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==Pathophysiology==
==Pathophysiology==
Bruxism is considered to have multifactorial etiology. SB and grinding have been associated with peripheral factors such as tooth interference in dental occlusion, psychosocial influences such as stress or anxiety and central or pathophysiological causes involving brain neurotransmitters or basal ganglia.
Central or Pathophysiological Factors
More and more pathophysiological factors are suggested to be involved in the precipitation of bruxism. As bruxism often occurs during sleep, the physiology of sleep has been studied extensively especially the ‘arousal response’ in search of possible causes of disorder. Arousal response is a sudden change in the depth of the sleep during which the individual either arrives in the lighter sleep stage or actually wakes up. Such a response is accompanied by gross body movements, increased heart rate, respiratory changes, and increased muscle activity. Macaluso et al. [10] in their study showed 86% of bruxism episodes were associated with arousal response along with involuntary leg movements. This shows that bruxism is a part of arousal response indeed.
Recently it is derived that disturbances in central neurotransmitter system may be involved in the etiology of bruxism. It is hypothesized that the direct and indirect pathways of the basal ganglion, a group of five subcortical nuclei that are involved in the coordination of movements is disturbed in bruxer. The direct output pathway goes directly from the stratum to the thalamus from where afferent signals project to the cerebral cortex. The indirect pathway on the other hand passes by several other nuclei before reaching it to the thalamus [13]. If there is imbalance between both the pathways, movement disorder results like Parkinson’s disease. The imbalance occurs with the disturbances in the dopamine-mediated transmission of an action potential. In case of bruxism there may be an imbalance in both pathways. Acute use of dopamine precursors like L-dopa inhibits bruxism activity and chronic long term use of l-dopa results in increased bruxism activity. SSRTs (serotonin reuptake inhibitors) which exert an indirect influence on the dopaminergic system may cause bruxism after long term use. Amphetamine which increases the dopamine concentration by facilitating its release has been observed to increase bruxism. Nicotine stimulates central dopaminergic activities which might explain the finding that cigarette smokers report bruxism two times more than the nonsmokers.
Psychosocial Factors
Number of studies is published in the literature regarding the role of psychosocial factors in the etiology of bruxism but none of these describe the conclusive nature because of the absence of large scale longitudinal trials. Bruxers differs from healthy individuals in the presence of depression, increased levels of hostility and stress sensitivity. Bruxing children are more anxious than non bruxers. A multifactorial large scale population study to sleep bruxism revealed highly stressful life as a significant risk factor. A study by Van Selms et al. demonstrated that daytime time clenching could significantly be explained by experienced stress, although experienced stress and anticipated stress were unrelated to sleep bruxism as recorded with ambulatory devices. All these studies show possible relationship between bruxism and various psychosocial factors is growing but not conclusive.
Peripheral Factors
Several occlusal factors were suggested to be related to self reported bruxism in a study with children. Giffin in his article has mentioned that for an effective management of bruxism, establishment of harmony between maximum intercuspation and centric relation is required. But most of studies published in the literature on this subject now agrees that there is no or hardly any relationship between clinically established bruxism and occlusal factors in adults. Manfredini et al. in their review of literature have stated that there is still a lack of methodological sound studies to definitely refute the importance of occlusal factors in the etiology of bruxism.


==Differential Diagnosis==
==Differential Diagnosis==

Revision as of 22:25, 10 February 2021

Bruxism

Bruxism is defined as repeated involuntary grinding and clenching of teeth which can occur either diurnal or nocturnally.

Historical Perspective

Classification

Bruxism can be classified into awake bruxism and sleep bruxism based on the physiological sleep status of the individual.

Awake Bruxism/Diurnal Bruxism Sleep Bruxism/Nocturnal Bruxism
Day Time /Awake Sleep
Semi-Voluntary Sterotyped
Clenching predominant Teeth grinding
Definitions
American Academy of Orofacial Pain (2008) Diurnal or nocturnal parafunctional activity including clenching, bracing, gnashing, and grinding of the teeth. I
The Academy of Prosthodontics (2005)
  • 1. The parafunctional grinding of teeth.
  • 2. An oral habit consisting of involuntary rhythmic or spasmodic non-functional gnashing, grinding or clenching of teeth, in other than chewing movements of the mandible, which may lead to occlusal trauma – called also tooth grinding, occlusal neurosis
The International Classification of Sleep Disorders (2005) Sleep-related bruxism is an oral activity characterized by grinding or clenching of the teeth during sleep, usually associated with sleep arousals.

Causes

Etiology of bruxism can be categorized into three groups psychosocial factors, peripheral factors and pathophysiological factors.

Etiology of Bruxism
Psychological Common psychological factors responsible for bruxism include
  • Stress induced bruxism
  • Depression associated bruxism
  • Anxiety related bruxism
Peripheral
  • Caffine intake
  • Smoking
  • Alcohol consumption
Pathological
  • Problem with arousal mechanism during sleep
  • Imbalance in the dopamine release in the basal ganglion

Pathophysiology

Bruxism is considered to have multifactorial etiology. SB and grinding have been associated with peripheral factors such as tooth interference in dental occlusion, psychosocial influences such as stress or anxiety and central or pathophysiological causes involving brain neurotransmitters or basal ganglia.

