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

Mutlu, Necip; Herken, Hasan; Özkaya, Mahmut; Erdal, Nurten; Öz, Gülsün; Bayazıt, Yıldırım A.

doi:10.1163/1568569053421663

Cited by 4 publications

(2 citation statements)

References 19 publications

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“…Among the human studies, different ethnic groups such as Koreans, Japanese, Brazilian, Finnish, and Turkish populations were studied ( Table 1 ). Three articles did not mention the ethnicity of the population studied [ 14 ] [ 15 ] [ 16 ]. One study indicated that in the miscegenetic Brazilian population, the age was significantly associated with TMDs [ 17 ].…”

Section: Resultsmentioning

confidence: 99%

“…Females are more affected by TMJ pain and degeneration due to the effects of β -estradiol on the TMJ [ 18 ]. Three studies show no statistically significant changes in candidate TMD causative genes: MAOA (monoamine oxidase-A), ESR 1 (estrogen receptor alpha), and TNF (tumor necrosis factor alpha) [ 16 ] [ 19 ] [ 20 ]. Several polymorphisms have been described in the promoter region of MMP genes, and these polymorphisms modify gene expression and function of the MMPs.…”

Section: Resultsmentioning

confidence: 99%

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Gene Mutations Associated with Temporomandibular Joint Disorders: A Systematic Review

Sangani¹,

Suzuki²,

VonVille³

et al. 2015

OALib

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Background The temporomandibular joint (TMJ) is a bilateral synovial joint between the mandible and the temporal bone of the skull. TMJ disorders (TMDs) are a set of complicated and poorly understood clinical conditions, in which TMDs are associated with a number of symptoms including pain and limited jaw movement. The increasing scientific evidence suggests that genetic factors play a significant role in the pathology of TMDs. However, the underlying mechanism of TMDs remains largely unknown. Objective The study aimed to determine the associated genes to TMDs in humans and animals. Methods The literature search was conducted through databases including Medline (Ovid), EMBASE (Ovid), and PubMed (NLM) by using scientific terms for TMDs and genetics in March 2015. Additional studies were identified by searching bibliographies of highly relevant articles and Scopus (Elsevier). Results Our systematic analyses identified 31 articles through literature searches. A total of 112 genes were identified to be significantly and specifically associated with TMDs. Conclusion Our systematic review provides a list of accurate genes associated with TMDs and suggests a genetic contribution to the pathology of TMDs.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Gene Mutations Associated with Temporomandibular Joint Disorders: A Systematic Review

Sangani¹,

Suzuki²,

VonVille³

et al. 2015

OALib

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show abstract

Genetic predictors of human chronic pain conditions

et al. 2016

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Chronic pain conditions are multifactorial disorders with a high frequency in the population. Their pathophysiology is often unclear, and treatment is inefficient. During the last 20years, genetic linkage analysis and association studies have made considerable strides toward identifying key molecular contributors to the onset and maintenance of chronic pain. Here, we review the genetic variants that have been implicated in chronic pain conditions, divided into the following etiologically-grouped categories: migraine, musculoskeletal pain disorders, neuropathic pain disorders, and visceral pain disorders. In rare familial monogenic pain conditions several strong-effect mutations have been identified. In contrast, the genetic landscape of common chronic pain conditions suggests minor contributions from a large number of single nucleotide polymorphisms representing different functional pathways. A comprehensive survey of up-to-date genetic association results reveals migraine and musculoskeletal pain to be the most investigated chronic pain disorders, in which nearly half of identified genetic variability alters neurotransmission pathways.

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Comorbidity of Alcohol Use Disorder and Chronic Pain: Genetic Influences on Brain Reward and Stress Systems

Yeung

Craggs

Gizer

2017

Alcoholism Clin & Exp Res

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Alcohol use disorder (AUD) is highly comorbid with chronic pain (CP). Evidence has suggested that neuroadaptive processes characterized by reward deficit and stress surfeit are involved in the development of AUD and pain chronification. Neurological data suggest that shared genetic architecture associated with the reward and stress systems may contribute to the comorbidity of AUD and CP. This monograph first delineates the prevailing theories of the development of AUD and pain chronification focusing on the reward and stress systems. It then provides a brief summary of relevant neurological findings followed by an evaluation of evidence documented by molecular genetic studies. Candidate gene association studies have provided some initial support for the genetic overlap between AUD and CP, however these results must be interpreted with caution until studies with sufficient statistical power are conducted and replications obtained. Genome-wide association studies have suggested a number of genes (e.g., TBX19, HTR7, and ADRA1A) that are either directly or indirectly related to the reward and stress systems in the AUD and CP literature. Evidence reviewed in this monograph suggests that shared genetic liability underlying the comorbidity between AUD and CP, if present, is likely to be complex. As the advancement in molecular genetic methods continues, future studies may show broader central nervous system involvement in AUD-CP comorbidity.

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

Cited by 4 publications

References 19 publications

Gene Mutations Associated with Temporomandibular Joint Disorders: A Systematic Review

Gene Mutations Associated with Temporomandibular Joint Disorders: A Systematic Review

Genetic predictors of human chronic pain conditions

Comorbidity of Alcohol Use Disorder and Chronic Pain: Genetic Influences on Brain Reward and Stress Systems

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