Molar Incisor Hypomineralisation: Possible aetiological factors in children from urban and rural areas

Souza, Juliana Feltrin de; Costa-Silva, Cristiane Maria da; Jeremias, Fabiano; Pinto, Luiz Gustavo Rodrigues; Zuanon, Ângela Cristina Cilense; Cordeiro, Rita de Cássia Loiola

doi:10.1007/bf03262865

Cited by 58 publications

(76 citation statements)

References 22 publications

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“…1) and hypomineralization has examined the genetic, environmental (drugs, chemicals, and trauma), and systemic (metabolic conditions and infections) factors that affect their formation (Brook and Smith 1998;Seow 2014;Souza et al 2012;Taji et al 2000). Studies have investigated how various health characteristics affect the development and severity of enamel hypoplasias.…”

Section: Advances In Our Understanding Of Lesion-formation Processesmentioning

confidence: 99%

“…For example, Skinner et al (2014) revealed that localized enamel defects occur more frequently in pigs that are sick at the time of death and that they co-occur with both infection and poor growth. Numerous studies have found that low birth weight and preterm birth are associated with increased risk of enamel hypoplasia and that maternal health plays a role in enamel hypoplasia formation in children (Gravina et al 2013;Jacobsen et al 2014;Masumo et al 2013;Silva-Sousa et al 2003;Souza et al 2012). Research among living people indicates that children with enamel hypoplasia are of significantly shorter stature than those without them (Lukacs et al 2001).…”

Section: Advances In Our Understanding Of Lesion-formation Processesmentioning

confidence: 99%

“…Research among living people indicates that children with enamel hypoplasia are of significantly shorter stature than those without them (Lukacs et al 2001). Other risk factors for enamel defects include low prenatal vitamin D (Schroth et al 2014), infections or high fever during childhood (Ford et al 2009;Ghanim et al 2013;Souza et al 2012), celiac disease (Munoz et al 2012), and immunodeficiency diseases (Meighani et al 2011). The established associations between enamel hypoplasia and poor health and the fact that enamel does not remodel after formation makes these lesions particularly useful for paleopathological analyses, some of which have begun to explore the developmental origins of poor adult health (see above).…”

Section: Advances In Our Understanding Of Lesion-formation Processesmentioning

confidence: 99%

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The Osteological Paradox 20 Years Later: Past Perspectives, Future Directions

2015

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More than 20 years ago, Wood et al. (Curr Anthropol 33:343-370, 1992) published ''The Osteological Paradox: Problems of Inferring Prehistoric Health from Skeletal Samples,'' in which they challenged bioarchaeologists to consider the effects of heterogeneous frailty and selective mortality on health inferences in past populations. Here, we review the paper's impact on bioarchaeology and paleopathology, focusing on recent advancements in studies of ancient health. We find the paper is often cited but infrequently engaged in a meaningful way. Despite an initial decade of limited progress, numerous researchers are now addressing components of the Paradox in more informed ways. We identify four areas of fruitful research: (1) intrasite, contextual perspectives, (2) subadults, (3) associating stress markers with demographic phenomena, and (4) skeletal lesion-formation processes. Although often seen as a problematic assumption, understanding the sources of heterogeneous frailty within human populations is a worthy research question in and of itself, and one that clearly links past and present health research within a global framework.

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Section: Advances In Our Understanding Of Lesion-formation Processesmentioning

confidence: 99%

Section: Advances In Our Understanding Of Lesion-formation Processesmentioning

confidence: 99%

Section: Advances In Our Understanding Of Lesion-formation Processesmentioning

confidence: 99%

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The Osteological Paradox 20 Years Later: Past Perspectives, Future Directions

