Masticationpedia

Bruxisme

Page Discussion
Go to top
Other languages:  

English · Italiano · Français · Deutsch · Español · 

IMG0103.jpg

Une brève description du bruxisme, pour ne pas perdre de temps sur des données communes à la plupart des collègues et par culture personnelle pour les non-spécialistes, suffit à approfondir le sujet sur Wikipediace qui, évidemment, ne sera pas exhaustif pour nos fins., mais, en substance, de cet aperçu de la recherche de la base de données, il ressort clairement que si d'une part le bruxisme est un phénomène complexe, d'autre part les efforts se sont concentrés presque exclusivement sur occlusal et les facteurs dentaires en général, laissant de côté un aspect, essentiel à nos yeux, celui de la fonctionnalité du système nerveux trijumeau.

Comme d'habitude, nous sommes confrontés au même problème d'imprécision du langage verbal que celui qui s'est produit avec la patiente Mary Poppins, le « bruxisme » peut n'être qu'un terme conventionnel à distinguer d'un terme tel que « tremblement », mais essentiellement le code machine peut ne pas être être lié au sens verbal.

Precisely by following the now acclaimed 'Masticationpedia' model, we are preparing to present a patient suffering from 'Bruxism' for 15 years and whose dental colleagues have obviously seen the significance given to the disorder, managed with an occlusal bite plane.In presenting this clinical case, of course, we will follow the same roadmap followed with our patient Mary Poppins suffering from 'Haemasticatory Spasm'. 

Masticationpedia

 

Introduction

A brief description of bruxism, in order not to waste time on data common to most colleagues and for personal culture for non-experts, is sufficient to deepen the topic on Wikipedia which, obviously, will not be exhaustive for our purposes. Let's start, therefore, by asking ourselves some specific questions: Is bruxism an oral parafunctional activity,[1] that is, is it not physiologically related to normal function such as eating or speaking? Is bruxism a common behavior despite reports of prevalence ranging from 8% to 31% in the general population?[2] Several symptoms are commonly associated with bruxism, including jaw muscle pain, headaches, hypersensitive teeth, tooth wear, and damage to dental restorations (e.g., crowns and fillings)?[3] Symptoms may be minimal, without the patient being aware of the condition. If no action is taken, after a while many teeth begin to wear out until they disappear completely, the question that arises is: do teeth wear out equally in the life cycle even without grinding?

A theory called 'Thegosis' studied by a group of New Zealand researchers[4] has always maintained that bruxism is a physiological function that increases masticatory capacity and organic muscle strength, therefore, where is the boundary between physiology and pathology?

They seem irrelevant questions but let's see what can be deduced from the literature. There are, of course, multiple factors[5][6] of which many theories are sometimes excessively supported and it is for this reason that we questioned Pubmed on specific keywords:

  • 'Bruxism'- The query was answered with 1750 results in 10 years[7] and 882 results combining the two keywords 'Bruxism AND sleep bruxism'.[8]
  • 'Bruxism AND sleep bruxism AND stress' - We had a dramatic reduction to 96 results[9] which made us wonder if there was an occlusal cause.
  • 'Bruxism AND sleep bruxism AND occlusal factor'- We had 32 results[10] that led us to wonder if there were any anxiety-producing causes in the phenomenon.
  • 'Bruxism AND sleep bruxism AND anxiety syndromes'- The reduction became more marked with 12 results[11] so that between stress and forms of anxiety we wondered if the phenomenon was somehow attributable to a form of neuro-excitability of the Central Nervous System.
  • 'Bruxism AND sleep bruxism AND trigeminal motoneuron'- and with immense surprise only two fantastic scientific papers came out that of İnan R et al.[12] and that of Jessica M D'Amico et al.[13] which we propose as a sub-chapter of Masticationpedia for its important specific scientific contribution on the excitability of trigeminal motor neurons in bruxism.

Substantially, from this overview of the database research it is clear that if on the one hand bruxism is a complex phenomenon on the other the efforts have concentrated almost exclusively on occlusal and dental factors in general, leaving out one aspect, essential in our opinion, that of functionality of the trigeminal nervous system.

From a synthetic extraction of the contents of the article by Jessica M D'Amico et al.,[13] which we recommend following in its entirety as reading in the dedicated sub-chapter, it is highlighted that the discharge of neurons in the raphe nuclei, in the locus coeruleus, in the subcoeruleus and in A5/A7 cells, they release serotonin and norepinephrine and facilitate PIC (persistent internal ionic currents referred to as 'PIC') to the trigeminal motor neuron pool. These episodes increase during micro-awakenings (Leung and Mason 1999,[14] Sakai and Crochet 2001,[15] Takahashi et al., 2010[16]). Individuals with bruxism experience an increase in the number of micro-awakenings during sleep (Kato et al. 2001,[17] 2003,[18] 2011[19]) with a probable increase in the monoaminergic drive towards trigeminal motor neurons. Accordingly, drugs such as serotonin reuptake inhibitors and amphetamines, which increase norepinephrine and serotonin levels, respectively, increase episodes of involuntary activity in bruxist participants (Lavigne et al. 2003,[20] See and Tan 2003[21]) and the amplitude of PICs in motor neurons of the limbs (D'Amico et al. 2013,[22] Udina et al. 2010[23]).

