Abstract Our aim is to propose a novel family-based preventive programme (Early Smiles) that uses promotional and preventive early interventions in the family, to reduce the onset and severity of caries lesions in rural preschool children. After conducting a baseline cross-sectional study with 2-, 4- and 6-year-old children under traditional dental care (Control Group; n=101), a non-randomized community trial including children aged 2, 4, and 6 years from rural areas in southern Chile was devised (Intervention Group; n=107). Dental caries lesions were assessed using the ICDAS index and the dmft and caries significance index (SiC) were determined. Caries prevalence, the dmft, and SiC in 2-year-old children intervened in the Early Smiles program decreased by 73.11%, 81.50%, and 74.78% respectively (p<0.001). The number of cavitated lesions decreased significantly in 2- and 4-year-old children by 77.38% and 86.88% respectively (p<0.001). In the intervention Group, caries lesion severity in 2- and 4-year-old children presented less severe codes (ICDAS 3 and 4) than the control group. Interventions based on behavioural change, with the family, within the interdisciplinary health team, and early in life, seems to be highly effective in reducing the burden of caries lesions in 2-year-old children from rural areas.

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.

To assess the impact of oral conditions on oral health-related quality of life (OHRQoL) in infants in ten Latin America countries (LAC). A cross-sectional study was conducted with 930 pairs of 1-to-3-year-old children/parents from 10 LAC, as a complementary study of the Research Observatory for Dental Caries of the Latin American Region. The scale ECOHIS, previously tested and valid in ten countries, was applied to parents/caregivers of children to measure OHRQoL. Statistical analysis included descriptive data analysis and one-way analysis of variance (ANOVA-One-Way) were performed to compare age groups with OHRQoL. Bootstrapping procedures (1000 re-samplings; 95%CI Bca) were performed. The mean scores of the 'Child Impact' section in the LAC was 4.0(±8.3), in the 'Family Impact' section was 2.0(±4.0), and in overall ECOHIS score was 6.0(±12.0). In the 'Child Impact' section, Argentina 10.0(+2.4) and Venezuela 17.8(±17.5) demonstrated mean scores higher than the LAC total data. In the 'Family Impact' section, the countries with higher mean scores were Argentina 4.9(±2.0), Ecuador 2.1(±3.1) and Venezuela 7.9(±7.8). In the overall ECOHIS score, Argentina 15.1 (±4.1) and Venezuela 25.7(±25.2) has higher mean scores than the values of LAC. There is an association between children's age and parents' report of impact on the OHRQoL (p<0.001). Three-year-olds had a higher mean when compared to one- and two-year-olds, both in the Impact on the Child and Impact on the Family (p<0.001) sections, as well as in the overall ECOHIS (p<0.001). In conclusion, there are differences in OHRQoL among Latin American countries, impacting older children more significantly.

Popularly known as “chalky teeth”, molar hypomineralisation (MH) affects over 1-in-5 children worldwide, triggering massive amounts of suffering from toothache and rapid decay. MH stems from childhood illness and so offers a medical-prevention avenue for improving oral and paediatric health. With a cross-sector translational research and education network (The D3 Group; thed3group.org) now highlighting this global health opportunity, aetiological understanding is urgently needed to enable better awareness, management and eventual prevention of MH. Causation and pathogenesis of “chalky enamel spots” (i.e., demarcated opacities, the defining pathology of MH) remain unclear despite 100 years of investigation. However, recent biochemical studies provided a pathomechanistic breakthrough by explaining several hallmarks of chalky opacities for the first time. This article outlines these findings in context of previous understanding and provides a working model for future investigations. The proposed pathomechanism, termed “mineralisation poisoning”, involves localised exposure of immature enamel to serum albumin. Albumin binds to enamel-mineral crystals and blocks their growth, leading to chalky opacities with distinct borders. Being centred on extracellular fluid rather than enamel-forming cells as held by dogma, this localising pathomechanism invokes a new type of connection with childhood illness. These advances open a novel direction for research into pathogenesis and causation of MH, and offer prospects for better clinical management. Future research will require wide-ranging inputs that ideally should be coordinated through a worldwide translational network. We hope this breakthrough will ultimately lead to medical prevention of MH, prompting global health benefits including major reductions in childhood tooth decay.

