Bruxism

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Bruxism

Bruxism is a complex phenomenon often reduced to dental and occlusal factors in medical discussions. However, these traditional perspectives frequently overlook a crucial aspect: the functionality of the trigeminal nervous system. This omission exemplifies the broader issue in medical diagnostics where conventional terms, such as bruxism, may not adequately represent the underlying complexities of the conditions they describe.

Bruxism is characterized as a non-functional oral activity, distinct from necessary functions like eating or speaking. Despite its prevalence, reported as ranging from 8% to 31% in the general population, bruxism often remains unnoticed until significant dental wear occurs. This raises questions about the inevitability of dental wear and whether it can occur even without bruxism.

The concept of 'Thegosis' suggests that bruxism might actually serve a physiological function to increase masticatory efficiency and muscular strength, challenging the distinction between physiological and pathological states. This perspective necessitates a deeper reassessment of how bruxism is perceived and managed in clinical settings.

The complexity of bruxism is evident in its diverse etiologies, which include 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.

Recent studies focusing on the trigeminal motoneurons have begun to reveal the neurological basis of bruxism, suggesting that it 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.

Bruxism may involve complex neurophysiological processes that include the activation and modulation of trigeminal motoneurons. Studies have indicated that bruxism could be related to specific neuronal discharges in areas such as the raphe nuclei and the locus coeruleus, which play roles in the modulation of sleep and arousal states that impact muscle activity.

These findings suggest that bruxism could be more than just a response to dental misalignment or stress, but also a manifestation of broader neurophysiological activities. Understanding these processes could lead to more targeted therapies that address the neurological components of bruxism, potentially offering relief for patients who do not respond to conventional treatments.

The management of bruxism is poised to benefit greatly from the integration of these neurophysiological insights. Instead of relying solely on dental guards and stress management, treatment protocols could include neuromodulatory approaches that address the central nervous system's role in bruxism.

Future research should continue to explore the complex interactions between neuronal circuits and bruxism behavior to develop more effective interventions. As the field advances, the integration of neurobiological insights with clinical practice is expected to improve outcomes for patients with bruxism, providing a more holistic approach to treatment.

The reevaluation of bruxism through the lens of basic knowledge and neurology underscores the need for a more nuanced understanding of this condition. It challenges the traditional boundaries between physiological and pathological states, suggesting that bruxism might not merely be a dental issue but a complex neurophysiological phenomenon that requires a comprehensive approach to diagnosis and treatment. This approach should incorporate not only the latest clinical practices but also ongoing research into the neural mechanisms underlying bruxism.

Keywords

Bruxism - Refers to the medical condition involving involuntary teeth grinding and clenching, often occurring during sleep.

Trigeminal Nervous System - Pertains to the network of nerves responsible for sensation in the face and motor functions such as biting and chewing; critical in understanding the neurological aspects of bruxism.

Dental Wear - Describes the damage and wear to teeth that result from chronic grinding, a common symptom of bruxism.

Oral Parafunctional Activity - Involves non-functional activities of the mouth and jaws, including bruxism, that are not related to normal functions like eating or speaking.

Neurophysiological Aspects of Bruxism - Explores the brain and nerve functions influencing bruxism, providing insight into how neurological conditions contribute to this behavior.

Treatment of Bruxism - Discusses various management strategies and therapies to alleviate and control the symptoms of bruxism.

Trigeminal Motoneurons - Focuses on the specific neurons in the trigeminal nerve that impact jaw movement, essential for understanding the pathophysiology of bruxism.

Sleep Disorders - Covers the range of medical conditions affecting sleep patterns, including how bruxism is often associated with other sleep disturbances.

Neuromodulatory Treatment - Refers to therapies that modify nerve activity, used in managing neurological aspects of bruxism such as reducing muscle activity.

Thegosis Theory - A theory suggesting that teeth grinding serves a physiological function, increasing masticatory efficiency and muscle strength.

Neurological Basis of Bruxism - Investigates the brain-based causes of bruxism, emphasizing the role of central nervous system in this condition.

PIC (Persistent Inward Currents) - Discusses the continuous electrical currents within neurons that are thought to contribute to sustained contractions in bruxism.

Bruxism and Neurotransmitters - Explores the relationship between chemical messengers in the brain and their impact on bruxism, focusing on how imbalances can trigger grinding behaviors.

Clinical Management of Bruxism - Details approaches used by healthcare professionals to diagnose, treat, and manage bruxism effectively.

Neurobiological Research on Bruxism - Highlights studies and findings in the field of neurobiology that shed light on the underlying causes and potential treatments for bruxism.

 

Article by  Gianni Frisardi · Flavio Frisardi

 

Introduction

Let's start by asking ourselves some specific questions:

• Is bruxism an oral parafunctional activity, not physiologically related to normal functions, such as eating or speaking?
• Is bruxism a common behavior despite reports of prevalence ranging from 8% to 31% in the general population?
• Are there any symptoms which are commonly associated with bruxism, including jaw muscle pain, headaches, hypersensitive teeth, tooth wear, and damage to dental restorations (e.g., crowns and fillings)?

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 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?

These might seem irrelevant questions, but let's see what can be deduced from the literature. There are, of course, multiple factors of which many theories are sometimes excessively supported and this is why we questioned Pubmed on specific keywords:

• 'Bruxism'
  The query was answered with 1750 results in 10 years and 882 results combining the two keywords 'Bruxism AND sleep bruxism'.
• 'Bruxism AND sleep bruxism AND stress' -
  We had a dramatic reduction to 96 results which made us wonder if there was an occlusal cause.
• 'Bruxism AND sleep bruxism AND occlusal factor'-
  We had 32 results 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 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'
  with immense surprise, only two fantastic scientific papers came out: that of İnan R et al. and that of Jessica M D'Amico et al. which we propose as a sub-chapter of Masticationpedia for their 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.

Evidences

A synthetic extraction of the contents of the article by Jessica M D'Amico et al.,, 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, Sakai and Crochet 2001, Takahashi et al., 2010). Individuals with bruxism experience an increase in the number of micro-awakenings during sleep (Kato et al. 2001, 2003, 2011) 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, See and Tan 2003) and the amplitude of PICs in motor neurons of the limbs (D'Amico et al. 2013, Udina et al. 2010).

Again on the same neurobiological tenor of GABA and Glutamate, the consideration of Andrisani G. 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. 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. 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: A patient suffering from severe diurnal and nocturnal bruxism

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'.

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 an other 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 and consequently managed with an occlusal bite plane.

Also in this clinical case the differential diagnosis, as reported by Merete Bakke et al., 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 'Hemimasticatory 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.

Bibliography & references