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==Overview== | ==Overview== | ||
Bruxism is defined as repeated involuntary grinding and clenching of [[teeth]] which can occur either diurnal or nocturnally. In 1907 Marie Pielkiewics coined the | Bruxism is defined as repeated involuntary grinding and clenching of [[teeth]] which can occur either diurnal or nocturnally. In 1907, Marie Pielkiewics coined the French term 'La Bruxomanie" for bruxism. Bruxism can be classified into awake bruxism and sleep bruxism based on the [[physiological]] [[sleep]] status of the individual. The [[etiology]] of bruxism can be categorized into three groups:[[psychosocial]] factors, peripheral factors, and [[pathophysiological]] factors. Multifactorial [[etiology]] causes involving [[brain]] [[neurotransmitters]] or [[basal ganglia]]. Bruxism affects [[men]] and [[women]] equally. Factors associated with an increased risk of bruxism include [[obstructive sleep apnea]], [[alcohol abuse]], [[caffeine]] intake, [[smoking]], and [[anxiety]]. The [[symptoms]] of bruxism usually develop in the first decade of life, and start with the appearance of the first primary upper and lower anterior [[teeth]]. Common [[complications]] of bruxism are [[tooth]] wear, and [[tooth]] hypersensitivity. Bruxism is primarily diagnosed based on the [[clinical]] presentation. History of complaints of disturbance from the clicking or grating sound by the accompanied partners. The most common [[symptoms]] of bruxism include involuntary rhythmic contractions of the masticator [[muscle]]<nowiki/>s during [[sleep]]. Removal of any offending agent responsible for bruxism is the primary step in the management. [[Surgery]] is the mainstay of [[treatment]] in the management of bruxism. | ||
==Historical Perspective== | ==Historical Perspective== | ||
*In 1907 Marie Pielkiewics coined | *In 1907, Marie Pielkiewics coined the French term 'La Bruxomanie" for bruxism. <ref name="pmid21886404">{{cite journal |vauthors=Shetty S, Pitti V, Satish Babu CL, Surendra Kumar GP, Deepthi BC |title=Bruxism: a literature review |journal=J Indian Prosthodont Soc |volume=10 |issue=3 |pages=141–8 |date=September 2010 |pmid=21886404 |pmc=3081266 |doi=10.1007/s13191-011-0041-5 |url=}}</ref> | ||
*In 1931, Frohman first coined the | *In 1931, Frohman first coined the English term bruxism. | ||
==Classification== | ==Classification== | ||
| Line 42: | Line 42: | ||
|- | |- | ||
|Semi-Voluntary | |Semi-Voluntary | ||
| | |Stereotyped | ||
|- | |- | ||
|Clenching predominant | |Clenching predominant | ||
| Line 64: | Line 64: | ||
==Causes== | ==Causes== | ||
The [[etiology]] of bruxism can be categorized into three groups [[psychosocial]] factors, peripheral factors, and pathophysiological factors.<ref name="pmid12531159">{{cite journal |vauthors=Bader G, Lavigne G |title=Sleep bruxism; an overview of an oromandibular sleep movement disorder. REVIEW ARTICLE |journal=Sleep Med Rev |volume=4 |issue=1 |pages=27–43 |date=February 2000 |pmid=12531159 |doi=10.1053/smrv.1999.0070 |url=}}</ref> | The [[etiology]] of bruxism can be categorized into three groups: [[psychosocial]] factors, peripheral factors, and pathophysiological factors.<ref name="pmid12531159">{{cite journal |vauthors=Bader G, Lavigne G |title=Sleep bruxism; an overview of an oromandibular sleep movement disorder. REVIEW ARTICLE |journal=Sleep Med Rev |volume=4 |issue=1 |pages=27–43 |date=February 2000 |pmid=12531159 |doi=10.1053/smrv.1999.0070 |url=}}</ref> | ||
{| class="wikitable" | {| class="wikitable" | ||
| Line 71: | Line 71: | ||
|- | |- | ||
|[[Psychological]] | |[[Psychological]] | ||