One hundred years ago, histopathology pioneer Bernhard Gottlieb described developmentally disrupted teeth as having “chalky enamel” and “chalky spots” that “crumble” easily. He also asked pivotal questions about the pathogenesis of “enamel hypoplasia” that remained enigmatic for almost a century. Today, breakthrough pathomechanistic investigations of chalky enamel are revealing surprising answers, and an allied translational initiative—The D3 Group for developmental dental defects (“D3s”) —is converting such scientific knowledge into social good surrounding prevention of tooth decay. Molar hypomineralisation (MH) affects 1-in-5 children worldwide and is well-evidenced, but poorly recognised, as a principal risk factor for childhood tooth decay. Given MH is causally linked to infantile illness, an exciting corollary is that medical prevention would lead to substantial reductions in decay. Here we reflect on the past century of chalky teeth research and retrace the path leading to recognition of MH as a global health concern. Five research eras, today's four major D3s, and diverse experimental attacks are outlined alongside translational wins that have benefitted global health. Addressing hopes for medical prevention of MH, this centennial year's pathomechanistic discovery is contextualised against past accomplishments and new opportunities. Finally, we note the translational value of accessible infographics for guiding future work, and forecast exciting prospects for the next century.

Enamel defects (i.e. hypoplasia, diffuse and demarcated opacities), in particular Molar Incisor Hypomineralization (MIH), are alterations of dental enamel with underlying implications in affected children. A proper diagnosis and clinical dental records are needed to improve clinical management of enamel defects in primary health setting. This cross-sectional study aimed to determine the prevalence of enamel defects in 6-year-old children attending to Family Health Centres in Talca city and comparing the clinical diagnosis with that registered by general dental practitioners (GDPs) on the clinical dental records. Children (n=318) were evaluated by a calibrated examiner using the modified DDE index criteria. Almost half of children had enamel defects (47.5%; n=151). The proportion of children affected by demarcated opacities (36.8%; n=117) was higher than those effected by hypoplasia (13.8%; n=44) and diffuse opacities (12.6%; n=40). MIH prevalence was 19.8% (n=63) and 22% (n=14) of MIH-affected children presented the severe form. Clinical dental records registered by GDPs recorded 6.6% (n=10) of enamel defects, but the type of defect was not consistent with the clinical examination undertaken by the calibrated examiner. These findings suggest that enamel defects are prevalent in the studied population, but only few cases were registered in clinical dental records. To achieve diagnosis consensus, the registration section for enamel defects in the clinical dental record at Family Health Centres may need some improvement. Further diagnostic training for GDPs working in the public sector may also be necessary.

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.

Molar hypomineralisation (MH) is becoming globally recognised as a significant public health problem linked to childhood tooth decay. However, with causation and pathogenesis unclear after 100 years of investigation, better pathological understanding is needed if MH is to become preventable. Our studies have implicated serum albumin in an extracellular pathomechanism for chalky enamel, opposing longheld dogma about systemic injury to enamel-forming cells. Hypothesising that chalky enamel arises through developmental exposure to serum albumin, this study used biochemical approaches to characterise demarcated opacities from 6-year molars. Addressing contradictory literature, normal enamel was found to completely lack albumin subject to removal of surface contamination. Querying surface permeability, intact opacities were found to lack salivary amylase, indicating that "enamel albumin" had become entrapped before tooth eruption. Thirdly, comparative profiling of chalky and hard-white enamel supported a dose-response relationship between albumin and clinical hardness of opacities. Moreover, albumin abundance delineated chalky enamel from white transitional enamel at opacity borders. Finally, addressing the corollary that enamel albumin had been entrapped for several years, clear signs of molecular ageing (oxidative aggregation and fragmentation) were identified. By establishing aged albumin as a biomarker for chalky enamel, these findings hold methodological, clinical, and aetiological significance. Foremost, direct inhibition of enamel-crystal growth by albumin (here termed "mineralisation poisoning") at last provides a cogent explanation for the clinical presentation of demarcated opacities. Together, these findings justify pursuit of an extracellular paradigm for the pathogenesis of MH and offer exciting new prospects for alleviating childhood tooth decay through medical prevention of MH.