Central or Pathophysiological Factors More and more pathophysiological factors are suggested to be involved in the precipitation of bruxism. As bruxism often occurs during sleep, the physiology of sleep has been studied extensively especially the ‘arousal response’ in search of possible causes of disorder. Arousal response is a sudden change in the depth of the sleep during which the individual either arrives in the lighter sleep stage or actually wakes up. Such a response is accompanied by gross body movements, increased heart rate, respiratory changes, and increased muscle activity. Macaluso et al. [10] in their study showed 86% of bruxism episodes were associated with arousal response along with involuntary leg movements. This shows that bruxism is a part of arousal response indeed.

Recently it is derived that disturbances in central neurotransmitter system may be involved in the etiology of bruxism. It is hypothesized that the direct and indirect pathways of the basal ganglion, a group of five subcortical nuclei that are involved in the coordination of movements is disturbed in bruxer. The direct output pathway goes directly from the stratum to the thalamus from where afferent signals project to the cerebral cortex. The indirect pathway on the other hand passes by several other nuclei before reaching it to the thalamus [13]. If there is imbalance between both the pathways, movement disorder results like Parkinson’s disease. The imbalance occurs with the disturbances in the dopamine-mediated transmission of an action potential. In case of bruxism there may be an imbalance in both pathways. Acute use of dopamine precursors like L-dopa inhibits bruxism activity and chronic long term use of l-dopa results in increased bruxism activity. SSRTs (serotonin reuptake inhibitors) which exert an indirect influence on the dopaminergic system may cause bruxism after long term use. Amphetamine which increases the dopamine concentration by facilitating its release has been observed to increase bruxism. Nicotine stimulates central dopaminergic activities which might explain the finding that cigarette smokers report bruxism two times more than the nonsmokers.

Psychosocial Factors Number of studies is published in the literature regarding the role of psychosocial factors in the etiology of bruxism but none of these describe the conclusive nature because of the absence of large scale longitudinal trials. Bruxers differs from healthy individuals in the presence of depression, increased levels of hostility and stress sensitivity. Bruxing children are more anxious than non bruxers. A multifactorial large scale population study to sleep bruxism revealed highly stressful life as a significant risk factor. A study by Van Selms et al. demonstrated that daytime time clenching could significantly be explained by experienced stress, although experienced stress and anticipated stress were unrelated to sleep bruxism as recorded with ambulatory devices. All these studies show possible relationship between bruxism and various psychosocial factors is growing but not conclusive.

Peripheral Factors Several occlusal factors were suggested to be related to self reported bruxism in a study with children. Giffin in his article has mentioned that for an effective management of bruxism, establishment of harmony between maximum intercuspation and centric relation is required. But most of studies published in the literature on this subject now agrees that there is no or hardly any relationship between clinically established bruxism and occlusal factors in adults. Manfredini et al. in their review of literature have stated that there is still a lack of methodological sound studies to definitely refute the importance of occlusal factors in the etiology of bruxism.

Differential Diagnosis


Orofacial movements Bruxism Loud noticeable teeth grinding noise during sleep
Pathological orofacial movements
  • Facial myoclonus
  • Chewing-like movements
  • Swallowing
  • Sleep talking
  • Expiratory groaning
Tooth wear
Jaw pain and fatigue


Epidemiology and Demographics

Gender

  • Bruxism affects men and women equally.

Age

  • Bruxism commonly affects individuals younger than 6 years of age and its incidence declines as age increases.

Screening

There is insufficient evidence to recommend routine screening for bruxism.

Risk Factors

Factors associated with an increased risk of bruxism include:

Natural History, Complications and Prognosis

Natural History

  • The symptoms of bruxism, usually develop in the first decade of life, and start with symptoms such as appearance of the first primary upper and lower anterior teeth.
  • The symptoms of bruxism typically develop in childhood and may persist into adult due to presence of other risk factors.
  • Usually bruxism follows a benign course.
  • If left untreated bruxism can lead to hypertrophy of masseter muscle accompanied by tenderness of TMJ, which manifests as otalgia.

Complications

Common complications of bruxism are

  • Tooth wear
  • Tooth hypersensitivity
  • Tooth mobility
  • Pain in the temporomandibular joint (TMJ) or jaw musculature
  • Temporal headache,
  • Poor sleep
  • Signs of this parafunctional habit
    • Indentation on the tongue
    • Presence of linea alba along the biting plane of the buccal mucosa
    • Gingival recessions

Treatment

Medical Therapy

  • Removal of any offending agent responsible for bruxism is primary step in the management.
  • Wait-and-see approach is recommended in cases with medical induced bruxism, as spontaneous remission is ensured with the cessation of the offending agent.
  • Pharmacotherapy mainly concentrated to alleviate symptoms
  • Buspirone and Gabapentin are the two recommended medications to manage bruxism
    • Preferred regimen 1 : Buspirone 15 to 20 mg/day PO q12.
    • Preferred regimen 2: Gabapentin 100 to 300 mg PO q24

Surgery

Surgery is the main stay of treatment in the management of bruxism.

Indications

The treatment of bruxism is indicated when there are any of these possible consequences:

  • Mechanical wear of the teeth, which results in loss of occlusal morphology and flattening of the occlusal surfaces
  • Hypersensitive teeth
  • Loss of periodontal support
  • Tooth fractures
  • Restorations fractures, usually class I and class II restorations, fracture of crowns, and fixed partial prosthesis
  • Restorations or dental implants failure
  • Hypertrophy of masticatory muscles
  • Tenderness and stiffness in jaw muscles
  • When bruxism leads to limited mouth opening
  • Temporomandibular pain
  • Pain in the preauricular region