Monoamine oxidase-A gene promoter polymorphism in temporomandibular joint pain and dysfunction

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dc.contributor.authorMutlu N.
dc.contributor.authorErdal M.E.
dc.contributor.authorHerken H.
dc.contributor.authorOzkaya M.
dc.contributor.authorErdal N.
dc.contributor.authorOz G.
dc.contributor.authorBayazit Y.A.
dc.date.accessioned2020-03-26T16:58:51Z
dc.date.available2020-03-26T16:58:51Z
dc.date.issued2005
dc.departmentSelçuk Üniversitesien_US
dc.description.abstractObjective: In this study we aimed to evaluate the relationship between temporomandibular joint pain and dysfunction (TMJPD) within the frame of monoamine oxidase-A gene (MAO-LPR) gene polymorphism. Methods: Ninety-three patients with TMJPD, and 91 healthy volunteers were included in the study. Symptom Checklist-90-Revised (SCL-90-R), Montgomery-Asberg Depression Rating Scale (MADRS), and State and Trait Anxiety Inventory tests (STAI-I and STAI-II) were applied to the patients that were diagnosed as having TMJPD according to the standard clinical examination protocol. Blood samples were taken from the patients, and the variability in the MAO-A gene was analyzed by amplification of DNA with polymerase chain reaction (PCR) for a genetic association study. Results: The analysis of allele and genotype distribution for MAO-A gene polymorphism showed no significant differences between patients and controls. There was no significant association between the MAO-A polymorphism and psychiatric status of the male patients. However, the average of obsession and depression subscales scores (SCL 90-R) and MADRS points of the female patients who were homozygous for high activity alleles (2-2) were higher than those who were homozygous (1-1) and heterozygous (1-2) for low activitiy allele (f = 8.83, p < 0.01; f = 7.98, p < 0.01; f = 3.37, p = 0.04, respectively). Conclusion: This study does not provide evidence to support the involvement of MAOA gene in TMJPD. Our findings probably indicate that only the presence of the high activity alleles may play a role in the clinical symptomatology of TMJPD. Further studies are required to confirm our results as well as to understand the genetic basis of TMJPD. © 2005 VSP.en_US
dc.identifier.doi10.1163/1568569053421663en_US
dc.identifier.endpage44en_US
dc.identifier.issn0169-1112en_US
dc.identifier.issue1en_US
dc.identifier.scopusqualityN/Aen_US
dc.identifier.startpage39en_US
dc.identifier.urihttps://dx.doi.org/10.1163/1568569053421663
dc.identifier.urihttps://hdl.handle.net/20.500.12395/20027
dc.identifier.volume17en_US
dc.indekslendigikaynakScopusen_US
dc.language.isoenen_US
dc.relation.ispartofPain Clinicen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.selcuk20240510_oaigen_US
dc.subjectDysfunctionen_US
dc.subjectMAO-A geneen_US
dc.subjectPainen_US
dc.subjectPolymorphismen_US
dc.subjectTemporomandibular jointen_US
dc.titleMonoamine oxidase-A gene promoter polymorphism in temporomandibular joint pain and dysfunctionen_US
dc.typeArticleen_US

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