Inheritance pattern of molar-incisor hypomineralization

Abstract

The aim of this study was to investigate the segregation patterns of molar incisor hypomineralization (MIH) in families, given the evidence that its etiology is influenced by genetics. Clinically, MIH may be detected in parents and/or siblings of MIH-affected children. Our study included children with at least one first permanent molar affected by MIH (proband) and their first-degree relatives (parents and siblings). The participants were examined clinically to detect MIH, according to the European Academy of Paediatric Dentistry criteria (2003). A total of 101 nuclear families (391 individuals) were studied. Proband diagnosis was followed by MIH classification of the subject, his parents and siblings, as affected, unaffected, or unknown. Segregation analysis was performed using the multivariate logistic regression model of the Statistical Analysis for Genetic Epidemiology package, and segregation models (general transmission, environmental, major gene, dominant, codominant and recessive models). The Akaike information criterion (AIC) was used to evaluate the most parsimonious model. In all, 130 affected individuals, 165 unaffected individuals, and 96 unknown individuals were studied. Severe MIH was found in 50.7% of the cases. A segregation analysis performed for MIH revealed the following different models: environmental and dominance (p = 0.05), major gene (p = 0.04), codominant (p = 0.15) and recessive models (p = 0.03). According to the AIC values, the codominant model was the most parsimonious (AIC = 308.36). Our results suggest that the codominant model could be the most likely for inheriting MIH. This result strengthens the evidence that genetic factors, such as multifactorial complex defect, influence MIH.

Molar‐incisor hypomineralization in a cohort of individuals born with cleft lip and palate

“…This high frequency should be explained as the result of corresponding pathogenic mechanisms for both disturbances of tooth structure and development of the primary palate 23 to the multifactorial genetic condition of both MIH and cleft lip and palate that shares the same genetic pathway. 12,13,18,24,25 This result supports the idea that cleft lip and palate were not isolated, but actually a syndrome of alterations of dentition. 18 Considering the cleft type, the low number of patients with cleft palate in the sample is not representative of the frequency of this cleft type in the centre.…”

“…Our study was performed in a cohort of 386 individuals born with cleft lip and/or palate previous to their orthodontic treatment and had not undergone an alveolar bone graft before the photos and clinical examination. This high frequency should be explained as the result of corresponding pathogenic mechanisms for both disturbances of tooth structure and development of the primary palate 23 to the multifactorial genetic condition of both MIH and cleft lip and palate that shares the same genetic pathway 12,13,18,24,25 . This result supports the idea that cleft lip and palate were not isolated, but actually a syndrome of alterations of dentition 18 …”

Etiological Factors of Molar Incisor Hypomineralization: A Systematic Review and Meta-Analysis

“…Therefore, it is probable that genetic susceptibility and genes might be involved in its phenotype. It has been suggested that the susceptibility to developing MIH is increased by exposure to risk factors such as medication use during amelogenesis [65,66]. Furthermore, although there seems to be an association between genetic polymorphism in enamel formation and MIH, more research is needed for clarification [67].…”

Is there an association between molar incisor hypomineralization and developmental dental anomalies? A case-control study

“…Etiological studies conducted to date have focused on maternal diseases, stress, medication, alcohol, and cigarette usage in the prenatal period; low birth weight, birth hypoxia, preterm birth, and other defects observed at birth; childhood diseases, exposure to environmental toxins, and long-term and frequent medication usage in the postnatal period [6][7][8][9][10]. It has also been shown that various genetic and epigenetic variants may be involved in the etiology of MIH [6,[11][12][13][14].…”