Abstract
Despite numerous case reports, the evidence for treatment of bruxism is still low. Different treatment modalities (behavioral techniques, intraoral devices, medications, and contingent electrical stimulation) have been applied. A clinical evaluation is needed to differentiate between awake bruxism and sleep bruxism and rule out any medical disorder or medication that could be behind its appearance (secondary bruxism). A polysomnography is required only in a few cases of sleep bruxism, mostly when sleep comorbidities are present. Counselling with regard to sleep hygiene, sleep habit modification, and relaxation techniques has been suggested as the first step in the therapeutic intervention, and is generally considered not harmful, despite low evidence of any efficacy. Occlusal splints are successful in the prevention of dental damage and grinding sounds associated with sleep bruxism, but their effects on reducing bruxism electromyographic (EMG) events are transient. In patients with psychiatric and sleep comorbidities, the acute use of clonazepam at night has been reported to improve sleep bruxism, but in the absence of double-blind randomized trials, its use in general clinical practice cannot be recommended. Severe secondary bruxism interfering with speaking, chewing, or swallowing has been reported in patients with neurological disorders such as in cranial dystonia; in these patients, injections of botulinum toxin in the masticatory muscles may decrease bruxism for up to 1-5 months and improve pain and mandibular functions. Long-term studies in larger and better specified samples of patients with bruxism, comparing the effects of different therapeutic modalities on bruxism EMG activity, progression of dental wear, and orofacial pain are current gaps of knowledge and preclude the development of severity-based treatment guidelines.