**3. Aetiological considerations**

Etiological factors of causing changes in organic/inorganic composition of MIH affected teeth are still unknown as showed by two systematic reviews. (Alaluusua, 2010, Crombie et al., 2009) As far, MIH may have a multifactor aetiology (Figure 3) acting additionally or even synergistically (Alaluusua, 2010, Crombie et al., 2009, Fagrell et al., 2011), with a genetic predisposition associated with one or more of a range of systemic insults occurring at a susceptible stage in the development of specific teeth. (Figure 3) It explains why in a seeming random manner several teeth are severely affected while their antimeres are unaffected. (Brook, 2009)

Notwithstanding, FAGRELL et al., 2011 (Fagrell et al., 2011) evaluated the etiological factors for severe demarcated enamel opacities in the first permanent molars from a database that contained approximately 4,000 variables with the purpose to prospectively investigate risk factors for immune mediate diseases in All Babies in Southeast Sweden project. Approximately, 17,000 children take part in the study. Medical data, information from interviews, questionnaires were collected at delivery, at 1, 2.5 years, of age with follow up at 5, at 8-9 and at 12 years. All information collected, about 4,000 variables for each child covering somatic growth: in pre-, peri-, and neonatal data from the child and its mother; diseases during first 3 years of child life; medication and vaccinations during the same

constituent mineral crystals; whereas for hypomineralised enamel micro cracking and subsequent crack growth were more evident in its less densely packed microstructure. (Xie et al., 2009) Thereafter, the ability of dental enamel to absorb energy and sustain deformation without catastrophic failure is attributed to its viscoelastic protein layers. Thus, the change in the protein content in teeth with MIH induces the enamel fracture when

In relation to the dentin of MIH affected teeth it was observed that the Ca/P ratios for dentin below hypomineralized enamel were in principle identical to those of normal enamel; but when the Ca/C ratio was analyzed, dentin below hypomineralized enamel had the lowest values and the level of C was highest for dentin below hypomineralized enamel. In addition, O and P levels in dentin below normal enamel were higher compared with values in dentin below hypomineralized and N values for dentin below hypomineralized

This enhanced knowledge concerning the microstructural changes in hypomineralised enamel improves the understanding of some of the problems associated with the clinical management of these teeth. In particular, the frequent occurrence of enamel fractures and inadequate retention of adhesive materials both of which are recognized as significant clinical challenges preventing successful restoration of these compromised teeth. It is known that organic matter such as proteins have poor acid solubility. The presence of increased amounts of organic matter in the hypomineralised enamel, specifically within both prism structure and sheath regions may inhibit the creation of an adequate etch profile which in turn compromises the adhesion between resin based restorative materials and the defective enamel. (William et al., 2006b) Improved clinical outcomes are likely to depend, at least in part, on the successful treatment of these proteins prior to any enamel etching or adhesive

Etiological factors of causing changes in organic/inorganic composition of MIH affected teeth are still unknown as showed by two systematic reviews. (Alaluusua, 2010, Crombie et al., 2009) As far, MIH may have a multifactor aetiology (Figure 3) acting additionally or even synergistically (Alaluusua, 2010, Crombie et al., 2009, Fagrell et al., 2011), with a genetic predisposition associated with one or more of a range of systemic insults occurring at a susceptible stage in the development of specific teeth. (Figure 3) It explains why in a seeming random manner several teeth are severely affected while their antimeres are

Notwithstanding, FAGRELL et al., 2011 (Fagrell et al., 2011) evaluated the etiological factors for severe demarcated enamel opacities in the first permanent molars from a database that contained approximately 4,000 variables with the purpose to prospectively investigate risk factors for immune mediate diseases in All Babies in Southeast Sweden project. Approximately, 17,000 children take part in the study. Medical data, information from interviews, questionnaires were collected at delivery, at 1, 2.5 years, of age with follow up at 5, at 8-9 and at 12 years. All information collected, about 4,000 variables for each child covering somatic growth: in pre-, peri-, and neonatal data from the child and its mother; diseases during first 3 years of child life; medication and vaccinations during the same

subjected to the masticatory efforts.

enamel are the highest. (Heijs et al., 2007)

strategies. (Baroni & Marchionni, 2011, Xie et al., 2008)

**3. Aetiological considerations** 

unaffected. (Brook, 2009)

period, socioeconomic factors and nutrition during first 3 years of child life were entered into databank. Besides, in this study, randomly, there were two-age and sex-matched children to each MIH child. After a regression logistic analyses, the results showed a positive association between severe demarcated opacities in permanent first molars with breastfeeding for more than 6 months, late introduction of gruel and late introduction of infant formula. Moreover, a combination of these variables increased the risk to develop severe demarcated opacities by more five times. According these results, the authors concluded that nutritional conditions during first 6 months of life may influence the risk to develop severe demarcated opacities in first permanent molars. (Fagrell et al., 2011)

Fig. 3. Multifactorial aetiology of MIH

Molar Incisor Hypomineralization:

A

B

restorations) (Lygidakis et al., 2008) (Figures 4B, C ).

Morphological, Aetiological, Epidemiological and Clinical Considerations 433

determined by dividing the affected teeth in only two groups: mild defect (demarcated opacities) (Figures 4A, B) and moderate/severe defect (enamel breakdown and atypical
