The causes for the genesis of molar incisor hypomineralization (MIH) have not been conclusively clarified to date. Although numerous potential etiological factors have been discussed so far, a monocausality with a high level of evidence has not yet been found or sufficiently demonstrated.1–4 The limitations of the studies published up to now include a lack of consistency in the study design and the type of study selected. Most studies are cross-sectional and retrospective, and their interpretation can lead to biased results. This is problematic insofar as there is the possibility that there is a combination effect and the probability is high that several influencing factors interact in the development of the defect.

In the following, the factors currently under discussion (Fig 5-1) will be examined in more detail. Influencing factors that interfere with tooth development during amelogenesis can be considered as triggers. The phases of enamel formation have already been described in detail in Chapter 3. For the first permanent molars and the incisors, this includes a period between the eighth month of pregnancy and the fourth year of life.

Fig 5-1 Currently discussed etiologic factors for the development of MIH.

5.1 Prenatal factors

Potential prenatal influences that have been found to promote the development of MIH include illness, medication use, stress, and maternal smoking.³ Prenatal illnesses of the mother during this period sometimes show an influence.^4,5 The problem with this factor is the considerable variability of the term illness. Some studies include only pregnancy-related diseases (eg, hypotensive anemia, hypertension, toxoplasmosis, pre-eclampsia),¹⁵ whereas other studies include general maternal diseases (eg, diseases in the last trimester of pregnancy, systemic diseases).11,14,15 Ghanim et al¹⁵ demonstrated that among prenatal maternal health conditions, factors such as hypotensive anemia and diseases in the last trimester of pregnancy were associated with an increased likelihood of developing MIH. A recent meta-anaylsis by Garot et al⁴ concluded that only the unspecified term “maternal illness” was associated with MIH.

No association was identified between maternal medication use^{5,6,8,10,12–14} and the occurrence of hypomineralization or maternal smoking^{5,8,11,12,16,17} during pregnancy and the development of MIH.

Maternal stress has been analyzed in only one study¹⁵ so far, which found a higher probability of MIH formation. However, this result should be interpreted with caution, as the number of studies on this topic is low and the conceptual understanding of stress is rather diffuse.

In summary, it can be critically noted that currently prenatal factors can rarely be associated with the occurrence of MIH.^3,4

5.2 Perinatal factors

Perinatal risk factors include events such as preterm birth, low birth weight, cesarean section, or birth complications. A problem with the studies published on this topic is again their heterogeneity in the methodology and documentation chosen, which does not allow any profound conclusions.³ In addition, the results found are partly contradictory.

Although the subject of several studies^{5,6,8,9,11, 12,14}, a significant association was found only once for cesarean section, for example.¹¹

Evidence for an association between MIH and low birth weight is also sparse^{5–12,18–20} and contradictory.³ A recently published review does conclude that both preterm birth and low birth weight increase the risk of MIH.²¹ However, the authors note that the included studies are too few in number and have a low level of evidence because of their design.

The factor of ‘birth complication’ must also be considered critically^{5–7,9–11,13,19,22} as it involves an equal amount of variability in interpretation and definition.³

Comparing and evaluating the results of the individual studies, it must be concluded that perinatal influences can currently only rarely be associated with the occurrence of MIH.³

5.3 Postnatal factors

5.3.1 Breastfeeding and dioxins in breast milk

Breast milk provides an important basis for the healthy development of a newborn. It is not only an important source of energy for the infant, but also provides the child with immunoglobulins and fat-soluble vitamins.²³ Finnish researchers tested the influence of dioxins on tooth development and found that dioxins present in breast milk can increase the risk of mineralization defects when breastfeeding is prolonged for more than 9 months.¹⁶ The severity and frequency of defects correlated with total dioxin exposure, which was calculated from the dioxin level in the milk of the respective mother and the duration of breastfeeding. However, the working group pointed out that the prolonged duration of breastfeeding alone was not responsible for the structural defect.

In further animal studies, in which the mode of action of dioxin on tooth germs of mice was investigated, it was further shown that dioxin binds to the epidermal growth factor receptor and this also influences tooth development.²⁴ A correlation between the exposure of dioxins and the occurrence of structural anomalies in the permanent teeth could be demonstrated.²⁵

Recent results show that after lowering dioxin concentrations in breast milk/placenta, there was no longer an association with MIH. Therefore, the study group concluded that exposure to breast milk is not associated with the development or severity of MIH.

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