# The Pathology of the First Permanent Molar during the Mixed Dentition Stage--Review
## 3 Results and Discussion
### Pathology of the Dental Hard Tissues
#### 3.2.1 Molar Incisor Hypomineralization
Histologically, the affected enamel shows varying degrees of porosity [42; 43] and contains higher carbon and lower calcium and phosphorus concentrations [42; 43]. Compared to healthy teeth, MIH-affected ones show less distinct prism sheaths and a lack of arrangement of the hydroxylapatite crystals [66]. Increased amounts of serum albumin, type I collagen, ameloblastoma, \(\alpha\)1-antitrypsin, and antithrombin III are found in the hypo-mineralized enamel [66]. The presence of these proteins inhibits the growth of hydroxylapatite crystals and influences the enzymatic activity during enamel maturation, thus leading to the reduction of mineral content and explaining the structural deficiencies of teeth affected by MIH [66; 67; 68]. Due to its porous structure, the enamel is very fragile and disintegrates under transticatory forces [45; 69]. A particular pattern of enamel destruction involving the occlusal surfaces and the cusps is a characteristic of MIH. Sometimes the enamel loss can be so rapid after the eruption that it looks like the enamel was not initially formed [45]. The destruction generates sensitivity, even pain which further determines the child to avoid oral hygiene practices. Plaque accumulates, caries rapidly develop, and even a subclinical inflammation of the dental pulp cells is reported [69]. As a consequence, dental fear and anxiety are more common in children with MIH than in non-affected children [69]. The severity of MIH lesions can differ between the four FPMs. Within one patient, only enamel opacities, without loss of hard dental tissue, can be present on one molar, while in another molar, large parts of the enamel are already broken down [45]. The risk for the onset of MIH lesions on upper incisors is higher when more FPMs are affected [45]. MIH case definition:  
* was introduced by the 6 th Congress of the European Academy of Paediatric Dentistry (EAPD) in 2002 [70]. * eight years of age was considered as the appropriate time for any examination for the condition because, at this age, in most children, all four FPMs and the majority of the incisors will be erupted [70]. Judgements related to individual teeth should include [70]:
* absence or presence of demarcated opacities;
* posteruptive enamel breakdown;
* atypical restorations (extended to the palatal surface and buccal surfaces; an opacity is frequently present at the border of the restoration);
* extraction of molars due to MIH. Extraction of molars due to MIH is suspected when the absence of an FPM is associated with opacities or atypical restorations in other FPMs [70]. When the absence of an FPM in a sound dentition is associated with demarcated opacities on the incisors, it is also suspected for MIH [70]. According to severity, MIH lesions fall into three categories [71]:  
Mild:  
* Demarcated opacities in non-stress-bearing area of molar. * Normal dental sensitivity Moderate:
* Intact atypical restoration present
* Occlusal/incisal third of teeth without initial posteruptive enamel breakdown. * Posteruptive enamel breakdown/caries limited to one or two surfaces without cuspal involvement. * Normal dental sensitivity. Severe:
* Rapid posteruptive enamel breakdown on erupting tooth
* Often develop widespread caries associated with affected enamel
* History of dental sensitivity. Differential diagnoses include:
* Amelogenesis imperfeta, a hereditary abnormality characterized by quantitative and structural disturbances of the enamel, without structural modifications of the dentine; it affects all teeth in the permanent dentition [52]. * Enamel hypoplasia, a quantitative abnormality identified as an external defect involving the enamel surface [42] and a localized reduction in the enamel thickness [52]. The damage occurs during the secretory phase of amelogenesis [52]. The margins of the lesion are smooth and round [42]. * Dental fluorosis is the result of excessive fluoride absorption during the mineralization stage and is characterized by diffuse white opacities affecting homologous teeth [42; 52].