BRUKSIZM TEDAVISI PDF

American Sleep Disorders Association defined bruxism as a periodic, stereotyped movement disorder of the masticatory system involving tooth grinding or clenching during sleep. Bruxism can occur durind the day or night. Generally, patients clench their teeth throughout the day and gnash and clench them during sleep. It is a destructive habit that may result in tooth wear. Although research on bruxism is extensive, its etiology remains debatable. In recent years, bruxism has become an increasing concern in children due to its negative effects on life quality and also for being considered an important risk factor for temporomandibular dysfunctions.

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Bruxism is an involuntary activity of the jaw musculature that is characterized, by jaw clenching and tooth grinding and it is a common condition. It has been postulated that disturbances in the central dopaminergic system, especially within the mesocortical tract, are linked to bruxism. In addition, it has been suggested that bruxism is considered to be a consequence of serotonergically mediated inhibition of the dopaminergic system in this brain region.

Bruxism can occur during the course of various diseases such as depression, schizophrenia, parkinsonism or it can be associated wit drug use. Tricyclic antidepressants are commonly used in the treatment of bruxism. These agents suppress the physiologic REM sleep state and increase in level four of NREM and this effect is considered a major factor in ameliorating bruxism.

It has been suggested a possible relation-ship between SSRI and bruxism, claiming that substances known to increase serotonin trans-mission in the CNS could affect bruxism. There seems to be a general agreement that these agents exacerbate bruxism.

In addition, it has been reported that venlafaxine, a serotonine noradrenaline reuptake inhibitor, may induce or exacerbate bruxism in humans. As stress has been implicated in the exacerbation of bruxism in humans anxiolytic or sedative hypnotic drugs are often suggested as effective in the treatment of bruxism. Thus, it has been found that clona-zepam therapy significantly improved not only the bruxism but also objective and subjective sleep quality, with unchanged performance upon awakening.

It has been reported that buspirone, a partial agonist of the 5-HT1A receptor, ameliorates especially drug-induced bruxism. Although an increasing number of studies on the etiology and management of bruxism, this clinical problem is still difficult to understand and as a subject open to discussion in our stands.

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