|Common [[psychological]] factors responsible for bruxism include | |Common [[psychological]] factors responsible for bruxism include: | ||
*[[Stress]] induced bruxism | *[[Stress]]-induced bruxism | ||
*[[Depression]] associated bruxism | *[[Depression]]-associated bruxism | ||
*[[Anxiety]] related bruxism | *[[Anxiety]]-related bruxism | ||
|- | |- | ||
|Peripheral | |Peripheral | ||
| Line 91: | Line 91: | ||
==Pathophysiology== | ==Pathophysiology== | ||
*Bruxism is caused by the activation of [[reflex]] [[chewing]] activity<ref name="pmid18557915">{{cite journal |vauthors=Lavigne GJ, Khoury S, Abe S, Yamaguchi T, Raphael K |title=Bruxism physiology and pathology: an overview for clinicians |journal=J Oral Rehabil |volume=35 |issue=7 |pages=476–94 |date=July 2008 |pmid=18557915 |doi=10.1111/j.1365-2842.2008.01881.x |url=}}</ref> | *Bruxism is caused by the activation of [[reflex]]ive [[chewing]] activity<ref name="pmid18557915">{{cite journal |vauthors=Lavigne GJ, Khoury S, Abe S, Yamaguchi T, Raphael K |title=Bruxism physiology and pathology: an overview for clinicians |journal=J Oral Rehabil |volume=35 |issue=7 |pages=476–94 |date=July 2008 |pmid=18557915 |doi=10.1111/j.1365-2842.2008.01881.x |url=}}</ref> | ||
*[[Mastication|Chewing]] is a [[neuromuscular]] activity that is controlled by [[reflex]] [[nerve]] pathways | *[[Mastication|Chewing]] is a [[neuromuscular]] activity that is controlled by the [[reflex]] [[nerve]] pathways. | ||
*During [[sleep]], the [[reflex]] part is active while the higher control is inactive, resulting in bruxism. | *During [[sleep]], the [[reflex]] part is active while the higher control is inactive, resulting in bruxism. | ||
*As stated bruxism is considered to have multifactorial [[etiology]]. Multifactorial [[etiology]] causes involving [[brain]] [[neurotransmitters]] or [[basal ganglia]]. | *As stated, bruxism is considered to have multifactorial [[etiology]]. Multifactorial [[etiology]] causes involving [[brain]] [[neurotransmitters]] or [[basal ganglia]]. | ||
*'''Pathophysiological Factors''' | *'''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.<ref name="pmid18557915">{{cite journal |vauthors=Lavigne GJ, Khoury S, Abe S, Yamaguchi T, Raphael K |title=Bruxism physiology and pathology: an overview for clinicians |journal=J Oral Rehabil |volume=35 |issue=7 |pages=476–94 |date=July 2008 |pmid=18557915 |doi=10.1111/j.1365-2842.2008.01881.x |url=}}</ref> | **As bruxism often occurs during [[sleep]], the [[physiology]] of [[sleep]] has been studied extensively, especially the ‘arousal response’, in search of possible [[causes]] of a disorder.<ref name="pmid18557915">{{cite journal |vauthors=Lavigne GJ, Khoury S, Abe S, Yamaguchi T, Raphael K |title=Bruxism physiology and pathology: an overview for clinicians |journal=J Oral Rehabil |volume=35 |issue=7 |pages=476–94 |date=July 2008 |pmid=18557915 |doi=10.1111/j.1365-2842.2008.01881.x |url=}}</ref> | ||
**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. | **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. | **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 derived that disturbances in the 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. | **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]]. | **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 | **If there is an imbalance between 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. | **The imbalance occurs with the disturbances in the [[dopamine]]-mediated transmission of an [[action potential]]. In the 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. | **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. | **[[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 smoking|cigarette smokers]] report bruxism two times more than the nonsmokers. | **[[Nicotine]] stimulates central [[dopaminergic]] activities, which might explain the finding that [[Cigarette smoking|cigarette smokers]] report bruxism two times more than the nonsmokers. | ||
*'''Psychosocial Factors''' | *'''Psychosocial Factors''' | ||