Objetivo: Creación de un currículo de competencias mínimas en Cariología, para la formación de los Cirujano-Dentistas egresados de las escuelas de Odontología de Chile.

The protease kallikrein 4 (KLK4) plays a pivotal role during dental enamel formation by degrading the major enamel protein, amelogenin, prior to the final steps of enamel hardening. KLK4 dysfunction is known to cause some types of developmental defect in enamel but the mechanisms responsible for transient retention of KLK4 in semi-hardened enamel matrix remain unclear. To address contradictory reports about the affinity of KLK4 for enamel hydroxyapatite-like mineral, we used pure components in quasi-physiological conditions and found that KLK4 binds hydroxyapatite directly. Hypothesising KLK4 self-destructs once amelogenin is degraded, biochemical analyses revealed that KLK4 progressively lost activity, became aggregated, and autofragmented when incubated without substrate in both the presence and absence of reducer. However, with non-ionic detergent present as proxy substrate, KLK4 remained active and intact throughout. These findings prompt a new mechanistic model and line of enquiry into the role of KLK4 in enamel hardening and malformation.

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 toward 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.

Introduction: Molar incisor hypomineralization (MIH) is a developmental condition resulting in defects in the enamel characterized by demarcated opacities mainly affecting first permanent molars and occasionally permanent incisors in 1 of every 6 children worldwide. Affected molars have greater susceptibility to post eruptive breakdown, extensive caries and, in severe cases, are difficult to restore. When the MIH-affected molar presents severe crown destruction, it is necessary to perform an intermediate restoration to preserve the remaining dental structure in order to maintain occlusion, proper hygiene and periodontal health. The case of an 11-year-old patient with severe MIH is reported. The patient had extensive crown destruction by caries in tooth 1.6 without clinical or radiographic signs of pulp pathology. After an initial preventive intervention, enamel without dentin support and carious dentin were removed from tooth 1.6. Subsequently, crown restoration was performed with resin-modified glass ionomer, followed by the cementation of an orthodontic band. After 18 months of follow-up, the patient reported no pain or discomfort. The restoration was preserved intact, maintaining occlusal functionality, pulp and gingival health. Conclusion: The interim treatment, cementing an orthodontic band over a tooth restored with glass ionomer seems to favor retention and compressive strength, keeping the MIH-affected molar asymptomatic for at least 18 months. Further studies evaluating this treatment option in similar clinical situations are recommended.Keywords:

Teeth are unique and complex organs formed from different embryonic layers. Mature tooth comprises enamel, dentin, cementum, and dental pulp. During its embryonic development, soft tissues of the dental germs begin to mineralize through a series of highly synchronized spatiotemporal events until the tooth erupts into the oral cavity. Enamel contains an exquisitely intricate and ordered arrangement of densely packed mineral crystals. Enamel mineralization involves the participation of multiple specific proteins that modulate the processes of crystal secretion and maturation. Dentin, on the other hand, is a less mineralized tissue than enamel and contains a higher amount of proteins. Like enamel, dentin mineralization requires participation of several proteins, some of them not yet fully characterized. Highly intricate cellular and molecular processes are required to form mature dentin. By a thorough revision of the existent literature on the topic, this chapter presents a state-of-the-art summary of the current understanding of tooth biomineralization.