Interactions with the aquaporin 5 gene increase the susceptibility to molar-incisor hypomineralization

Pang, Liangyue; Li, Xia; Wang, Ketian; Tao, Ye; Cui, Tianqiang; Xu, Qiong; Lin, Huancai

doi:10.1016/j.archoralbio.2019.104637

Cited by 20 publications

(48 citation statements)

References 31 publications

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“…All the above suggest that MIH follows a multifactorial model with genetic and/or epigenetic components becoming more prominent in the more recently established evidence (Pang et al 2020;Bussaneli et al 2021).…”

Section: Genetics/epigeneticsmentioning

confidence: 95%

“…The SCUBE1 gene plays a role in the development of the craniofacial region, and in a mouse model, it was found to be localised to the dental papilla of both incisor and molar teeth (Xavier et al 2009 ). A genetic predisposition to MIH in conjunction with one or several other aetiological factors has been proposed, as some authors identified certain variants in amelogenesis-related genes ENAM, AMELX or MMP20 (Jeremias et al 2013a , b , 2016 ; Kühnisch et al 2014 ; Hočevar et al 2020 ; Pang et al 2020 ) or immune response-related genes (Bussaneli et al 2019 ) in children with MIH. More recently, epigenetic influences of certain environmental factors have also been established (Teixeira et al 2018 ; Vieira 2019 ; Vieira and Manton 2019 ).…”

Section: Aetiology Of Mihmentioning

confidence: 99%

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Best clinical practice guidance for clinicians dealing with children presenting with molar-incisor-hypomineralisation (MIH): an updated European Academy of Paediatric Dentistry policy document

Lygidakis

Garot

Somani

et al. 2021

Eur Arch Paediatr Dent

158

192

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Aim To update the existing European Academy of Paediatric Dentistry (EAPD) 2010 policy document on the ‘Best Clinical Practice guidance for clinicians dealing with children presenting with Molar-Incisor-Hypomineralisation (MIH).’ Methods Experts, assigned the EAPD, worked on two different topics: (A) Aetiological factors involved in MIH, and (B) Treatment options for the clinical management of MIH. The group prepared two detailed systematic reviews of the existing literature relevant to the topics and following a consensus process produced the updated EAPD policy document on the ‘Best Clinical Practice guidance for clinicians dealing with children presenting with molar-incisor-hypomineralisation (MIH).’ The GRADE system was used to assess the quality of evidence regarding aetiology and treatment which was judged as HIGH, MODERATE, LOW or VERY LOW, while the GRADE criteria were used to indicate the strength of recommendation regarding treatment options as STRONG or WEAK/CONDITIONAL. Results (A) Regarding aetiology, it is confirmed that MIH has a multifactorial aetiology with the duration, strength and timing of occurrence of the aetiological factors being responsible for the variable clinical characteristics of the defect. Perinatal hypoxia, prematurity and other hypoxia related perinatal problems, including caesarean section, appear to increase the risk of having MIH, while certain infant and childhood illnesses are also linked with MIH. In addition, genetic predisposition and the role of epigenetic influences are becoming clearer following twin studies and genome and single-nucleotide polymorphisms analyses in patients and families. Missing genetic information might be the final key to truly understand MIH aetiology. (B) Regarding treatment options, composite restorations, preformed metal crowns and laboratory indirect restorations provide high success rates for the posterior teeth in appropriate cases, while scheduled extractions provide an established alternative option in severe cases. There is great need for further clinical and laboratory studies evaluating new materials and non-invasive/micro-invasive techniques for anterior teeth, especially when aesthetic and oral health related quality of life (OHRQoL) issues are concerned. Conclusions MIH has been studied more extensively in the last decade. Its aetiology follows the multifactorial model, involving systemic medical and genetic factors. Further focused laboratory research and prospective clinical studies are needed to elucidate any additional factors and refine the model. Successful preventive and treatment options have been studied and established. The appropriate choice depends on the severity of the defects and the age of the patient. EAPD encourages the use of all available treatment options, whilst in severe cases, scheduled extractions should be considered.

