Predisposing factors involved in the aetiology of Molar Incisor Hypomineralization: a case-control study

Aim The aetiology of Molar Incisor Hypomineralisation (MIH) is currently unclear. Over time, several aetiological hypotheses have come forward, including pre and perinatal medical problems and postnatal illness. The aim of this case-control study is the identification of possible predisposing factors involved in MIH aetiology. Methods Study Design: By hypothesising the probability of at least one predisposing factor present 2.5 times more in MIH cases than in controls, with an estimated prevalence of MIH patients requiring therapy equal to 30%, at a unilateral alpha level of 5% and a power of 80%, 63 couples of subjects are needed with an allocation ratio of 1:1; individual matching for age and gender was carried out. After clinical examination, 78 children with MIH (EAPD criteria) were recruited (mean age 9.36 years). An anamnestic form filled-in by a parent was used to collect data on possible predisposing factors including demographic characteristics, pregnancy, birth, childhood medical illness and medications’ intake. Statistics: One-tail McNemar chi square test was used to evaluate the significance of the association between predisposing factor and MIH; odds ratio and 95% confidence intervals were computed. Results Defects were detected in 249 permanent teeth. Demarcated white-creamy opacities were more frequent in incisors, while yellowbrown opacities were found in first permanent molars (p<0.001). The frequency of enamel breakdown was higher in molars with yellowbrown opacities than white-creamy (p<0.001). Among prenatal factors, smoking during pregnancy (p=0.0005) and among perinatal and postnatal factors, newborn jaundice (p=0.020), genetic syndromes (p=0.009) and antibiotic intake during the second year of life (p=0.033) were associated to MIH. As for genetic syndromes odds ratio was equal to 1.30 (95% CI:1.14–1.48) being that a syndromic child risk 30% more to develop MIH. Conclusions A multifactorial aetiology may be advocated for MIH development; in particular, further investigations are required to confirm and clarify the role of genetic factors.