59 60 N/A17 Journal of Oral Rehabilitation Page 18 of 40

1 2 3 may be osteoarthrosis of the TMJ (degeneration), or dental occlusion with a need to 4 5 increase the vertical dimension (VD) to find the CR, which also increases the CR/MI 6 7 distance (116, 117). 8 9 10 In young or adolescent patients, the dentist must proceed with caution, given that 11 12 the longevity of treatments tends to be short. Again, it is essential to establish etiology and 13 14 to initiate preventative measures (118). 15 16 Dental attrition is a very slow process and sometimes it is better not to intervene. 17 18 But once SB and/orFor VB have Peer been diagnosed Review and the etiology sought, there is no need to 19 20 21 delay restorative treatment. Abrupt changes in vertical dimension (complete rehabilitation) 22 23 or in occlusion (orthodontic treatments) will not bring about any repercussions for SB and 24 25 VB pathology, will neither increase nor reduce the parafunction (119, 120). 26 27 Dental wear is a natural process that does not usually require a specific treatment; 28 29 30 even when wear is severe it may not need oral rehabilitation, providing adaptation is 31 32 satisfactory. In cases where restoration is indicated, there is time enough to deliberate 33 34 treatment carefully. It has been shown that dentoalveolar compensation can cause the 35 36 vertical dimension of occlusion (VDO) to remain relatively constant, or even increase in 37 38 spite of dental wear, which means that increasing VDO as an element of restoration is 39 40 41 unnecessary. If restoration is necessary, it must be established whether or not the space 42 43 required by restoration is available in MI position and that the restoration’s retention and 44 45 strength will be adequate (121123). With fixed cemented prostheses, the design of tooth 46 47 preparation is key to increasing retention and reducing the chances of debonding. It would 48 49 50 appear that the endodontic treatment/ screw post technique is a worse option than good 51 52 tooth preparation. Splinting should be avoided whenever possible; with a short post the 53 54 addition of a second post is not indicated, given that debonding, rotation, or other 55 56 vicissitudes are equally probable. There is no evidence to suggest that the use of occlusal 57 58 59 60 N/A18 Page 19 of 40 Journal of Oral Rehabilitation

1 2 3 splints in cases of severe wear in patients with fixed prostheses improves the restorations’ 4 5 prognoses (124). 6 7 In cases of reduced VDO due to dental wear, VDO should be maintained and not 8 9 10 modified (in any case, a compensating overeruption usually occurs). Providing there are no 11 12 functional problems, it will be better to conserve the patient’s worn occlusion and it is not 13 14 essential to increase VDO to meet some preconceived standard of normality. However, it 15 16 will be necessary to increase VDO in cases with interocclusal space problems or 17 18 whenever aestheticsFor are severely Peer compromised. Review In these two circumstances, the dentist 19 20 21 should not hesitate to increase VDO, and problems of adaptation to the new vertical 22 23 dimension are rare. Under conditions of heavy loading, metal (ideally gold), porcelain, or 24 25 ceromer restorations would appear the better option, although no material will resist for 26 27 long. In children, resin based composite materials can be used for restoration (low 28 29 30 sensitivity and they prevent VDO loss), instead of other more permanent restoration 31 32 materials, although their survival will be only short term (125). Plastic or resin restorations 33 34 (removable prostheses) also suffer early fracture and antagonist dentoalveolar extrusion 35 36 (126, 127). 37 38 39 40 41 SB and VB and implant dentistry 42 43 SB and VB are considered an absolute counter indication for implantbased rehabilitation, 44 45 due to the risk of short or mediumterm failure of both the implant itself and the implant 46 47 supported prosthesis. When implants are placed, they must not have excessive cantilevers, 48 49 50 must be kept out of occlusion and only make contact in MI. The more implants placed to 51 52 support prostheses, the better the prognosis. In totally edentulous patients, fixed bonded 53 54 metalporcelain prostheses are recommended in the upper maxillary, and hybrid 55 56 metal/resin in the mandible. To date, no scientific evidence exists to link cause and effect 57 58 59 60 N/A19 Journal of Oral Rehabilitation Page 20 of 40

1 2 3 between SB and VB and implant failure. When performing a total rehabilitation with 4 5 implants, all patients should be treated as potential bruxists as this may be the case, even 6 7 though the patient is unaware of the SB/VB and there may be no clinical signs that confirm 8 9 10 the presence of SB and/or VB. It has not been established that occlusal splints are essential 11 12 for these patients and the most important factor is to create a satisfactory occlusion (128, 13 14 129). When patients present wear to various natural teeth on both sides, canine guidance 15 16 must be reconstructed and then an occlusal splint fabricated. Canine guidance is a better 17 18 option than groupFor function asPeer only two teeth Review will suffer wear, instead of the eight or more 19 20 21 teeth involved in group function (130, 131). 22 23 24 25 Conclusions 26 27 The etiology of SB resides in the CNS, while VB is associated with emotional factors; the 28 29 30 two types are different. SB and VB are mediated fundamentally by the central rather than 31 32 the peripheral nervous system (occlusion/TMJ), although betterdesigned studies are 33 34 needed into this pathology, one that presents such a fascinating but frustrating challenge to 35 36 the dental professional. SB and VB are without doubt one of the least studied oral 37 38 pathologies and yet one of the most common pathologies in dentistry. Its etiopathology 39 40 41 remains unknown. 42 43 Higher education teaching should treat SB and VB as a separate subject, rather than as a 44 45 subsection mentioned in passing, as at present. 46 47 Occlusal splints do not cure SB and VB, but act on the consequences; they do not prevent 48 49 50 the process and do not affect its genesis. Occlusal interferences (whether natural or 51 52 artificial) may reduce and alleviate SB and VB episodes. In normal CR, only antagonist 53 54 dental pieces are in contact; in the past the selective wear of antagonist pairs were 55 56 57 58 59 60 N/A20 Page 21 of 40 Journal of Oral Rehabilitation

