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| [[File:IMG0103.jpg|left|225x225px]]Bruxism is often reduced to dental and occlusal factors, but this overlooks the crucial role of the trigeminal nervous system. This chapter emphasizes that conventional terms like bruxism may not adequately represent the complexities of the conditions they describe.
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| Bruxism is characterized as a non-functional oral activity, distinct from eating or speaking. Despite its prevalence, it often goes unnoticed until significant dental wear occurs. This raises questions about whether dental wear can occur without bruxism.
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| The concept of 'Thegosis' suggests that bruxism might serve a physiological function to increase masticatory efficiency and muscular strength, challenging the distinction between physiological and pathological states. This perspective necessitates a reassessment of how bruxism is perceived and managed in clinical settings.
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| Bruxism has diverse etiologies, including psychological stress, physiological anomalies, and especially the involvement of the trigeminal nervous system. Traditional views of bruxism as primarily a dental or occlusal issue do not account for its neurological dimensions, which are critical for effective management.
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| Recent studies on trigeminal motoneurons suggest that bruxism may be linked to decreased inhibitory control within the trigeminal network. This emerging understanding opens new avenues for comprehending and treating bruxism beyond conventional dental interventions, emphasizing the importance of integrating neurobiological research into clinical practice.
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| Bruxism may involve complex neurophysiological processes, including the activation and modulation of trigeminal motoneurons. Studies indicate that bruxism could be related to specific neuronal discharges in areas like the raphe nuclei and the locus coeruleus, which modulate sleep and arousal states that impact muscle activity.
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| These findings suggest that bruxism could be more than a response to dental misalignment or stress but also a manifestation of broader neurophysiological activities. Understanding these processes could lead to more targeted therapies addressing the neurological components of bruxism, offering relief for patients unresponsive to conventional treatments.
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| Integrating neurophysiological insights into bruxism management can significantly benefit treatment protocols. Future research should explore the interactions between neuronal circuits and bruxism behavior to develop effective interventions. Integrating neurobiological insights with clinical practice is expected to improve patient outcomes, providing a holistic treatment approach.
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| Reevaluating bruxism through neurology underscores the need for a nuanced understanding. It challenges traditional boundaries between physiological and pathological states, suggesting bruxism is a complex neurophysiological phenomenon requiring a comprehensive diagnostic and treatment approach, incorporating the latest clinical practices and ongoing research into neural mechanisms.{{ArtBy|
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| | autore = Gianni Frisardi | | | autore = Gianni Frisardi |
| | autore2 = | | | autore2 = |
| | autore3 = Flavio Frisardi | | | autore3 = Flavio Frisardi |
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| | '''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.' |
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| | 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. |
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| | 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. |
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| | 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 == | | == Introduction to the Bruxism == |
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