| Line 146: | Line 146: | ||
*[https://www.wikidoc.org/index.php/Obstructive_sleep_apnea Obstructive sleep apnea] | *[https://www.wikidoc.org/index.php/Obstructive_sleep_apnea Obstructive sleep apnea] | ||
*[https://www.wikidoc.org/index.php/Alcohol_abuse Alcohol abuse] | *[https://www.wikidoc.org/index.php/Alcohol_abuse Alcohol abuse] | ||
*Caffeine intake | *[[Caffeine]] intake | ||
*[https://www.wikidoc.org/index.php/Smoking Smoking] | *[https://www.wikidoc.org/index.php/Smoking Smoking] | ||
*[https://www.wikidoc.org/index.php/Anxiety Anxiety] | *[https://www.wikidoc.org/index.php/Anxiety Anxiety] | ||
| Line 156: | Line 156: | ||
*The [[symptoms]] of bruxism typically develop in [[childhood]] and may persist into [[adult]] due to presence of other [[risk factors]]. | *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. | *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]]. | *If left untreated, bruxism can lead to [[hypertrophy]] of [[masseter muscle]] accompanied by tenderness of [[TMJ]], which manifests as [[otalgia]]. | ||
===Complications=== | ===Complications=== | ||
Common [[complications]] of bruxism are | Common [[complications]] of bruxism are: | ||
*Tooth wear | *Tooth wear | ||
*Tooth hypersensitivity | *[[Tooth]] hypersensitivity | ||
*Tooth mobility | *[[Tooth]] mobility | ||
*Pain in the temporomandibular joint (TMJ) or jaw musculature | *[[Pain]] in the [[temporomandibular joint]] (TMJ) or [[jaw]] musculature | ||
*Temporal headache, | *Temporal [[headache]], | ||
*Poor sleep | *Poor [[sleep]] | ||
*Signs of this parafunctional habit | *Signs of this parafunctional habit | ||
**Indentation on the tongue | **Indentation on the [[tongue]] | ||
**Presence of linea alba along the biting plane of the buccal mucosa | **Presence of [[linea alba]] along the biting plane of the [[buccal mucosa]] | ||
**Gingival recessions | **[[Gingival]] recessions | ||
==Diagnosis== | ==Diagnosis== | ||
| Line 176: | Line 176: | ||
Bruxism is primarily diagnosed based on the clinical presentation. | Bruxism is primarily diagnosed based on the clinical presentation. | ||
*History of tooth grinding during sleep | *History of tooth grinding during [[sleep]] | ||
*Confirmation by parents or bed partners. | *Confirmation by parents or bed partners. | ||
| Line 182: | Line 182: | ||
===History=== | ===History=== | ||
* | *History of complaints of disturbance from the clicking or grating sound by the accompanied partners. | ||
===Symptoms=== | ===Symptoms=== | ||
The most common [[symptoms]] of bruxism include | The most common [[symptoms]] of bruxism include:<ref name="MacedoMacedo2014">{{cite journal|last1=Macedo|first1=Cristiane R|last2=Macedo|first2=Elizeu C|last3=Torloni|first3=Maria R|last4=Silva|first4=Ademir B|last5=Prado|first5=Gilmar F|last6=Macedo|first6=Cristiane R|title=Pharmacotherapy for sleep bruxism|year=2014|doi=10.1002/14651858.CD005578.pub2}}</ref> | ||
*Involuntary rhythmic contractions of the masticator muscles during [[sleep]]. | *Involuntary rhythmic contractions of the masticator muscles during [[sleep]]. | ||
| Line 192: | Line 192: | ||