Again on the same neurobiological tenor of GABA and Glutamate, the consideration of Andrisani G.[24] is expressed which leaves everyone somewhat surprised, namely 'the bruxism is not a parafunction, and it functions to activate the ascending reticular formation (ARAS) to regulate the loss of neurotransmitters such as noradrenaline, dopamine, serotonin, acetylcholine and glutamate.

It emerged from another interesting study by M C Verhoeff et al.[25] that although bruxism is present in subjects with Parkinson's this is not associated with the dose of the dopaminergic drug.

While for Merete Bakke et al.[26] exposure to dopamine receptor blocking agents such as antipsychotics, antitussives and antiemetics can induce dystonia including bruxism making the differential diagnosis between similar and possibly related disorders such as Parkinson's disease, essential tremor, Tourette's syndrome, temporomandibular disorders, nocturnal bruxism.

Figure 1: Patient suffering from severe diurnal and nocturnal bruxism

The conclusion, unfortunately, remains the same and that is that the external manifestation of an organic and/or functional disturbance is a macroscopic effect which transfers a series of mesoscopic abnormalities of the system over time. Here we were able to test only some of these neurobiological mesoscopic phenomena but the clinical result must be interpreted as a whole phenomenon because current scientific knowledge does not allow us to weigh the physiopathological value of the neurotransmitters, the PIC, the basal nuclei, the ascending reticular formation, etc. . What is certain is that an abnormality in one of these sites can generate an 'encrypted code' as a message in machine language of the Central Nervous System which in itself could not be 'Bruxism' but a form of 'Neuromotor Hyperexcitability'

As usual we are faced with the same problem of vagueness of verbal language as happened with the patient Mary Poppins,the 'Bruxism' may just be a conventional term to be distinguished from a term such as 'Tremor' but essentially the machine code may not be related to the verbal meaning.

Precisely by following the now acclaimed 'Masticationpedia' model, we are preparing to present a patient suffering from 'Bruxism' for 15 years and whose dental colleagues have obviously seen the significance given to the disorder, managed with an occlusal bite plane.

Also in this clinical case the differential diagnosis, as reported by Merete Bakke et al.,[26] remains very complex.

In presenting this clinical case (figure 1), of course, we will follow the same roadmap followed with our patient Mary Poppins suffering from 'Haemasticatory Spasm'. The subject was a 32-year-old man suffering from pronounced nocturnal and diurnal bruxism and chronic bilateral OP prevalent in the temporoparietal regions, with greater intensity and frequency on the left side. Neurological examination showed a contraction of the masseter muscles with pronounced stiffness of the jaw, diplopia and loss of visual acuity in the left eye, left gaze nystagmus with a rotary component, papillae with blurred borders and positive bilateral Babynski's, and polykinetic tendon reflexes in all four limbs.

