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Bruxism Abstract

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Bruxism

Masticationpedia
Masticationpedia

Abstract
This chapter examines bruxism through a neurophysiological and systems-oriented perspective, challenging its traditional classification as a purely oral parafunctional activity. Although bruxism is widely reported in the literature with a prevalence ranging from 8% to 31% in the general population, its clinical meaning remains controversial. It has been variably interpreted as a pathological condition associated with jaw muscle pain, headaches, tooth wear, and restorative damage, or alternatively as a physiological function enhancing masticatory capacity, as proposed by the theory of “thegosis.” This persistent ambiguity reflects deeper limitations in conventional diagnostic frameworks, which tend to privilege occlusal, dental, or behavioral explanations while marginalizing the role of the trigeminal nervous system.

Through a structured analysis of the available literature, this chapter highlights a striking imbalance in research focus. While thousands of publications address bruxism in relation to occlusal factors, stress, anxiety, and sleep disturbances, only a very limited number directly investigate trigeminal motoneuron excitability. Notably, the works of İnan et al. and D’Amico et al. provide compelling evidence that bruxism is associated with a reduced inhibitory control of trigeminal motoneurons and altered activation properties within the trigeminal motor neuron pool. These findings suggest that bruxism may represent an expression of neuromotor hyperexcitability rather than an isolated dental or behavioral disorder.

The chapter explores the neurobiological mechanisms underlying this hypothesis, focusing on persistent inward currents (PICs) in trigeminal motoneurons and the modulatory role of monoaminergic systems. During sleep micro-awakenings—known to occur more frequently in individuals with bruxism—neuronal activity in the raphe nuclei, locus coeruleus, and related brainstem structures increases the release of serotonin and norepinephrine. This neuromodulatory drive facilitates PICs, enhancing motoneuron excitability and predisposing to involuntary rhythmic or sustained muscle activity. The clinical relevance of this mechanism is further supported by pharmacological observations, whereby agents that increase serotonergic or noradrenergic transmission, such as selective serotonin reuptake inhibitors or amphetamines, are associated with an exacerbation of bruxist activity.

Importantly, the chapter situates bruxism within a broader spectrum of neuromotor disorders. Evidence from studies on spinal and cranial motoneurons indicates that similar mechanisms of hyperexcitability and impaired inhibitory control underlie conditions such as dystonia, cramps, and other paroxysmal motor phenomena. In this context, bruxism emerges not as a discrete disease entity but as a macroscopic manifestation of mesoscopic neurophysiological alterations within the central and peripheral nervous system.

The clinical implications of this paradigm are illustrated through the introduction of a patient with severe diurnal and nocturnal bruxism persisting for over fifteen years. By applying the same diagnostic roadmap previously used in hemimasticatory spasm, the chapter emphasizes the necessity of an expanded differential diagnosis that goes beyond occlusal management. Ultimately, it argues for the integration of probabilistic and quantum-like diagnostic models capable of accommodating the intrinsic complexity and variability of neuromotor systems. Within this framework, bruxism is reinterpreted as a potential marker of underlying neuromotor hyperexcitability rather than a diagnosis in itself, opening new perspectives for research, diagnosis, and treatment.


🧠 Three guiding questions (with essential answers)

1️⃣ Is bruxism a pathological parafunction or a physiological activity? — Current evidence indicates that bruxism cannot be reduced to a purely dental parafunction; it represents a neuromotor phenomenon that may range from physiological adaptive activity to pathological expression depending on the underlying neurophysiological context.

2️⃣ What role does the trigeminal nervous system play in bruxism? — Neurophysiological studies show that bruxism is associated with reduced inhibitory control and increased excitability of trigeminal motoneurons, driven by persistent inward currents and monoaminergic modulation during sleep micro-awakenings.

3️⃣ Why are traditional diagnostic models insufficient to explain bruxism? — Deterministic and compartmentalized models fail because bruxism is a macroscopic manifestation of mesoscopic neurobiological alterations; a probabilistic, system-based framework is required to distinguish neuromotor hyperexcitability from secondary dental effects.

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