**[[Jaw pain]] | **[[Jaw pain]] | ||
**Clicking in the [[temporomandibular joint]]<nowiki/>s | **Clicking in the [[temporomandibular joint]]<nowiki/>s | ||
*[[Dental]] deformities may be seen however not [[disease]] specific not limited to | *[[Dental]] deformities may be seen, however not [[disease]] specific, and not limited to: | ||
**Thermal sensitivity in the [[teeth]] | **Thermal sensitivity in the [[teeth]] | ||
**Hypermobility | **Hypermobility | ||
| Line 198: | Line 198: | ||
**[[Tooth]] wear on [[tooth]] surfaces that contact during biting or [[chewing]] | **[[Tooth]] wear on [[tooth]] surfaces that contact during biting or [[chewing]] | ||
**Lateral grinding forces in particular can be particularly destructive. | **Lateral grinding forces in particular can be particularly destructive. | ||
* | *Severe cases of bruxism do present with: | ||
**Injury to soft tissues of the [[mouth]] | **Injury to soft tissues of the [[mouth]] | ||
**[[Dental fractures]] | **[[Dental fractures]] | ||
| Line 204: | Line 204: | ||
**[[Temporomandibular joint]] [[pain]] and dysfunction | **[[Temporomandibular joint]] [[pain]] and dysfunction | ||
**[[Head]] and [[neck pain]] | **[[Head]] and [[neck pain]] | ||
===Physical Examination=== | |||
Patients with bruxism usually appear normal. | |||
===Laboratory Findings=== | ===Laboratory Findings=== | ||
There are no diagnostic [[laboratory]] findings associated with | There are no diagnostic [[laboratory]] findings associated with bruxism. | ||
===Electrocardiogram=== | ===Electrocardiogram=== | ||
There are no [[ECG]]findings associated with | There are no [[ECG]]findings associated with bruxism. | ||
===X-ray=== | ===X-ray=== | ||
There are no [[x-ray]] findings associated with | There are no [[x-ray]] findings associated with bruxism. | ||
===Echocardiography or Ultrasound=== | ===Echocardiography or Ultrasound=== | ||
There are no [[echocardiography]]/[[ultrasound]] | There are no [[echocardiography]]/[[ultrasound]] findings associated with bruxism . | ||
===CT scan=== | ===CT scan=== | ||
There are no [[CT scan]] findings associated with | There are no [[CT scan]] findings associated with bruxism. | ||
===MRI=== | ===MRI=== | ||
There are no [[MRI]] findings associated with | There are no [[MRI]] findings associated with bruxism. | ||
===Other Imaging Findings=== | ===Other Imaging Findings=== | ||
There are no other imaging findings associated with | There are no other imaging findings associated with bruxism. | ||
===Other Diagnostic Studies=== | ===Other Diagnostic Studies=== | ||
There are no other diagnostic studies associated with | There are no other diagnostic studies associated with bruxism. | ||
==Treatment== | ==Treatment== | ||
===Medical Therapy=== | ===Medical Therapy=== | ||
*Removal of any offending agent responsible for bruxism is primary step in the management. | *Removal of any offending agent responsible for bruxism is the primary step in management.<ref name="MacedoMacedo2014">{{cite journal|last1=Macedo|first1=Cristiane R|last2=Macedo|first2=Elizeu C|last3=Torloni|first3=Maria R|last4=Silva|first4=Ademir B|last5=Prado|first5=Gilmar F|last6=Macedo|first6=Cristiane R|title=Pharmacotherapy for sleep bruxism|year=2014|doi=10.1002/14651858.CD005578.pub2}}</ref><ref name="pmid21356412">{{cite journal |vauthors=Ommerborn MA, Taghavi J, Singh P, Handschel J, Depprich RA, Raab WH |title=Therapies most frequently used for the management of bruxism by a sample of German dentists |journal=J Prosthet Dent |volume=105 |issue=3 |pages=194–202 |date=March 2011 |pmid=21356412 |doi=10.1016/S0022-3913(11)60029-2 |url=}}</ref><ref name="pmid17949541">{{cite journal |vauthors=Huynh N, Manzini C, Rompré PH, Lavigne GJ |title=Weighing the potential effectiveness of various treatments for sleep bruxism |journal=J Can Dent Assoc |volume=73 |issue=8 |pages=727–30 |date=October 2007 |pmid=17949541 |doi= |url=}}</ref> | ||
