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Bruxism

Bruxism is defined as repeated involuntary grinding and clenching of teeth which can occur either diurnal or nocturnally. In 1907 Marie Pielkiewics coined a 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. 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 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 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. Removal of any offending agent responsible for bruxism is primary step in the management. Surgery is the main stay of treatment in the management of bruxism.

Historical Perspective

• In 1907 Marie Pielkiewics coined a french term 'La Bruxomanie" for bruxism.
• 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)	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 caused by the activation of reflex chewing activity; it is not a learned habit.
• Chewing is a complex neuromuscular activity that is controlled by reflex nerve pathways, with higher control by the brain.
• During sleep, the reflex part is active while the higher control is inactive, resulting in bruxism. In most people, bruxism is mild enough not to be a health problem; however, some people suffer from significant bruxism that can become symptomatic.
• 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 Facial myoclonus Chewing-like movements Swallowing Sleep talking Expiratory groaning
Tooth wear
Jaw pain and fatigue

A profile of a smile, exhibiting significant wear, especially on the maxillary incisors. Even though the teeth are in an edge-to-edge position, the teeth are in maximum intercuspation; this patient possesses a Class III occlusion.

The etiology of bruxism is unknown; the following factors may be associated with the condition.

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

• 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

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

• H/o complain of disturbance from the clicking or grating sound by the accompanied partners.

Symptoms

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
  • Hypermobility
  • 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

