Systemic and Environmental Risk Factors Associated with Molar Incisor Hypomineralisation.

The etiology of molar incisor hypomineralisation (MIH) has been attributed to systemic and environmental factors since 2001. The identification of MIH etiology is fundamental to better understand this condition, for differential diagnosis, and to identify the patient group at risk of MIH. Although the etiology of MIH is still unclear, it is stated as a multifactorial origin, with an overlap of systemic and genetic risk factors. The aim of this chapter was to discuss the systemic and environmental factors associated with MIH according to scientific evidence in the literature, relating it to the basic knowledge of amelogenesis and tooth development chronology. In this chapter, amelogenesis is described and illustrated in detail. Some characteristics of the amelogenesis process could explain some clinical features of the developmental defect of enamel, especially MIH. The chronology of tooth development was also referred to as a characteristic for the occurrence of MIH. Finally, the literature about systemic and environmental risk factors was revised, and the prenatal, perinatal, and postnatal factors associated with MIH were discussed. During the prenatal period, maternal health status, including illnesses during pregnancy and maternal smoking, are the main investigated factors associated with MIH. Prematurity (<37 weeks), low birth weight, and cesarean delivery are the factors associated with MIH during the perinatal period. Moreover, postnatal factors, such as common childhood illnesses, respiratory disease, infections, and antibiotic use, have been associated with MIH. New longitudinal studies that consider the synergy between exposure to environmental factors and biological susceptibility are likely to provide a new understanding of the etiology of MIH.

Prolonged breastfeeding, sugar consumption and dental caries at 2 years of age: A birth cohort study.

OBJECTIVES: Previous cohort studies have found a positive association between prolonged breastfeeding (≥12 months) on dental caries, but few of them analysed the mediated effect of sugar consumption on this association. This study investigated whether prolonged breastfeeding is a risk factor for caries at 2-year follow-up assessment (21-27 months of age) and whether this effect is mediated by sugar consumption. METHODS: A birth cohort study was performed in the Brazilian Amazon (n = 800). Dental caries was assessed using the dmf-t index. Prolonged breastfeeding was the main exposure. Data on baseline covariables and sugar consumption at follow-up visits were analysed. We estimated the OR for total causal effect (TCE) and natural indirect effect (NIE) of prolonged breastfeeding on dental caries using the G-formula. RESULTS: The prevalence of caries was 22.8% (95% CI: 19.8%-25.8%). Children who were breastfed for 12-23 months (TCE = 1.13, 95% CI: 1.05-1.20) and for ≥24 months (TCE = 1.27, 95% CI: 1.14-1.40) presented a higher risk of caries at age of 2 years than those breastfed <12 months. However, this risk was slightly mediated by a decreased frequency of sugar consumption at age of 2 years only for breastfeeding from 12 to 23 months (NIE; OR = 0.95, 95% CI: 0.91-0.97). CONCLUSIONS: In this study, the effect of prolonged breastfeeding on the increased risk of dental caries was slightly mediated by sugar consumption. Early feeding practices for caries prevention and promoting breastfeeding while avoiding sugar consumption should be targeted in the first 2 years of life.

Diagnosis training and calibration for epidemiological studies on primary and permanent teeth with hypomineralization.

PURPOSE: The objective of this study was to assess the impact on diagnostic accuracy and Kappa values improvement during the three-phase training and calibration process for MIH/HSPM. METHODS: Thirty dentists were calibrated as examiners for diagnosis of Molar Incisor Hypomineralization (MIH) using Ghanim's index. The whole process was divided into three phases. Phase 1: three meetings with the dentists for the first diagnosis training and calibration (sessions 1a and 1b); phase 2: for a period of 1 month, the dentists started practicing MIH/HSPM diagnosis in the Basic Health Units and an online follow-up group was created to discuss cases and resolve doubts; phase 3: two meetings with the dentists for the second calibration (sessions 2a and 2b). A webpage with educational material was prepared as support during the whole process to improve the dentists' skills in diagnosing MIH/HSPM. The examiners' responses were compared to a gold standard and the Kappa value was obtained. RESULTS: The average clinical criteria kappa value of the examiners was 0.76 ± 0.19 for the first calibration and 0.93 ± 0.07 (p < 0.05) for the second calibration. For the eruption criteria, the average kappa value was 0.89 ± 0.14 for the first calibration and 0.98 ± 0.08 for the second calibration. Extension criteria had an average kappa value of 0.59 ± 0.15 during the first calibration and 0.75 ± 0.14 during the second calibration. CONCLUSION: This study demonstrated that the methodology used was an effective tool for improving the diagnostic accuracy of MIH/HSPM.