Difference between revisions of "Bruxism"

* '''<nowiki/>'''<nowiki/>'Bruxism AND sleep bruxism AND occlusal factor'''<nowiki/>'''<nowiki/>'- We had 32 results<ref>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</ref> that led us to wonder if there were any anxiety-producing causes in the phenomenon.

* '''<nowiki/>'''<nowiki/>'Bruxism AND sleep bruxism AND anxiety syndromes'''<nowiki/>'''<nowiki/>'- The reduction became more marked with 12 results<ref>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</ref> 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.

</blockquote>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.<blockquote>From a synthetic extraction of the contents of the article by Jessica M D'Amico et al.,<ref name=":12" /> 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,<ref>Leung CG, Mason P. Physiological properties of raphe magnus neurons during sleep and walking. J Neurophysiol 81: 584–595, 1999 [PubMed]</ref> Sakai and Crochet 2001,<ref>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]</ref> Takahashi et al., 2010<ref>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]</ref>). Individuals with bruxism experience an increase in the number of micro-awakenings during sleep (Kato et al. 2001,<ref>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]</ref> 2003,<ref>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]</ref> 2011<ref>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]</ref>) 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,<ref>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]</ref> See and Tan 2003<ref>See SJ, Tan EK. Case Report: severe amphetamine-induced bruxism: treatment with botulinum toxin. Acta Neurol Scand 107: 161–163, 2003 [PubMed] [Google Scholar]</ref>) and the amplitude of PICs in motor neurons of the limbs (D'Amico et al. 2013,<ref>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]</ref> Udina et al. 2010<ref>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]</ref>).

</ref> 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.</blockquote>[[File:IMG0103.jpg|thumb|'''Figure 1''': Patient suffering from severe diurnal and nocturnal bruxism|300x300px]]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'

Also in this clinical case the differential diagnosis, as reported by Merete Bakke et al.,<ref name=":0" /> remains very complex.