* | |||
*The wait-and-see approach is recommended in cases with medically induced bruxism, as spontaneous remission is ensured with the cessation of the offending agent. | |||
*[[Pharmacotherapy]] mainly concentrated to alleviate [[symptoms]] | *[[Pharmacotherapy]] mainly concentrated to alleviate [[symptoms]] | ||
*[[Buspirone]] and [[Gabapentin]] are the two recommended medications to manage bruxism | *[[Buspirone]] and [[Gabapentin]] are the two recommended medications to manage bruxism | ||
| Line 240: | Line 244: | ||
===Surgery=== | ===Surgery=== | ||
Surgery is the | Surgery is the mainstay of treatment in the management of bruxism. | ||
====Indications==== | ====Indications==== | ||
The treatment of bruxism is indicated when there are any of these possible consequences: | The treatment of bruxism is indicated when there are any of these possible consequences:<ref name="MacedoMacedo2014">{{cite journal|last1=Macedo|first1=Cristiane R|last2=Macedo|first2=Elizeu C|last3=Torloni|first3=Maria R|last4=Silva|first4=Ademir B|last5=Prado|first5=Gilmar F|last6=Macedo|first6=Cristiane R|title=Pharmacotherapy for sleep bruxism|year=2014|doi=10.1002/14651858.CD005578.pub2}}</ref><ref name="pmid21356412">{{cite journal |vauthors=Ommerborn MA, Taghavi J, Singh P, Handschel J, Depprich RA, Raab WH |title=Therapies most frequently used for the management of bruxism by a sample of German dentists |journal=J Prosthet Dent |volume=105 |issue=3 |pages=194–202 |date=March 2011 |pmid=21356412 |doi=10.1016/S0022-3913(11)60029-2 |url=}}</ref> | ||
*Mechanical wear of the [[teeth]], which results in loss of occlusal morphology and flattening of the occlusal surfaces | *Mechanical wear of the [[teeth]], which results in loss of occlusal morphology and flattening of the occlusal surfaces | ||
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[[Category:Neurology]] | [[Category:Neurology]] | ||
[[Category:Psychiatry]] | [[Category:Psychiatry]] | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]
Overview
Bruxism is defined as repeated involuntary grinding and clenching of teeth which can occur either diurnal or nocturnally. In 1907, Marie Pielkiewics coined the French term 'La Bruxomanie" for bruxism. Bruxism can be classified into awake bruxism and sleep bruxism based on the physiological sleep status of the individual. The etiology of bruxism can be categorized into three groups:psychosocial factors, peripheral factors, and pathophysiological factors. Multifactorial etiology causes involving brain neurotransmitters or basal ganglia. Bruxism affects men and women equally. Factors associated with an increased risk of bruxism include obstructive sleep apnea, alcohol abuse, caffeine intake, smoking, and anxiety. The symptoms of bruxism usually develop in the first decade of life, and start with the appearance of the first primary upper and lower anterior teeth. Common complications of bruxism are tooth wear, and tooth hypersensitivity. Bruxism is primarily diagnosed based on the clinical presentation. History of complaints of disturbance from the clicking or grating sound by the accompanied partners. The most common symptoms of bruxism include involuntary rhythmic contractions of the masticator muscles during sleep. Removal of any offending agent responsible for bruxism is the primary step in the management. Surgery is the mainstay of treatment in the management of bruxism.
