N Mutlu1, M E Erdal, H Herken, G Oz, Y A Bayazit. 1. Department of Oral and Maxillofacial Surgery, Faculty of Dentistry, Selcuk University, Konya, Turkey. nmutlu@selcuk.edu.tr
Abstract
OBJECTIVE: To assess whether a relationship existed between the T102C polymorphism of 5-HT2A receptor gene and temporomandibular dysfunction. METHODS: Sixty-three patients with temporomandibular dysfunction, and 54 healthy volunteer controls were included in the study. Molecular analysis of the T102C polymorphism of the 5-HT2A receptor gene was performed using PCR technique. RESULTS: The C/C genotype was over represented in the patients whereas T/T genotype was over represented in the controls (P < 0.05). The genotype distribution of the patients who had temporomandibular dysfunction was not different than those who did not have temporomandibular dysfunction (P > 0.05). CONCLUSION: The T102C polymorphism may be involved in the etiology of temporomandibular dysfunction. The overrepresentation of the C/C variant of 5-HT2A receptor gene in temporomandibular dysfunction suggests a possible role of the serotonergic system in this disease, particularly at the receptor level.
OBJECTIVE: To assess whether a relationship existed between the T102C polymorphism of 5-HT2A receptor gene and temporomandibular dysfunction. METHODS: Sixty-three patients with temporomandibular dysfunction, and 54 healthy volunteer controls were included in the study. Molecular analysis of the T102C polymorphism of the 5-HT2A receptor gene was performed using PCR technique. RESULTS: The C/C genotype was over represented in the patients whereas T/T genotype was over represented in the controls (P < 0.05). The genotype distribution of the patients who had temporomandibular dysfunction was not different than those who did not have temporomandibular dysfunction (P > 0.05). CONCLUSION: The T102C polymorphism may be involved in the etiology of temporomandibular dysfunction. The overrepresentation of the C/C variant of 5-HT2A receptor gene in temporomandibular dysfunction suggests a possible role of the serotonergic system in this disease, particularly at the receptor level.
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