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Difference between revisions of "Bruxism"
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| autore = Gianni Frisardi | | autore = Gianni Frisardi | ||
| autore2 = | | autore2 = | ||
| autore3 = Flavio Frisardi | | autore3 = Flavio Frisardi | ||
}} | }} | ||
== Introduction == | '''Abstract:'''This chapter explores the neurophysiological mechanisms behind bruxism, a condition commonly viewed as an oral parafunctional activity not related to normal functions like eating or speaking. While the literature reports bruxism prevalence ranging from 8% to 31% in the general population, it remains a complex phenomenon often associated with jaw muscle pain, tooth wear, and headaches. There are ongoing debates about whether bruxism is pathological or a physiological function that enhances masticatory capacity, as suggested by the theory of 'Thegosis.' | ||
Through extensive literature analysis, we question whether bruxism is linked to occlusal factors, stress, anxiety syndromes, or trigeminal motoneuron excitability. Studies reveal that while occlusal factors are frequently discussed, little attention has been given to the functionality of the trigeminal nervous system. Research by İnan et al. and Jessica M. D'Amico et al. highlights the role of decreased inhibitory control in trigeminal motoneurons in individuals with bruxism, suggesting a neurophysiological basis for the condition. | |||
The chapter delves into neurobiological mechanisms, examining persistent internal ionic currents (PIC) in the trigeminal motor neuron pool and the influence of serotonin and norepinephrine during micro-awakenings, which are frequent in bruxist individuals. The relationship between drugs affecting neurotransmitter levels and the involuntary activity seen in bruxism is also discussed. However, despite advancements in understanding the neurophysiological aspects, the full pathophysiology of bruxism remains elusive, often presenting as a symptom of broader neuromotor hyperexcitability. | |||
Finally, the chapter presents a clinical case of a 32-year-old patient suffering from severe bruxism for 15 years, emphasizing the need for a thorough differential diagnosis. Using the same clinical roadmap as in the case of hemimasticatory spasm, the chapter offers insights into how the complexities of neurophysiological systems manifest in conditions like bruxism and stresses the importance of integrating a quantum probability model for a more comprehensive understanding. | |||
== Introduction to the Bruxism == | |||
Let's start by asking ourselves some specific questions: | Let's start by asking ourselves some specific questions: | ||
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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. | 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. | ||
== | ===Trigeminal motor neuron pool evidences=== | ||
A synthetic extraction of the contents of the article by Jessica M D'Amico et al.,<ref name=":12" />, shows evidence that the discharge of neurons in the raphe nuclei, in the locus coeruleus, in the subcoeruleus and in A5/A7 cells, releases serotonin and norepinephrine and facilitates 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>{{cita libro | A synthetic extraction of the contents of the article by Jessica M D'Amico et al.,<ref name=":12" />, shows evidence that the discharge of neurons in the raphe nuclei, in the locus coeruleus, in the subcoeruleus and in A5/A7 cells, releases serotonin and norepinephrine and facilitates 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>{{cita libro | ||
| autore = Leung CG | | autore = Leung CG | ||
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| OCLC = | | OCLC = | ||
}}</ref>). Individuals with bruxism experience an increase in the number of micro-awakenings during sleep (Kato et al. 2001,<ref>{{cita libro | }}</ref>). Individuals with bruxism experience an increase in the number of micro-awakenings during sleep (Kato et al. 2001,<ref>{{cita libro | ||
<nowiki> </nowiki><nowiki>|</nowiki> autore = Kato T | |||
<nowiki> </nowiki><nowiki>|</nowiki> autore2 = Rompre PH | |||
<nowiki> </nowiki><nowiki>|</nowiki> autore3 = Montplaisir JY | |||
<nowiki> </nowiki><nowiki>|</nowiki> autore4 = Sessle BJ | |||
<nowiki> </nowiki><nowiki>|</nowiki> autore5 = Lavigne GJ | |||
<nowiki> </nowiki><nowiki>|</nowiki> titolo = Sleep bruxism: an oromotor activity secondary to microarousal | |||
<nowiki> </nowiki><nowiki>|</nowiki> url = https://pubmed.ncbi.nlm.nih.gov/11706956 | |||
| volume = | | volume = | ||
| opera = J Dent Res | | opera = J Dent Res | ||
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[[File:IMG0103.jpg|thumb|'''Figure 1''': A patient suffering from severe diurnal and nocturnal bruxism|200px]] | [[File:IMG0103.jpg|thumb|'''Figure 1''': A patient suffering from severe diurnal and nocturnal bruxism|200px]] | ||
==Conclusion== | ==Neurophysiological Conclusion== | ||
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'. | 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'. | ||