Bibliography & references
  1. ↑ Wassell R, Naru A, Steele J, Nohl F (2008). Applied occlusion. London: Quintessence. pp. 26–30. ISBN 9781850970989.
  2. ↑ Manfredini D, Winocur E, Guarda-Nardini L, Paesani D, Lobbezoo F (2013). "Epidemiology of bruxism in adults: a systematic review of the literature". Journal of Orofacial Pain. 27 (2): 99–110. doi:10.11607/jop.921. PMID 23630682.
  3. ↑ Tyldesley WR, Field A, Longman L (2003). Tyldesley's Oral medicine (5th ed.). Oxford: Oxford University Press. p. 195. ISBN 978-0192631473.
  4. ↑ C G Murray, G D Sanson. Thegosis--a critical review. Aust Dent J. 1998 Jun;43(3):192-8. doi: 10.1111/j.1834-7819.1998.tb00164.x.
  5. ↑ Cawson RA, Odell EW, Porter S (2002). Cawsonś essentials of oral pathology and oral medicine(7th ed.). Edinburgh: Churchill Livingstone. pp. 6, 566, 364, 366. ISBN 978-0443071065.
  6. ↑ Shetty S, Pitti V, Satish Babu CL, Surendra Kumar GP, Deepthi BC (September 2010). "Bruxism: a literature review". Journal of Indian Prosthodontic Society. 10 (3): 141–8. doi:10.1007/s13191-011-0041-5. PMC 3081266. PMID 21886404.
  7. ↑ Bruxism: https://pubmed.ncbi.nlm.nih.gov/?term=bruxism&filter=datesearch.y_10
  8. ↑ Bruxism AND sleep bruxism. https://pubmed.ncbi.nlm.nih.gov/?term=%27Bruxism+AND+sleep+bruxism+&filter=datesearch.y_10
  9. ↑ Bruxism AND sleep bruxism AND stress: https://pubmed.ncbi.nlm.nih.gov/?term=%27Bruxism+AND+sleep+bruxism+AND+stress&filter=datesearch.y_10
  10. ↑ Bruxism AND sleep bruxism AND occlusal factor.https://pubmed.ncbi.nlm.nih.gov/?term=%27Bruxism+AND+sleep+bruxism+AND+occlusal+factor&filter=datesearch.y_10
  11. ↑ Bruxism AND sleep bruxism AND anxiety syndrome. https://pubmed.ncbi.nlm.nih.gov/?term=%27Bruxism+AND+sleep+bruxism+AND+anxiety+syndromes&filter=datesearch.y_10
  12. ↑ Rahşan İnan, Gülçin Benbir Şenel, Figen Yavlal, Derya Karadeniz, Ayşegül Gündüz, Meral E Kızıltan. Sleep bruxism is related to decreased inhibitory control of trigeminal motoneurons, but not with reticulobulbar system. Neurol Sci. 2017 Jan;38(1):75-81.doi: 10.1007/s10072-016-2711-x. Epub 2016 Sep 14.
  13. ↑ 13.0 13.1 Jessica M D'Amico, Ş Utku Yavuz, Ahmet Saraçoglu, Elif Sibel Atiş, Monica A Gorassini, Kemal S Türker. Activation properties of trigeminal motoneurons in participants with and without bruxism. J Neurophysiol. 2013 Dec;110(12):2863-72. doi: 10.1152/jn.00536.2013. Epub 2013 Sep 25.
  14. ↑ Leung CG, Mason P. Physiological properties of raphe magnus neurons during sleep and walking. J Neurophysiol 81: 584–595, 1999 [PubMed]
  15. ↑ Sakai K, Crochet S. Differentiation of presumed serotonergic dorsal raphe neurons in relation to behaviour and wake-sleep states. Neuroscience 104: 1141–1155, 2001 [PubMed] [Google Scholar]
  16. ↑ Takahashi K, Kayama Y, Lin JS, Sakai K. Locus coeruleus neuronal activity during the sleep-waking cycle in mice. Neuroscience 169: 1115–1126, 2010 [PubMed] [Google Scholar]
  17. ↑ Kato T, Rompre PH, Montplaisir JY, Sessle BJ, Lavigne GJ. Sleep bruxism: an oromotor activity secondary to microarousal. J Dent Res 80: 1940–1944, 2001 [PubMed] [Google Scholar]
  18. ↑ Kato T, Montplaisir JY, Guitard F, Sessle BJ, Lavigne GJ. Evidence that experimentally induced sleep bruxism is a consequence of transient arousal. J Dent Res 82: 284–288, 2003 [PubMed] [Google Scholar]
  19. ↑ Kato T, Masuda Y, Yoshida A, Morimoto T. Masseter EMG activity during sleep and sleep bruxism. Arch Ital Biol 149: 478–491, 2011 [PubMed] [Google Scholar]
  20. ↑ Lavigne GJ, Kato T, Kolta A, Sessle BJ.Neurobiological mechanisms involved in sleep bruxism. Crit Rev Oral Biol Med 14: 30–46, 2003 [PubMed] [Google Scholar]
  21. ↑ See SJ, Tan EK. Case Report: severe amphetamine-induced bruxism: treatment with botulinum toxin. Acta Neurol Scand 107: 161–163, 2003 [PubMed] [Google Scholar]
  22. ↑ D'Amico JM, Murray KC, Li Y, Chan KM, Finlay MG, Bennett DJ, Gorassini MA. Constitutively-active 5HT2/α1 receptors facilitate muscle spasms after human spinal cord injury. J Neurophysiol 109: 1473–1484, 2013 [PMC free article] [PubMed] [Google Scholar]
  23. ↑ Udina E, D'Amico J, Bergquist AJ, Gorassini MA.Amphetamine increases persistent inward currents in human motoneurons estimated from paired motor unit activity. J Neurophysiol 103: 1295–1303, 2010 [PMC free article] [PubMed] [Google Scholar]
  24. ↑ Andrisani Giovanni, Andrisani Giorgia . The neurophysiological basis of bruxism.Heliyon. 2021 Jul 3;7(7):e07477. doi: 10.1016/j.heliyon.2021.e07477.eCollection 2021 Jul.
  25. ↑ M C Verhoeff, M Koutris, M K A van Selms, A N Brandwijk, M S Heres, H W Berendse, K D van Dijk, F Lobbezoo. Is dopaminergic medication dose associated with self-reported bruxism in Parkinson's disease? A cross-sectional, questionnaire-based study.Clin Oral Investig. 2021 May;25(5):2545-2553. doi: 10.1007/s00784-020-03566-0.Epub 2020 Sep 12.
  26. ↑ 26.0 26.1 Merete Bakke, Tove Henriksen, Heidi Bryde Biernat, Torben Dalager, Eigild Møller . Interdisciplinary recognizing and managing of drug-induced tardive oromandibular dystonia: two case reports.Clin Case Rep. 2018 Sep 26;6(11):2150-2155. doi: 10.1002/ccr3.1548.eCollection 2018 Nov.
Retrieved from "https://www.masticationpedia.org/index.php?title=Bruxisme&oldid=15954"