Abstract
Objectives: Analyze defects in the state of maturation of the enamel result in an adequate volume of enamel, but in an insufficient mineralization, which can affect both deciduous teeth and permanent teeth. Among the most common defects, we recognize Deciduous Molar Hypominerlization (DMH), Hypomineralized Second Primary Molar (HSPM), and Molar Incisor Hypomineralization (MIH). These, in fact, affect the first deciduous molars, the second deciduous molars and molars, and permanent incisors, respectively, but their etiology remains unclear. The objective of the paper is to review studies that focus on investigating possible associations between genetic factors or prenatal, perinatal, and postnatal causes and these enamel defects. Materials and methods: A comprehensive and bibliometric search for publications until January 2021 was conducted. The research question was formulated following the Population, Intervention, Comparison, Outcome strategy. Case-control, cross-sectional, cohort studies, and clinical trials investigating genetic and environmental etiological factors of enamel defects were included. Results: Twenty-five articles are included. For genetic factors, there is a statistical relevance for SNPs expressed in the secretion or maturation stage of amelogenesis (16% of studies and 80% of studies that investigated these factors). For prenatal, perinatal, and postnatal causes, there is a statistical relevance for postnatal factors, such as the breastfeeding period (2%), asthma (16%), high fever episodes (20%), infections/illnesses (20%), chickenpox (12%), antibiotic intake (8%), diarrhea (4%), and pneumonia (4%). Conclusions: The results are in agreement with the multifactorial idea of the dental enamel defects etiology, but to prove this, further studies enrolling larger, well-diagnosed, and different ethnic populations are necessary to expand the investigation of the genetic and environmental factors that might influence the occurrence of DMH, HPSM, and MIH.
Highlights
Dental enamel is a highly mineralized tissue consisting of 95% of hydroxyapatite crystals arranged into highly ordered units called enamel prism, which creates a structure with remarkable mechanical resistance
If we speak of insufficient mineralization, we can include enamel defects such as Deciduous Molar Hypomineralization (DMH), Hypomineralized Second Primary Molar (HPSM), and Molar Incisor Hypomineralization (MIH)
Which genetic factors and problems related to the prenatal, perinatal, and postnatal period cause enamel defects like Deciduous Molar Hypomineralization (DMH), Hypomineralized Second Primary Molar (HPSM) and Molar Incisor Hypomineralization (MIH)? In particular, can they influence the development of MIH?
Summary
Dental enamel is a highly mineralized tissue consisting of 95% of hydroxyapatite crystals arranged into highly ordered units called enamel prism, which creates a structure with remarkable mechanical resistance. Ameloblasts produce and secrete the organic component, and they polarize and are removed from the surface of the enamel For this reason, the mature enamel does not have the capacity of regeneration, due to not having any more living supporting cells [1,2]. A fragile and quantitatively defective enamel or a normal volume enamel but with insufficient mineralization can be found, depending on which phase of the ameloblasts life cycle is affected [3]. In this case, if we speak of insufficient mineralization, we can include enamel defects such as Deciduous Molar Hypomineralization (DMH), Hypomineralized Second Primary Molar (HPSM), and Molar Incisor Hypomineralization (MIH). MIH is characterized by demarcated qualitative defects of enamel of systemic origin affecting one or more first permanent molars with or without incisor involvement [8]; its prevalence varies between 2.9% and 4.4% [7]
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