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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, Anxiety. The symptoms of bruxism, usually develop in the first decade of life, and start with symptoms such as the appearance of the first primary upper and lower anterior teeth. Common complications of bruxism are tooth wear, tooth hypersensitivity. Bruxism is primarily diagnosed based on the clinical presentation. H/o complains 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.
- In 1907 Marie Pielkiewics coined a french term 'La Bruxomanie" for bruxism. 
- In 1931, Frohman first coined the term English term bruxism.
|Awake Bruxism/Diurnal Bruxism||Sleep Bruxism/Nocturnal Bruxism|
|Day Time /Awake||Sleep|
|Clenching predominant||Teeth grinding|
|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.|
|Etiology of Bruxism|
|Psychological||Common psychological factors responsible for bruxism include|
- Bruxism is caused by the activation of reflex chewing activity
- Chewing is a neuromuscular activity that is controlled by 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 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.
- Disturbed sleep pattern/other sleep disorders (obstructive sleep apnea, snoring, moderate daytime sleepiness)
- 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
- High levels of alcohol consumption
- High levels of anxiety and/or stress
- 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
- Excessive use of (i.e., frequent redosing and dependency on) GHB and similar GABA-inducing analogues such as Phenibut 
- Disorders such as Huntington's and Parkinson's diseases 
Epidemiology and Demographics
- Bruxism commonly affects individuals younger than 6 years of age and its incidence declines as age increases.
There is insufficient evidence to recommend routine screening for bruxism.
Factors associated with an increased risk of bruxism include:
Natural History, Complications and Prognosis
- 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.
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
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.
- H/o complain 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.
- 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 not limited to
- Thermal sensitivity in the teeth
- Need for dental restorations
- Tooth wear on tooth surfaces that contact during biting or chewing
- Lateral grinding forces in particular can be particularly destructive.
- Sever 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
There are no diagnostic laboratory findings associated with Bruxism.
There are no ECGfindings associated with Bruxism.
There are no x-ray findings associated with Bruxism.
Echocardiography or Ultrasound
There are no CT scan findings associated with Bruxism.
There are no MRI findings associated with [disease name].
[Location] MRI may be helpful in the diagnosis of [disease name]. Findings on MRI suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
There are no MRI findings associated with [disease name]. However, a MRI may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].
Other Imaging Findings
There are no other imaging findings associated with [disease name].
[Imaging modality] may be helpful in the diagnosis of [disease name]. Findings on an [imaging modality] suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
Other Diagnostic Studies
There are no other diagnostic studies associated with [disease name].
[Diagnostic study] may be helpful in the diagnosis of [disease name]. Findings suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
Other diagnostic studies for [disease name] include [diagnostic study 1], which demonstrates [finding 1], [finding 2], and [finding 3], and [diagnostic study 2], which demonstrates [finding 1], [finding 2], and [finding 3].
- 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
Surgery is the main stay of treatment in the management of bruxism.
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
- 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.
- 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.
- 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.
- 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.
- 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