1 2 3 considered as interference; today, this is considered iatrogenic, and in an any case there 4 5 will always be a new ‘interference’ in CR before long. 6 7 It is important to make patients aware of their VB, so that the habit shifts from being sub 8 9 10 conscious to conscious. 11 12 No dental restoration material to date has provided satisfactory longterm outcomes under 13 14 duress from SB and/or VB. The ideal material can withstand physiological wear without 15 16 affecting the antagonist. Working in the centric relation means working in a situation of 17 18 tendon and jointFor tension. Maximum Peer intercuspation Review is the only stable occlusal relation. 19 20 21 In bruxist patients, the survival of dental treatment outcomes may be shortlived. 22 23 Once SB and VB have been diagnosed and the etiology sought, there is no need to delay 24 25 restorative treatment. Abrupt changes in vertical dimension (complete rehabilitation) or in 26 27 occlusion (orthodontic treatments) will not produce any repercussions for SB and VB 28 29 30 pathology, will neither increase nor reduce the parafunction. 31 32 When the occlusal vertical dimension is reduced due to wear, it is recommendable to 33 34 maintain this OVD rather than modify it; it should only be modified in severe cases that 35 36 compromise facial aesthetics, and problems rarely occur as a result of adapting to the new 37 38 OVD. 39 40 41 Canine guidance is better than group function as only two teeth will be subjected to wear, 42 43 while eight teeth or more are affected in group function. 44 45 46 47 48 References 49 50 1.Svensson P, BaadHansen L, Pigg M, List T, Eliav E et al ; Special Interest Group of 51 52 Orofacial Pain. Guidelines and recommendations for assessment of somatosensory 53 54 function in orofacial pain conditionsa taskforce report. J Oral Rehabil. 2011;38:366394. 55 56 57 58 59 60 N/A21 Journal of Oral Rehabilitation Page 22 of 40

1 2 3 2.Lobbezoo F1, Ahlberg J, Manfredini D, Winocur E. Are bruxism and the bite causally 4 5 related? J Oral Rehabil. 2012;39:489501. 6 7 8 9 10 3. Falisi G, Rastelli C, Panti F, Maglione H, Quezada Arcega R. Psychotropic drugs and 11 12 bruxism. Expert Opin Drug Saf . 2014;13:13191326. 13 14 15 16 4. Winocur E, Gavish A, Voikovitch M, EmodiPerlman A, Eli I. Drugs and bruxism: a 17 18 critical review. JFor Orofacial Pain.Peer 2002;17:99111. Review 19 20 21 22 23 5. DíazSerrano KV, da Silva CBA, de Albuquerque S, Pereira Saraiva MDC, Nelson 24 25 Filho P. Is there an association between bruxism and intestinal parasitic infestation in 26 27 children?. J Dent Child. 2008;75:276279. 28 29 30 31 32 6. Munerato MC, Moure SP, Machado V, Gomes FG. Selfmutilation of tongue and in a 33 34 patient with simple schizophrenia. Clin Med Res. 2011;9:4245. 35 36 37 38 7. Chikhani L, Dichamp J. Bruxism, temporomandibular dysfunction and botulinum toxin. 39 40 41 Ann Readapt Med Phys. 2003;46:333337. 42 43 44 45 8. Widmalm SE, Christiansen RL, Gunn SM. Oral parafunctions as temporomandibular 46 47 disorder risk factors in children. Cranio. 1995;13:242246. 48 49 50 51 52 9. Cheifetz AT, Osganian SK, Allred EN, Needleman HL. Prevalence of bruxism and 53 54 associated correlates in children as reported by parents. J Dent Child. 2005;72:6773. 55 56 57 58 59 60 N/A22 Page 23 of 40 Journal of Oral Rehabilitation

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1 2 3 31. Rosales VP, Ikeda K, Hizaki KO, Naruo T, Nozoe SI et al . Emotional stress and brux - 4 5 like activity of the masseter muscle in rats. Eur J Orthod. 2002;24:107117. 6 7 8 9 10 32. Manfredini D, Lobbezoo F. Role of psychosocial factors in the etiology of bruxism. J 11 12 Orofacial Pain. 2008;23:153166. 13 14 15 16 17 33. Manfredini D, GuardaNardini L, MarcheseRagona R, Lobbezoo F. Theories on 18 For Peer Review 19 possible temporal relationships between sleep bruxism and obstructive sleep apnea events. 20 21 An expert opinion. Sleep Breath. 2015 Mar 22. 22 23 24 25 34. Lobbezoo F, Lavigne GJ, Tanguay R, Montplaisir JY. The effect of the catecholamine 26 27 28 precursor L ‐Dopa on sleep bruxism: A controlled clinical trial. Mov Disord . 1997;12:73 29 30 78. 31 32 33 34 35 35. Ahlberg J, Savolainen A, Rantala M, Lindholm H, Könönen M. Reported bruxism and 36 37 biopsychosocial symptoms: a longitudinal study. Community Dent Oral 38 39 Epidemiol. 2014;32:307311. 40 41 42 43 36. Brand HS, Van Zalingen D, Veerman EC. Heroin and oral health. Ned Tijdschr 44 45 46 Tandheelkd. 2006;116:479482. 47 48 49 50 37. Hublin C, Kaprio J, Partinen M, Koskenvuo M. Sleep bruxism based on self -report in a 51 52 53 nationwide twin cohort. J Sleep Res. 1998;7:6167. 54 55 56 57 58 59 60 N/A26 Page 27 of 40 Journal of Oral Rehabilitation

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