Historical Perspective
- In 1907, Marie Pielkiewics coined the French term 'La Bruxomanie" for bruxism. [1]
- In 1931, Frohman first coined the English term bruxism.
Classification
Bruxism can be classified into awake bruxism and sleep bruxism based on the physiological sleep status of the individual.[2][3]
| Awake Bruxism/Diurnal Bruxism | Sleep Bruxism/Nocturnal Bruxism |
|---|---|
| Day Time /Awake | Sleep |
| Semi-Voluntary | Stereotyped |
| 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
The etiology of bruxism can be categorized into three groups: psychosocial factors, peripheral factors, and pathophysiological factors.[3]
| Etiology of Bruxism | |
|---|---|
| Psychological | Common psychological factors responsible for bruxism include:
|
| Peripheral |
|
| Pathological |
|
Pathophysiology
- Bruxism is caused by the activation of reflexive chewing activity[4]
- Chewing is a neuromuscular activity that is controlled by the reflex nerve pathways.
- During sleep, the reflex part is active while the higher control is inactive, resulting in bruxism.
- 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 a disorder.[4]
- 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 the 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 an imbalance between 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 the 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.
Associated Factors
- Disturbed sleep pattern/other sleep disorders[5][6] (obstructive sleep apnea,[7] snoring,[8] moderate daytime sleepiness[5])
- Malocclusion, in which the upper and lower teeth fit together in a dysfunctional way, typically through lateral asymmetry and dysocclusion of the front teeth through premature contact of back teeth.
- Relatively high levels of consumption of caffeinated drinks and foods, such as coffee, colas, and chocolate[5]
- High levels of alcohol consumption[5]
- Smoking[5]
- High levels of anxiety and/or stress[5]
- SSRIs
- Digestive problems
- Hypersensitivity of the dopamine receptors in the brain.
- Consumption of stimulant drugs and medications, such as those of the amphetamine-based family, such as MDMA[9]
- Excessive use of (i.e., frequent redosing and dependency on) GHB and similar GABA-inducing analogues such as Phenibut [9]
- Disorders such as Huntington's and Parkinson's diseases [10]
Epidemiology and Demographics
Bruxism often occurs during sleep and can even occur during short naps. Bruxism is one of the most common sleep disorders: 30 to 40 million Americans grind their teeth during sleep.
Gender
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
Diagnosis
Diagnostic study of choice
Bruxism is primarily diagnosed based on the clinical presentation.
- History of tooth grinding during sleep
- Confirmation by parents or bed partners.
History
- History of complaints of disturbance from the clicking or grating sound by the accompanied partners.
Symptoms
The most common symptoms of bruxism include:[11]
- Involuntary rhythmic contractions of the masticator muscles during sleep.
- Secondary symptoms may develop due to forceful grinding in some patients which include:
- Morning headaches
- Jaw pain
- Clicking in the temporomandibular joints
- Dental deformities may be seen, however not disease specific, and not limited to:
- Severe cases of bruxism do present with:
- Injury to soft tissues of the mouth
- Dental fractures
- Difficulty with chewing
- Temporomandibular joint pain and dysfunction
- Head and neck pain
Physical Examination
Patients with bruxism usually appear normal.
Laboratory Findings
There are no diagnostic laboratory findings associated with bruxism.
Electrocardiogram
There are no ECGfindings associated with bruxism.
X-ray
There are no x-ray findings associated with bruxism.
Echocardiography or Ultrasound
There are no echocardiography/ultrasound findings associated with bruxism .
CT scan
There are no CT scan findings associated with bruxism.
MRI
There are no MRI findings associated with bruxism.
Other Imaging Findings
There are no other imaging findings associated with bruxism.
Other Diagnostic Studies
There are no other diagnostic studies associated with bruxism.
