Epidemiology (2011):
Kim Seow and colleagues from Brisbane have compared the prevalence of D3s in baby (primary) and adult (secondary) teeth of school children. They found that the primary teeth had almost half as many enamel defects as secondary teeth, and that these were mostly demarcated opacities with about 1 in 7 exhibiting surface breakdown. These findings confirm that Hypomin lesions could contribute substantially to caries risk in the primary dentition. (read more)

Lab (2011):
Rami Farah and colleagues from Dunedin investigated Molar Hypomin lesions of varying severity using X-ray microtomography. They took particular care over density calibration, so enhancing their quantitative interpretations. Mineral density was found to vary according to position on the tooth, depth within the lesion, and relationship to developmental lines. (read more)

Clinic/epidemiology (2011):
In a world-first study asking whether ethnicity influences the prevalence of Molar Hypomin, Wellington researchers (Mahoney & Morrison) found equal rates in children representing Maori, Pacific Island and NZ European groups. The overall prevalence (15%) and heightened risk for caries (up to 12-fold increase in DMFT) puts this NZ subpopulation in line with reports from other countries. (read more)

A follow-up study comparing children from a central-city environment with "out-of-towners" revealed a somewhat higher prevalence for city kids (about 19% had Molar Hypomin, vs 15% as above) but no obvious association with socioeconomic status was found. Compared with Hypomineralisation, Hypoplastic defects were an uncommon finding (affecting less than 1% of kids). (read more


Clinic/aetiology (2009):
Felicity Crombie (then a PhD student) and her Melbourne colleagues critically reviewed previous reports about suspected causes of Molar Hypomin. Although specific causes were unable to be established, some potential risk factors were identified. Overall, the level of evidence was found to be low and the need for long-term prospective epidemiological studies was highlighted. (read more)

Aetiology (2009):
Following from his prevalence study (see below), Peter Arrow investigated the potential risk factors associated with Molar Hypomin in Western Australian schoolchildren. Children with an infection during the neonatal period were found to be over six times more likely to have demarcated enamel defects. (read more)


Clinic (2008):
A retrospective study of 182 children with Molar Hypomin seen in a Melbourne paediatric dental practice led Chawla, Silva and Messer to describe an “MIH spectrum”. That is, cases ranged from mild, where only the molars were affected, to severe with involvement of both incisors and molars. Aetiological associations with combinations of antibiotic use, ear infections, fevers, perinatal conditions and other illnesses in the child’s first three years of life were also found. (read more)

These data were also used to develop a Hypomineralisation Severity Index intended to help clinicians determine the best management options for Molar Hypomin. (read more)

Clinic (2008):
The knowledge, clinical experience and opinions of specialist practitioners in regards to Molar Hypomin have been assessed by Felicity Crombie and colleagues. Questioning members of the Australia and New Zealand Society for Paediatric Dentistry revealed that Molar Hypomin was widely recognized and posed significant clinical problems. A majority of respondents felt a need for further research in this area. (read more)

Epidemiology (2008):
Peter Arrow reported the first comprehensive study of Molar Hypomin prevalence in Australian schoolchildren (n= 511). Investigating a Western Australian population, 22% were found to have demarcated opacities on at least one first permanent molar, a figure that is somewhat higher than the average reported elsewhere in the world. (read more)