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Section: Genetics/epigeneticsmentioning

confidence: 95%

Section: Aetiology Of Mihmentioning

confidence: 99%

Best clinical practice guidance for clinicians dealing with children presenting with molar-incisor-hypomineralisation (MIH): an updated European Academy of Paediatric Dentistry policy document

Lygidakis

Garot

Somani

et al. 2021

Eur Arch Paediatr Dent

158

192

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“…Knowing that enamel development of first permanent molars is completed around 4 years of age [23], a possible mechanism underlying MIH is an interference in enamel formation due to an organic stress in response to illness or infection. This organic stress could happen at any time between birth and past 4 years of age in children with a particular genetic background that includes hypomorphic alleles of IRF6, TGFA, and other genes such as TGFBR1 [29], and AQP5 [28]. It is likely that disturbances of first permanent molar development may happen after the first year of life, since mineralization of these teeth is not complete until later.…”

Section: Plos Onementioning

confidence: 99%

“…Different systematic reviews concluded that most of the previously studied environmental factors that were believed to be risk factors for MIH did not fully explain the disease etiology [5,26,27]. In contrast, etiological factors associated with enamel forming genes [2,28] or in immune response-related genes [28,29] have been reported to play a role in the condition's onset.…”

Section: Introductionmentioning

confidence: 99%

Gene-environment interaction in molar-incisor hypomineralization

et al. 2021

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Molar incisor hypomineralization (MIH) is an enamel condition characterized by lesions ranging in color from white to brown which present rapid caries progression, and mainly affects permanent first molars and incisors. These enamel defects usually occur when there are disturbances during the mineralization or maturation stage of amelogenesis. Both genetic and environmental factors have been suggested to play roles in MIH’s development, but no conclusive risk factors have shown the source of the disease. During head and neck development, the interferon regulatory factor 6 (IRF6) gene is involved in the structure formation of the oral and maxillofacial regions, and the transforming growth factor alpha (TGFA) is an essential cell regulator, acting during proliferation, differentiation, migration and apoptosis. In this present study, it was hypothesized that these genes interact and contribute to predisposition of MIH. Environmental factors affecting children that were 3 years of age or older were also hypothesized to play a role in the disease etiology. Those factors included respiratory issues, malnutrition, food intolerance, infection of any sort and medication intake. A total of 1,065 salivary samples from four different cohorts were obtained, and DNA was extracted from each sample and genotyped for nine different single nucleotide polymorphisms. Association tests and logistic regression implemented in PLINK were used for analyses. A potential interaction between TGFA rs930655 with all markers tested in the cohort from Turkey was identified. These interactions were not identified in the remaining cohorts. Associations (p<0.05) between the use of medication after three years of age and MIH were also found, suggesting that conditions acquired at the age children start to socialize might contribute to the development of MIH.

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“…The neonatal causes could be related to premature birth, systemic upset, nephrotic or gastrointestinal disturbances. Recent studies have also shown a possible genetic link to MIH [ 6 , 7 ].…”

Section: Introductionmentioning

confidence: 99%

Molar Incisor Hypomineralisation—To Extract or to Restore beyond the Optimal Age?

Elhussein

Jamal

2020

Children

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The management of compromised first permanent molars (FPMs) in children presents a clinical challenge to the dental team. Hypomineralised FPMs in molar incisor hypomineralisation (MIH) conditions could undergo post-eruptive breakdown, making them susceptible to caries, leading to their subsequent loss. The planned extraction of compromised FPMs is a valid alternative to complex restorative treatment. However, establishing the presence or absence of third permanent molars, amongst other considerations, is crucial to reaching a successful outcome. Clinicians should understand the importance of an orthodontic examination around the age of 8 years old with regard to establishing a differential therapeutic decision about the ideal timing of MIH-affected FPMs’ extraction in children. The aim of this article is to highlight that, with an interdisciplinary approach, a good outcome can be achieved following the extraction of poorly prognosed FPMs. The most cost-effective way of addressing MIH-affected FPMs is extraction, followed by orthodontic space closure when indicated. This obviates the need for the repeated restorative replacement and saves perfectly healthy premolars from being extracted for space creation in orthodontic treatment in several clinical scenarios.

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Interactions with the aquaporin 5 gene increase the susceptibility to molar-incisor hypomineralization

Cited by 20 publications

References 31 publications

Best clinical practice guidance for clinicians dealing with children presenting with molar-incisor-hypomineralisation (MIH): an updated European Academy of Paediatric Dentistry policy document

Best clinical practice guidance for clinicians dealing with children presenting with molar-incisor-hypomineralisation (MIH): an updated European Academy of Paediatric Dentistry policy document

Gene-environment interaction in molar-incisor hypomineralization

Molar Incisor Hypomineralisation—To Extract or to Restore beyond the Optimal Age?

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