Treatment
Medical Therapy
- Removal of any offending agent responsible for bruxism is the primary step in management.[11][12][13]
- The wait-and-see approach is recommended in cases with medically 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 mainstay of treatment in the management of bruxism.
Indications
The treatment of bruxism is indicated when there are any of these possible consequences:[11][12]
- 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
- Temporomandibularpain
- Pain in the preauricular region
References
- ↑ Shetty S, Pitti V, Satish Babu CL, Surendra Kumar GP, Deepthi BC (September 2010). "Bruxism: a literature review". J Indian Prosthodont Soc. 10 (3): 141–8. doi:10.1007/s13191-011-0041-5. PMC 3081266. PMID 21886404.
- ↑ Thorpy MJ (October 2012). "Classification of sleep disorders". Neurotherapeutics. 9 (4): 687–701. doi:10.1007/s13311-012-0145-6. PMC 3480567. PMID 22976557.
- ↑ 3.0 3.1 Bader G, Lavigne G (February 2000). "Sleep bruxism; an overview of an oromandibular sleep movement disorder. REVIEW ARTICLE". Sleep Med Rev. 4 (1): 27–43. doi:10.1053/smrv.1999.0070. PMID 12531159.
- ↑ 4.0 4.1 Lavigne GJ, Khoury S, Abe S, Yamaguchi T, Raphael K (July 2008). "Bruxism physiology and pathology: an overview for clinicians". J Oral Rehabil. 35 (7): 476–94. doi:10.1111/j.1365-2842.2008.01881.x. PMID 18557915.
- ↑ 5.0 5.1 5.2 5.3 5.4 5.5 Maurice M. Ohayon, MD, DSc, PhD; Kasey K. Li, DDS, MD and Christian Guilleminault, MD: "Risk Factors for Sleep Bruxism in the General Population";Stanford University School of Medicine, Sleep Disorders Center, Stanford, CA;
- ↑ Y. Kobayashi, M. Yokoyama, H. Shiga, and N. Namba: 1198 Sleep Condition and Bruxism in Bruxist, Nippon Dental University, Tokyo, Japan
- ↑ Oksenberg A, Arons E.: "Sleep bruxism related to obstructive sleep apnea: the effect of continuous positive airway pressure.";Sleep Disorders Unit, Loewenstein Hospital-Rehabilitation Center, P.O. Box 3, Raanana, Israel
- ↑ Ng DK, Kwok KL, Poon G, Chau KW "Habitual snoring and sleep bruxism in a paediatric outpatient population in Hong Kong." Department of Paediatrics, Kwong Wah Hospital, Waterloo Road, Hong Kong, SAR China.
- ↑ 9.0 9.1 Winocur E, Gavish A, Voikovitch M, Emodi-Perlman A, Eli I: "Drugs and bruxism: a critical review.";Department of Occlusion and Behavioral Sciences, Maurice and Gabriela Goldschleger, School of Dental Medicine, Tel Aviv University, Tel Aviv, Israel.
- ↑ Bruxism/Teeth grinding - MayoClinic.com
- ↑ 11.0 11.1 11.2 Macedo, Cristiane R; Macedo, Elizeu C; Torloni, Maria R; Silva, Ademir B; Prado, Gilmar F; Macedo, Cristiane R (2014). "Pharmacotherapy for sleep bruxism". doi:10.1002/14651858.CD005578.pub2.
- ↑ 12.0 12.1 Ommerborn MA, Taghavi J, Singh P, Handschel J, Depprich RA, Raab WH (March 2011). "Therapies most frequently used for the management of bruxism by a sample of German dentists". J Prosthet Dent. 105 (3): 194–202. doi:10.1016/S0022-3913(11)60029-2. PMID 21356412.
- ↑ Huynh N, Manzini C, Rompré PH, Lavigne GJ (October 2007). "Weighing the potential effectiveness of various treatments for sleep bruxism". J Can Dent Assoc. 73 (8): 727–30. PMID 17949541.