THE CURE FOR BRUXISM

HISTORY

“La bruxomanie” (a French term, translates to bruxomania) was suggested by Marie Pietkiewics in 1907. In 1931, Frohman first coined the term bruxism. Occasionally recent medical publications will use the word bruxomania with bruxism, to denote specifically bruxism that occurs while awake; however, this term can be considered historical and the modern equivalent would be awake bruxism or diurnal bruxism. It has been shown that the type of research into bruxism has changed over time. Overall between 1966 and 2007, most of the research published was focused on occlusal adjustments and oral splints. Behavioral approaches in research declined from over 60% of publications in the period 1966–86 to about 10% in the period 1997–2007.In the 1960s, a periodontist named Sigurd Peder Ramfjord championed the theory that occlusal factors were responsible for bruxism. Generations of dentists were educated by this ideology in the prominent textbook on occlusion of the time, however therapy centered around removal of occlusal interference remained unsatisfactory. The belief among dentists that occlusion and bruxism are strongly related is still widespread, however the majority of researchers now disfavor malocclusion as the main etiologic factor in favor of a more multifactorial, biopsychosocial model of bruxism.

DEFINITION OF BRUXISM

Bruxism is derived from the Greek word βρύκειν (brúkein), meaning “bite/gnash”. People who suffer from bruxism are called bruxists or bruxers and the verb itself is “to brux”. There is no widely accepted definition of bruxism, but some suggested definitions include:

• “Bruxism is a repetitive jaw-muscle activity characterized by clenching or grinding of the teeth and/or by bracing or thrusting of the mandible. Bruxism has two distinct circadian manifestations: it can occur during sleep (indicated as sleep bruxism) or during wakefulness (indicated as awake bruxism)”
• All forms of bruxism entail forceful contact between the biting surfaces of the upper and lower teeth. In grinding and tapping this contact involves movement of the mandible and unpleasant sounds which can often awaken sleeping partners and even people asleep in adjacent rooms. Clenching (or clamping), on the other hand, involves inaudible, sustained, forceful tooth contact unaccompanied by mandibular movements.
• “A movement disorder of the masticatory system characterized by teeth-grinding and clenching during sleep as well as wakefulness.”
• “Non-functional contact of the mandibular and maxillary teeth resulting in clenching or tooth grinding due to repetitive, unconscious contraction of the masseter and temporalis muscles.”
• “Parafunctional grinding of teeth or 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.”
• “Periodic repetitive clenching or rhythmic forceful grinding of the teeth.”

Bruxism is excessive teeth grinding or jaw clenching. It is an oral parafunctional activity; i.e., it is unrelated to normal function such as eating or talking. Bruxism is a common behavior; reports of prevalence range from 8–31% in the general population.Several symptoms are commonly associated with bruxism, including hypersensitive teeth, aching jaw muscles, headaches, tooth wear, and damage to dental restorations (e.g. crowns and fillings) to teeth.[3] But symptoms may be minimal, without patient awareness of the condition.

There are two main types of bruxism: one occurs during sleep (sleep bruxism) and one during wakefulness (awake bruxism). Dental damage may be similar in both types, but the symptoms of sleep bruxism tend to be worse on waking and improve during the course of the day, and the symptoms of awake bruxism may not be present at all on waking, and then worsen over the day. The causes of bruxism are not completely understood, but probably involve multiple factors. Awake bruxism is thought to have different causes from sleep bruxism, and is more common in females, whereas males and females are affected in equal proportions by sleep bruxism. Several treatments are in use, although there is little evidence of robust efficacy for any particular treatment.
Most people who brux are unaware of the problem, either because there are no symptoms, or because the symptoms are not understood to be associated with a clenching and grinding problem. The symptoms of sleep bruxism are usually most intense immediately after waking, and then slowly abate, and the symptoms of a grinding habit which occurs mainly while awake tend to worsen through the day, and may not be present on waking.

BRUXISM MAY CAUSE A VARIETY OF SIGNS AND SYMPTOMS, INCLUDING:

1.Excessive tooth wear,particularly attrition, which flattens the occlusal (biting) surface, but also possibly other types of tooth wear such as abfraction, where notches form around the neck of the teeth at the gumline.
2. Tooth fractures, and repeated failure of dental restorations (fillings, crowns, etc.).
3. Hypersensitive teeth,(e.g. dental pain when drinking a cold liquid) caused by wearing away of the thickness of insulating layers of dentin and enamel around the dental pulp.
4.Inflammation of the periodontal ligament of teeth, which may make them sore to bite on, and possibly also a degree of loosening of the teeth.
5. A grinding or tapping noise during sleep, sometimes detected by a partner or a parent. This noise can be surprisingly loud and unpleasant, and can wake a sleeping partner. Noises are rarely associated with awake bruxism.
6. Other parafunctional activity which may occur together with bruxism: cheek biting (which may manifest as morsicatio buccarum and/or linea alba), and/or lip biting.
7. A burning sensation on the tongue (see: glossodynia),possibly related to a coexistent “tongue thrusting” parafunctional activity.
8. Indentations of the teeth in the tongue (“crenated tongue” or “scalloped tongue”).
9. Hypertrophy of the muscles of mastication (increase in the size of the muscles that move the jaw), particularly the masseter muscle.
10. Tenderness, pain or fatigue of the muscles of mastication, which may get worse during chewing or other jaw movement.
Trismus (restricted mouth opening).
11.Pain or tenderness of the temporomandibular joints, which may manifest as preauricular pain (in front of the ear), or pain referred to the ear (otalgia).
12.Clicking of the temporomandibular joints.
13. Headaches, particularly pain in the temples,caused by muscle pain associated with the temporalis muscle.