2015

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“…However, the aetiology of MIH remains unclear [Alaluusua, 2010;Sönmez et al, 2013;Wuollet et al, 2014]. There are studies demonstrating a potential environmental contribution to MIH [Jan et al, 2007;Alaluusua, 2010;Souza et al, 2012;Loli et al, 2015;Oyedele et al, 2015] and other studies demonstrating evidence of the genetic influence on the occurrence of MIH [Jeremias et al, 2013b;Kühnisch et al, 2014]. Kuscu et al [2013] mentioned that MIH is a multifactorial disturbance, but the specific environmental factors and the genetic contribution are still not completely understood.…”

mentioning

confidence: 99%

Family-Based Genetic Association for Molar-Incisor Hypomineralization

Jeremias

Pierri²,

Souza³

et al. 2016

Caries Res

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Despite some evidence of genetic and environmental factors on molar-incisor hypomineralization (MIH), its aetiology remains unclear. This family-based genetic association study aimed more comprehensively to investigate the genetic carriage potentially involved in MIH development. DNA was obtained from buccal cells of 391 individuals who were birth family members of 101 Brazilian nuclear families. Sixty-three single nucleotide polymorphisms (SNPs) were investigated in 21 candidate genes related to amelogenesis using the TaqMan™ OpenArray™ Genotyping platform. All SNPs were genotyped in 165 birth family members unaffected by MIH, 96 with unknown MIH status and 130 affected individuals (50.7% with severe MIH). Association analysis was performed by the transmission/disequilibrium test (TDT), and statistical results were corrected using the false discovery rate. Significant results were obtained for SNPs rs7821494 (FAM83H gene, OR = 3.7; 95% CI = 1.75-7.78), rs34367704 (AMBN gene, OR = 2.7; 95% CI = 1.16-6.58), rs3789334 (BMP2 gene, OR = 2.9; 95% CI = 1.34-6.35), rs6099486 (BMP7 gene, OR = 2.2; 95% CI = 1.14-4.38), rs762642 (BMP4 gene, OR = 2.3; 95% CI = 1.38-3.65), rs7664896 (ENAM gene, OR = 2.1; 95% CI = 1.19-3.51), rs1711399 (MMP20 gene, OR = 0.4; 95% CI = 0.20-0.72), rs1711423 (MMP20 gene, OR = 2.1; 95% CI = 1.18-3.61), rs2278163 (DLX3 gene, OR = 2.8; 95% CI = 1.26-6.41), rs6996321 (FGFR1 gene, OR = 2.7; 95% CI = 1.20-5.88), and rs5979395 (AMELX gene, OR = 11.7; 95% CI = 1.63-84.74). Through this family-based association study, we concluded that variations in genes related to amelogenesis were associated with the susceptibility to develop MIH. This result is in agreement with the multifactorial idea of the MIH aetiology, but further studies are necessary to investigate more thoroughly the factors that could influence MIH.

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“…It has not been possible to name one singular influence or even a combination of several influences working together as being responsible for the disease [3]. Genetic and environmental factors have been proposed to contribute to MIH [28,29]. The environmental factors considered include illnesses occurring during mineralization of the FPMs and permanent incisors, such as fevers, chicken pox, ear infections, tonsillitis, asthma, and allergies [28].…”

Section: Etiology Of Molar Incisor Hypomineralizationmentioning

confidence: 99%

Molar Incisor Hypomineralization in Children: A Review of Literature

Meligy¹

2014

Oral Hyg Health

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Molar incisor hypomineralization (MIH), which refers to the clinical picture of hypomineralization of systemic origin affecting one or more first permanent molars (FPMs), frequently in association with affected incisors, is one of the major developmental defects of dental enamel. While this condition is of interest to clinical practitioners worldwide, there is little information regarding its prevalence and etiology, especially in the Middle East. The purpose of this review was to describe the prevalence and possible etiological factors of molar incisor hypomineralization in children. About 252 articles were reviewed as well as some references of selected articles. Twenty-six recent studies described the prevalence and possible etiological factors of molar incisor hypomineralization in children. The prevalence of MIH appears to be increasing and was associated with health problems during early childhood, including asthma, adenoid infection, tonsillitis, fevers, and antibiotic intake. Although the etiology may be multifactorial, children born preterm and those with poor general health or systemic conditions in their early life may develop MIH.

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Molar Incisor Hypomineralisation: Possible aetiological factors in children from urban and rural areas

Abstract: This study suggests a link between MIH and health problems during pregnancy, as well as environmental factors.

Cited by 58 publications

References 22 publications

The Osteological Paradox 20 Years Later: Past Perspectives, Future Directions

The Osteological Paradox 20 Years Later: Past Perspectives, Future Directions

Family-Based Genetic Association for Molar-Incisor Hypomineralization

Molar Incisor Hypomineralization in Children: A Review of Literature

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