Developmental dental defects (DDDs, hereafter 'D3s') hold significance for scientists and practitioners from both medicine and dentistry. Although attention has classically dwelt on three other D3s (amelogenesis imperfecta, dental fluorosis and enamel hypoplasia), dental interest has recently swung towards Molar Hypomineralisation (MH), a prevalent condition characterised by well-delineated ('demarcated') opacities in enamel. MH imposes a significant burden on global health and has potential to become medically preventable, being linked to infantile illness. Yet even in medico-dental research communities there is only narrow awareness of this childhood problem and its link to tooth decay, and of allied research opportunities. Major knowledge gaps exist at population, case and tooth levels and salient information from enamel researchers has sometimes been omitted from clinically-oriented conclusions. From our perspective, a cross-sector translational approach is required to address these complex inadequacies effectively, with the ultimate aim of prevention. Drawing on experience with a translational research network spanning Australia and New Zealand (The D3 Group; www.thed3group.org), we firstly depict MH as a silent public health problem that is generally more concerning than the three classical D3s. Second, we argue that diverse research inputs are needed to undertake a multi-faceted attack on this problem, and outline demarcated opacities as the central research target. Third, we suggest that, given past victories studying other dental conditions, enamel researchers stand to make crucial contributions to the understanding and prevention of MH. Finally, to focus geographically diverse research interests onto this nascent field, further internationalisation of The D3 Group is warranted.

Molar Hypomineralisation (MH) is gaining cross-sector attention as a global health problem, making deeper enquiry into its prevention a research priority. However, causation and pathogenesis of MH remain unclear despite 100 years of investigation into “chalky” dental enamel. Contradicting aetiological dogma involving disrupted enamel-forming cells (ameloblasts), our earlier biochemical analysis of chalky enamel opacities implicated extracellular serum albumin in enamel hypomineralisation. This study sought evidence that the albumin found in chalky enamel reflected causal events during enamel development rather than later association with pre-existing enamel porosity. Hypothesising that blood-derived albumin infiltrates immature enamel and directly blocks its hardening, we developed a “molecular timestamping” method that quantifies the adult and fetal isoforms of serum albumin ratiometrically. Applying this novel approach to 6-year molars, both isoforms of albumin were detectable in 6 of 8 chalky opacities examined (corresponding to 4 of 5 cases), indicating developmental acquisition during early infancy. Addressing protein survival, in vitro analysis showed that, like adult albumin, the fetal isoform (alpha-fetoprotein) bound hydroxyapatite avidly and was resistant to kallikrein-4, the pivotal protease involved in enamel hardening. These results shift primary attention from ameloblast injury and indicate instead that an extracellular mechanism involving localised exposure of immature enamel to serum albumin constitutes the crux of MH pathogenesis. Together, our pathomechanistic findings plus the biomarker approach for onset timing open a new direction for aetiological investigations into the medical prevention of MH.

The aim of this multicenter study was to explore the early-life sugar consumption and dietary practices in Latin America as well as to investigate the association between breastfeeding duration and the age at which foods and beverages with added sugars are introduced. A cross-sectional study was conducted with 805 1- to 3-year-old children from 10 Latin American countries, as a complementary study to the Research Observatory for Dental Caries of the Latin American Region (OICAL). A Food Frequency Questionnaire previously tested in different countries was applied to children’s mothers and data on breastfeeding and age at introduction of sugary foods and beverages was collected. Statistical analysis included the Kruskal-Wallis test and Poisson regression with robust variance, with the calculation of crude and adjusted mean ratios (MR) and 95% of confidence intervals (CI). The average age at introduction of sugary foods and beverages was 10.1 months (95%CI 9.7–10.4) and 9.6 (95%CI 9.2–9.9) months, respectively, with a significant variation between countries (p < 0.001). The average daily frequency of sugary foods-beverages was 3.3 times per day (95%CI 3.1–3.5) and varied significantly between countries (p = 0.004). Breastfeeding duration of over six months was associated with an increase in the age of introduction of sweet drinks (16%; MR 1.16; 95%CI 1.05–1.28) and foods (21%; MR 1.21; 95%CI 1.10–1.33). In conclusion, most children from vulnerable settings in Latin America start consuming sugary products in the first year of life and a high frequency of consumption was reported through early childhood. Additionally, breastfeeding contributes to a delay in the introduction of sugary products.

PALABRAS CLAVE: Educación; Cariología; Educación en odontología; Caries dental