Drugs and bruxism: a critical review.
Lykilorð
Útdráttur
OBJECTIVE
Bruxism associated with drugs can be destructive, resulting in severe consequences to health that include destruction of tooth structure, irreversible harm to the temporomandibular joint, severe myofascial pain, and muscle contraction headache. However, reports concerning a possible association between bruxism and various pharmacologic drugs are scarce and mostly anecdotal. The purpose of this article was to review the existing literature concerning the exacerbating or ameliorating effect of drugs on bruxism in humans.
METHODS
A search of the MEDLINE, EMBASE, and PsicINFO databases from 1982 to 2001 was conducted, and the term bruxism and one of the following terms were used: drugs, medicine(s), pharmaceutical, movement disorders, akathisia, dyskinesia, dystonia, central or autonomic nervous system, dopamine, serotonin, and GABA. Furthermore, a search using the term bruxism was carried out on the weekly journal Reactions, which deals with side effects of drugs. Several chemical terms were searched separately (e.g., caffeine, nicotine). Relevant information was also derived from reference lists of the retrieved publications.
RESULTS
The search yielded complex information referring to the association between bruxism and dopamine-related drugs, antidepressant drugs, sedative and anxiolytic drugs, and drugs of abuse.
CONCLUSIONS
There is insufficient evidence-based data to draw definite conclusions concerning the effects of various drugs on bruxism. Although certain substances related to the dopaminergic, serotonergic, and adrenergic systems suppress or exacerbate bruxist activity in humans and animals, the literature is still controversial, and based mostly on anecdotal case reports. More controlled, evidence-based research on this under-explored subject is needed.