Molar incisor hypomineralisation (MIH) is a qualitative developmental enamel defect with a prevalence of 13% worldwide. This review aims to outline the current evidence regarding the impact of MIH on children’s oral health and, more broadly, their day-to-day activities. MIH is associated with negative sequelae, including hypersensitivity, post-eruptive breakdown, the rapid development of carious lesions and poor aesthetics. Other concerns pertain to the clinical management of MIH and include difficulty in achieving local anaesthesia, increased dental fear and anxiety (DFA) and increased behaviour management problems. Oral health-related quality of life (OHRQoL) is the most standardised measure of patient impact; however, no instruments have been validated for use in MIH populations. The few existing observational studies investigating the impact of MIH on OHRQoL in children have produced conflicting results. Interventions to alleviate hypersensitivity and improve aesthetics had a positive impact on the OHRQoL of MIH-affected children. Multiple methodological issues make it difficult to measure the impact of MIH, including heterogeneity in the MIH severity classification, an overlap in the indices used to diagnose dental caries and MIH as well as the subjectivity of outcome measures for hypersensitivity and DFA.

Purpose: Molar incisor hypomineralisation (MIH) is a qualitative defect of enamel characterised by demarcated opacities. Aesthetic and functional sequelae of MIH may manifest as reduced oral health related quality of life (OHRQoL). This study aims to investigate the impact of the presence and severity of MIH on children’s OHRQoL. Methods: This cross-sectional study recruited children aged 7–16 years-of-age attending specialist paediatric dental clinics in Melbourne, Australia. Clinical examination utilised the modified European Academy of Paediatric Dentistry index to quantify the presence and severity of MIH. OHRQoL data was collected via the Child Perception Questionnaire, Parent-Caregiver Perception Questionnaire and Family Impact Statement. Causal analysis used quantile regression and included poor medical health as a confounding variable. Sensitivity analysis used the same model and different strata of MIH lesion location and severity. Results: 131 participants with complete self-reported OHRQoL data were included in the causal analysis. The estimated average causal effect after adjusting for poor medical health showed the estimated difference in medians of child-reported OHRQoL was 6 (CI = 2.62, 12.25, p = 0.02) in the MIH group compared to the unaffected group. The estimated difference in medians of self-reported OHRQoL after adjusting for poor medical health was 7 (CI = 1.87, 11.99, p = 0.01) for severe MIH group and − 1 (CI = − 5.16, 3.62, p = 0.63) for the mild group compared to those unaffected. The estimated difference in medians of self-reported OHRQoL after adjusting for poor medical health was 5.16 (CI = − 2.42, 10.99, p = 0.15) for participants with MIH-affected incisors compared to the rest of the cohort. Conclusions: MIH impacts children’s OHRQoL as reported by self and parent/caregiver.

Molar incisor hypomineralisation (MIH) is a common developmental dental defect of unknown etiology and considerable morbidity. Observational and experimental studies suggest systemic inflammation as a key mechanism, but there are no prospective human data. This study aimed to describe how the prevalence and severity of MIH vary with early childhood inflammation. It also aimed to investigate the extent to which early childhood inflammation affects the risk of MIH. Data were from the Barwon Infant Study, a population-based prebirth cohort. Glycoprotein acetyls (GlycA), measured by nuclear magnetic resonance, and high-sensitivity C-reactive protein (hsCRP), measured by immunoassay, were quantified from prenatal maternal serum and infant plasma from birth, 6 mo, 12 mo, and 4 y. Cytokine/chemokine responses were also measured from samples collected at 4 y of age. MIH was diagnosed by standardized clinical dental examination at 9 to 13 y of age via the modified European Association of Paediatric Dentistry index. In total, 1,074 mother–infant dyads consented to participate; 481 participants had dental examinations at a mean of 11.9 y (standard deviation = 0.96), and the prevalence of MIH was 27% (n = 129). The unadjusted odds ratio for standardized hsCRP and GlycA showed no difference in the odds of MIH and when comparing the mild and severe MIH subgroups to the non-MIH group at any time point. The estimated average causal effect after adjusting for confounding showed that a 1-unit increase of GlycA measured at 12 mo of age led to a decrease of 0.03 in the risk of MIH (95% confidence interval = −0.07, 0.02, P = 0.24). In this present study, there was no clear evidence of an association between systemic inflammation in early childhood and the risk of MIH.