Molar incisor hypomineralisation (MIH) is common, clinically challenging, and still poorly understood. Children affected by MIH may present with demarcated enamel opacities, hypersensitivity, post-eruptive breakdown, and atypical caries.
A new prospective population-based cohort study has now investigated this question using biological markers of inflammation.
Looking for inflammation before MIH appeared
The researchers used data from the Barwon Infant Study, a population-based prebirth cohort in Australia. Inflammation was assessed prospectively using two markers: high-sensitivity C-reactive protein (hsCRP) and glycoprotein acetyls (GlycA).
Samples were collected during pregnancy and at birth, 6 months, 12 months and 4 years of age. Cytokine and chemokine responses were also assessed at 4 years. The children subsequently underwent standardized dental examinations between 9 and 13 years of age to determine whether they had MIH.
Of the 1,064 participants in the cohort, 481 underwent dental examination at a mean age of 11.9 years. MIH was diagnosed in 129 children, giving a prevalence of 27%. One-third of those affected had severe MIH.
This prospective design is important. Earlier studies have often relied on retrospective reports of childhood illness or fever, which can introduce recall and measurement bias. Here, inflammatory markers were measured before MIH was diagnosed.
No clear association was found
Despite the detailed inflammatory measurements, the researchers found no significant association between hsCRP or GlycA levels and the presence of MIH at any of the measured time points.
There was also no significant association between these inflammatory markers and whether MIH was classified as mild or severe.
The causal analyses produced similar results. After adjustment for factors including childhood infections, breastfeeding, gestational age and mode of delivery—and, in additional models, maternal smoking and socioeconomic position—there was still no clear evidence that early-childhood GlycA levels affected the risk of MIH.
The analysis of cytokine responses at four years also failed to show differences between children with and without MIH.
When a child presents with MIH, clinicians often hear a history of repeated fever, respiratory infections or other illnesses during early childhood. Previous research has made it tempting to connect these events directly with the enamel defect.
This study suggests that such a conclusion may be premature.
The researchers measured systemic inflammation prospectively at multiple stages of early development and did not find a clear relationship with subsequent MIH. This strengthens the argument that MIH should continue to be viewed as a multifactorial developmental condition, rather than attributed to a single inflammatory exposure.
It also reinforces an important clinical distinction: an association between childhood illness and MIH does not necessarily mean that systemic inflammation is the mechanism responsible.
A history of childhood illness or fever may be relevant when discussing a child's history, but current evidence does not allow us to confidently tell parents that systemic inflammation caused their child's MIH.
The search for the underlying causes of MIH, it seems, is still very much open.