Bruxism is usually detected because of the effects of the process (most commonly tooth wear and pain), rather than the process itself. The large forces that can be generated during bruxism can have detrimental effects on the components of masticatory system, namely the teeth, the periodontium and the articulation of the mandible with the skull (the temporomandibular joints). The muscles of mastication that act to move the jaw can also be affected since they are being utilized over and above of normal function.

THE CAUSES

The muscles of mastication (the temporalis, masseter, medial and lateral pterygoid muscles) are paired on either side and work together to move the mandible, which hinges and slides around its dual articulation with the skull at the temporomandibular joints. Some of the muscles work to elevate the mandible (close the mouth), and others also are involved in lateral (side to side), protrusive or retractive movements. Mastication (chewing) is a complex neuromuscular activity that can be controlled either by subconscious processes or by conscious processes. In individuals without bruxism or other parafunctional activities, during wakefulness the jaw is generally at rest and the teeth are not in contact, except while speaking, swallowing or chewing. It is estimated that the teeth are in contact for less than 20 minutes per day, mostly during chewing and swallowing. Normally during sleep, the voluntary muscles are inactive due to physiologic motor paralysis, and the jaw is usually open.

Some bruxism activity is rhythmic with bite force pulses of tenths of a second (like chewing), and some have longer bite force pulses of 1 to 30 seconds (clenching). Some individuals clench without significant lateral movements. Bruxism can also be regarded as a disorder of repetitive, unconscious contraction of muscles. This typically involves the masseter muscle and the anterior portion of the temporalis (the large outer muscles that clench), and the lateral pterygoids, relatively small bilateral muscles that act together to perform sideways grinding.

The cause of bruxism is largely unknown, but it is generally accepted to have multiple possible causes. Bruxism is a parafunctional activity, but it is debated whether this represents a subconscious habit or is entirely involuntary. The relative importance of the various identified possible causative factors is also debated.

Awake bruxism is thought to be usually semivoluntary, and often associated with stress caused by family responsibilities or work pressures.Some suggest that in children, bruxism may occasionally represent a response to earache or teething. Awake bruxism usually involves clenching (sometimes the term “awake clenching” is used instead of awake bruxism),but also possibly grinding, and is often associated with other semivoluntary oral habits such as cheek biting, nail biting, chewing on a pen or pencil absent mindedly, or tongue thrusting (where the tongue is pushed against the front teeth forcefully).

There is evidence that sleep bruxism is caused by mechanisms related to the central nervous system, involving sleep arousal and neurotransmitter abnormalities. Underlying these factors may be psychosocial factors including daytime stress which is disrupting peaceful sleep. Sleep bruxism is mainly characterized by “rhythmic masticatory muscle activity” (RMMA) at a frequency of about once per second, and also with occasional tooth grinding. It has been shown that the majority (86%) of sleep bruxism episodes occur during periods of sleep arousal. One study reported that sleep arousals which were experimentally induced with sensory stimulation in sleeping bruxists triggered episodes of sleep bruxism. Sleep arousals are a sudden change in the depth of the sleep stage, and may also be accompanied by increased heart rate, respiratory changes and muscular activity, such as leg movements. Initial reports have suggested that episodes of sleep bruxism may be accompanied by gastroesophageal reflux, decreased esophageal pH (acidity), swallowing, and decreased salivary flow. Another report suggested a link between episodes of sleep bruxism and a supine sleeping position (lying face up).

Disturbance of the dopaminergic system in the central nervous system has also been suggested to be involved in the etiology of bruxism. Evidence for this comes from observations of the modifying effect of medications which alter dopamine release on bruxing activity, such as levodopa, amphetamines or nicotine. Nicotine stimulates release of dopamine, which is postulated to explain why bruxism is twice as common in smokers compared to non-smokers.

MEDICATION

Treatment for bruxism revolves around repairing the damage to teeth that has already occurred, and also often, via one or more of several available methods, attempting to prevent further damage and manage symptoms, but there is no widely accepted, best treatment. Since bruxism is not life-threatening, and there is little evidence of the efficacy of any treatment, it has been recommended that only conservative treatment which is reversible and that carries low risk of morbidity should be used.

Certain drugs, including both prescribed and recreational drugs are thought by some to cause the development of bruxism,however others argue that there is insufficient evidence to draw such a conclusion.Examples may include dopamine agonists, dopamine antagonists, tricyclic antidepressants, selective serotonin reuptake inhibitors, alcohol, cocaine, and amphetamines (including those taken for medical reasons). In some reported cases where bruxism is thought to have been initiated by selective serotonin reuptake inhibitors, decreasing the dose resolved the side effect. Other sources state that reports of selective serotonin reuptake inhibitors causing bruxism are rare, and it only happens with long-term use.

Specific examples include levodopa (when used in the long term, as in Parkinson’s disease), fluoxetine, metoclopramide, lithium, cocaine, venlafaxine, citalopram, fluvoxamine, methylenedioxyamphetamine (MDA), methylphenidate (used in attention deficit hyperactive disorder),and gamma-hydroxybutyric acid (GHB) and similar gamma-aminobutyric acid-inducing analogues such as phenibut. Bruxism can also be exacerbated by excessive consumption of caffeine,as in coffee, tea or chocolate. Bruxism has also been reported to occur commonly comorbid with drug addiction. Methylenedioxymethamphetamine (MDMA, ecstasy) has been reported to be associated with bruxism, which occurs immediately after taking the drug and for several days afterwards. Tooth wear in people who take ecstasy is also frequently much more severe than in people with bruxism not associated with ecstasy.

 

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