Systemic Inflammation and Molar Incisor Hypomineralisation: A Cohort Study

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.