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

Labrynthitis

Diseases	Clinical manifestations					Para-clinical findings		Gold standard	Additional findings
	Symptoms				Physical examination
						Lab Findings	Imaging
	Acute onset	Recurrency	Nystagmus	Hearing problems
Peripheral
BPPV	+	+	+/−	−	+ Dix-Hallpike maneuver	−	−	Dix-Hallpike maneuver	May be associated with nausea, vomiting, and gait instability
Vestibular neuritis	+	+/−	+ /− (unilateral)	−	+ Head thrust test	−	−	History/ Physical exam	May be associated with nausea, vomiting, gait instability and previous upper respiratory infection
HSV oticus	+	+/−	−	+/−	Taste loss in the front two-thirds of the tongue Acute facial nerve paralysis Vesicles in the ear canal, the tongue, and/or hard palate	+ VZV antibody titres	In MRI with gadolinium dye we may have enhancement of the facial nerve and cranial nerve VIII	History/ Physical exam	May be associated with otalgia, dry mouth, and dry eyes
Meniere disease	+/−	+	+/−	+ (Progressive)	Sensorineural hearing loss	−	In CT scan we may see small or invisible vestibular aqueduct	History/ Physical exam/ Rulling out other diagnoses	May be associated with nausea, vomiting, and tinnitus
Labyrinthine concussion	+	−	−	+	high frequency hearing loss	−	We may see other evidences of head trauma or temporal bone fracture	History/ Physical exam	It happens following blunt head trauma May be associated with dizziness or tinnitus
Perilymphatic fistula	+/−	+	−	+	Tullio phenomenon	−	CT scan may show fluid around the round window recess	History/ Physical exam/Imaging	Can be a complication of a stapedectomy, head injury, or heavy lifting It may be provoked by sneezing, lifting, straining, coughing, and loud sounds
Semicircular canal dehiscence syndrome	+/−	+	−	+ (air-bone gaps on audiometry)	Tullio phenomenon	−	CT scan may show defect in the arcuate eminence of the superior semicircular canal	History/ Physical exam/Imaging	It may be provoked by Valsalva maneuver, coughing, and sneezing
Vestibular paroxysmia	+	+	+/− (Induced by hyperventilation)	−	Impaired caloric testing	−	We may see evidence of vestibulocochlear nerve compression on MRI	History/ Physical exam/Imaging	It may be provoked by head turn or other action They respond well to treatment with carbamazepine or oxcarbazepine
Cogan syndrome	−	+	+/−	+	Interstitial keratitis Oscillopsia Absent vestibular function on caloric test Systemic vasculitis (Aortitis)	Increased ESR and cryoglobulins	In CT scan we may see calcification or soft tissue attenuation obliterating the intralabyrinthine fluid spaces	History/ Physical exam	It may cause Ménière-like attacks
Vestibular schwannoma	−	+	+/−	+	Sensorineural hearing loss + Rinne test Lateralization of Weber test to the normal ear	−	In CT scan we may see erosion, and widening of the internal acoustic meatus Hypointense mass on T1-weighted MRI, and hyperintense mass on T2-weighted MRI	Imaging	Gadolinium-enhanced MRI scan is definitive diagnostic test of acoutic neuroma
Otitis media	+	−	−	+/−	Fever Presence of effusion in the middle ear	Increased acute phase reactants	Opacification of the middle ear	History/ Physical exam	Patient may show other signs and symptoms of upper respiratory infection such az cough, nasal discharge, and fever
Aminoglycoside toxicity	+	−	−	+	Oscillopsia	−	−	History/ Physical exam	May be associated with nausea, vomiting, and ataxia It may be irreversible Gentamicin is the most common one
Recurrent vestibulopathy	+	−	−	−	−	−	−	History/ Physical exam	The underlying pathophysiology is unknown It may happen infrequently, every one to two years It may be associated with nausea and vomiting It may overlap with vestibular migraine
Central
Vestibular migrain	–	+	+/−	+/−	History of migraine headaches	−	They may have white-matter hyperintensities (WMHs) on MRI	ICHD-3 criteria	It may be associated with anxiety and depression
Epileptic vertigo	−	+	+/−	−	They may experience loss of consciousness and motor/sensory problems	−	−	EEG	They response well to anti-seizure drugs
Multiple sclerosis	−	+	+/−	−	Lhermitte's sign Spasticity Increased reflexes Internuclear ophthalmoplegia Optic neuritis Gait disturbance	Elevated concentration of CSF oligoclonal bands	Brain atrophy and some contrast enhancing plaques on CT scan Cerebral plaques disseminating in space and time on MRI	History and physical examination Imaging CSF analysis	MS is at least two times more common among women than men The onset of symptoms is mostly between the age of fifteen to forty years, rarely before age fifteen or after age sixty
Brain tumors	+/−	+	+	+	Papilledema Focal neurological deficits	Cerebral spinal fluid (CSF) may show cancerous cells	On CT scan most of the brain tumors appears as a hypodense mass lesions On MRI most of the brain tumors appears as a hypointense or isointense on T1-weighted scans, or hyperintense on T2-weighted MRI.	Imaging Biopsy	Patieny may experience headache, seizures, visual changes and changes in personality, mood and concentration
Cerebellar infarction/hemorrhage	+	−	++/−	−	Limb ataxia Gait disturbance Dysarthria	−	Based on the time interval between stroke and imaging we may have different presentations	Imaging	Posterior inferior cerebellar artery is the most common artery that causes vertigo
Brain stem ischemia	+	−	+/−	−	Contralateral body weakness Visual field deficits Oculomotor abnormalities Bulbar findings	−	Based on the time interval between stroke and imaging we may have different presentations For more information click here	Imaging	It may be associated with subclavian steal syndrome
Chiari malformation	−	+	+	−	Tachycardia Pupillary dilatation Impaired gag reflex Impaired coordination	−	In CT scan we may see hydrocephalus, herniated cerebellar tonsils, and a flattened spinal cord In MRI we may see cerebellar tonsillar herniation, wedge shaped tonsils, syringohydromyelia, small posterior fossa, obstructive hydrocephalus, and brainstem anomalies	Imaging	Patient may experience ringing in the ears
Parkinson	−	+	−	−	Hypomimia Cogwheel rigidity Resting tremor Gait problems Bradykinesia	−	On brain CT scan, Parkinson disease is characterized by cortical and subcortical atrophy MRI findings in Parkinson disease are reduction in T2 relaxation time and reduced iron content in putamen and GPe	History and physical examination	Patients may present with slowness of movement (bradykinesia), shaking hands while they are at rest (resting tremor) and muscle stiffness (rigidity).