DT News - ASEAN - Study examines role of systemic inflammation in molar incisor hypomineralisation

Iveta Ramonaite, Dental Tribune International

Fri. 21. August 2026

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MELBOURNE, Australia: Molar incisor hypomineralisation (MIH) is a common developmental dental defect associated with considerable morbidity, yet its aetiology remains poorly understood. Previous observational and experimental research has suggested that systemic inflammation may play a role in its development. Now, a new study has investigated whether early childhood inflammation is associated with the prevalence, severity and risk of MIH.

According to paediatric dentist Dr Mihiri Silva, systemic inflammation in early childhood does not appear to be a major driver of molar incisor hypomineralisation. (Image: Dr Mihiri Silva)

“MIH is one of the most common developmental dental conditions. Affected children have poorer oral health-related quality of life and experience 4.8 times more dental treatment by age 18 compared with those without MIH. Although millions of children worldwide have MIH, its cause remains unknown. Answering this question is essential if we want to prevent it,” senior author Dr Mihiri Silva, associate professor of paediatrics at the Melbourne Dental School, told Dental Tribune International.

In the study, the researchers used data from the population-based Barwon Infant Study, which is following participants over time as they grow and develop, to investigate whether the prevalence and severity of MIH were associated with systemic inflammation during early childhood. Two key markers of systemic inflammation were measured in maternal serum during pregnancy and in offspring plasma at birth and at 6 months, 12 months and 4 years of age. The researchers also looked at the children’s immune systems at age 4 by measuring specific immune signalling proteins in their blood samples.

The study found no clear link between inflammation in early childhood and the development of MIH. Children who later developed MIH had similar levels of key inflammatory markers before birth, at birth, and at 6 months, 12 months and 4 years of age to those of children who did not develop MIH. This was true even when comparing children with mild or severe MIH to those without the condition. Overall, the results suggest that systemic inflammation in early life is unlikely to be a major cause of MIH.

Previous research had suggested that childhood infections and fevers might contribute to MIH by increasing systemic inflammation and thereby disrupting tooth development. “We were surprised to find that systemic levels of inflammatory markers were not associated with MIH,” Dr Silva commented.

According to the researchers, MIH is likely to have a multifactorial aetiology involving genetic and environmental influences. Other forms of inflammation may also be relevant, including inflammation associated with atopic conditions such as asthma and eczema. The researchers emphasised that large-scale studies using robust, standardised data will be needed to investigate these and other potential contributors.

“While the search for the cause of MIH is not yet complete, our findings provide a valuable resource for researchers worldwide as they continue to unravel the causes of this complex condition,” Dr Silva commented. “Collaboration will be crucial to further our understanding of MIH aetiology.”

The study, titled “Systemic inflammation and molar incisor hypomineralisation: A cohort study”, was published online on 22 July 2026 in the Journal of Dental Research, ahead of final publication.