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==Causes== | ==Causes== | ||
Etiology of bruxism can be categorized | Etiology of bruxism can be categorized into three groups psychosocial factors, peripheral factors and pathophysiological factors. | ||
{| class="wikitable" | {| class="wikitable" | ||
|+ | |+ | ||
Line 67: | Line 67: | ||
==Pathophysiology== | ==Pathophysiology== | ||
* As stated bruxism is considered to have multifactorial etiology. Multifactorial etiology causes involving brain neurotransmitters or basal ganglia. | |||
* '''Pathophysiological Factors''' | |||
** 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. | |||
** 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. | |||
** 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''' | |||
** There is no proper description of conclusive nature of psychological factors role in bruxism because of the absence of large scale longitudinal trials. | |||
Psychosocial Factors | |||
==Differential Diagnosis== | ==Differential Diagnosis== | ||
Line 108: | Line 113: | ||
|}<br /> | |}<br /> | ||
== Epidemiology and Demographics == | ==Epidemiology and Demographics== | ||
==== Gender ==== | ====Gender==== | ||
* Bruxism affects men and women equally. | *Bruxism affects men and women equally. | ||
==== Age ==== | ====Age==== | ||
* Bruxism commonly affects individuals younger than 6 years of age and its incidence declines as age increases. | *Bruxism commonly affects individuals younger than 6 years of age and its incidence declines as age increases. | ||
* | * | ||
== Screening == | ==Screening== | ||
There is insufficient evidence to recommend routine screening for bruxism. | There is insufficient evidence to recommend routine screening for bruxism. | ||
Revision as of 22:30, 10 February 2021
Bruxism
Bruxism is defined as repeated involuntary grinding and clenching of teeth which can occur either diurnal or nocturnally.
Historical Perspective
- In 1907 Marie Pielkiewics coined a french term 'La Bruxomanie" for bruxism. (https://pubmed.ncbi.nlm.nih.gov/21886404/)
- In 1931, Frohman first coined the term english term bruxism.
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) |
|
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
|
Peripheral |
|
Pathological |
|
Pathophysiology
- As stated bruxism is considered to have multifactorial etiology. Multifactorial etiology causes involving brain neurotransmitters or basal ganglia.
- Pathophysiological Factors
- 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.
- 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.
- 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
- There is no proper description of conclusive nature of psychological factors role in bruxism because of the absence of large scale longitudinal trials.
Differential Diagnosis
Orofacial movements | Bruxism | Loud noticeable teeth grinding noise during sleep |
Pathological orofacial movements
|
||
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:
- Obstructive sleep apnea
- Alcohol abuse
- Caffeine intake
- Smoking
- Anxiety
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