To better understand the pathogenesis of molar incisor hypomineralization (MIH), it is essential to know and understand the structural, mechanical, and chemical differences of hypomineralized enamel compared to healthy tooth structure. In the present chapter, the processes of regular amelogenesis are first described before the characteristics of hypomineralized enamel are discussed.

3.1 Tooth enamel

Dental enamel is the most mineralized and hardest tissue in the human body. It consists of 95% inorganic substance (calcium and phosphate in the form of hydroxyapatite), 1% organic substance, and approx. 4% water.¹ Thus, enamel has an almost pure crystalline structure. The crystalline portion mainly consists of calcium and phosphorus. It also contains small amounts of sodium, magnesium, chlorine, and potassium. In mature enamel a number of trace elements can also be found.¹

Enamel is mainly transparent, but has a grayish-yellow inherent shade. Depending on the enamel thickness, the tooth color is determined by the yellowish natural color of the dentin and the degree of transparency, as well as the homogeneity of the enamel.¹

3.2 Amelogenesis

Enamel formation begins at the bell stage of tooth development by the ameloblasts. They develop by differentiation from the cells of the inner enamel epithelium. The process starts at the dentino-enamel junction with the help of preameloblasts by reciprocal signaling interaction.² The preameloblasts initiate the deposition of an initial dentin layer in the odontoblasts, then start the secretory phase themselves and form the enamel matrix. Thereby, the enamel matrix is not formed simultaneously at the entire interface to the dentin. The formation of enamel starts at the cusp tips or in the middle of the incisal edge and is further deposited layer by layer towards the cervical area. In parallel, enamel formation proceeds in a centrifugal direction, so that the last matrix formed – in contrast to the dentin – is on the outside of the tooth. Per year, human ameloblasts move about 1 mm, which corresponds to a daily enamel formation rate of about 3 to 4 μm.¹ When the ameloblasts begin to function as secretory cells, they develop a distal projection called Tomes´ process. This has the ability to simultaneously secrete and resorb the matrix.

Amelogenesis is a three-stage process: it begins with the secretion phase, followed by a short transition/mineralization phase, and then the maturation phase. Enamel formation ends in the area of the incisal edges or the occlusal relief when the maximum enamel thickness is reached. The ameloblasts end their secretion activity at this point.¹

3.2.1 Secretion

The organic enamel matrix produced and secreted by the ameloblasts at the beginning of enamel formation comprises proteins and enzymes (proteases).³ The latter gradually degrade the proteins again. The proteins themselves can be divided into the group of amelogenins (about 80–90%) and non-amelogenins (tuftelin, sheatlin, and enamelin).⁴ Matrix secretion and immediate mineralization proceed in rhythmic phases. The secreted amelogenins arrange themselves into nanospheres, which in turn group together to form a matrix for crystallite incorporation. Subsequently, proteinases reabsorb these nanospheres to allow further crystal growth. To the extent the matrix is degraded, the crystallites grow in length and thickness until they touch and possibly connect.¹ However, despite immediate mineralization, this matrix remains only partially mineralized until subsequent maturation.

During enamel matrix secretion, ameloblasts migrate coronally from the dentino-enamel junction in such a way that the final shape of the tooth is formed. After reaching the prospective enamel surface, the ameloblasts stop the process of matrix secretion and start mineralizing the enamel.

Disturbances in the secretion phase result in less matrix being secreted. This leads to a quantitative defect: hypoplastic enamel results. Causes can be genetic influences or direct trauma.

3.2.2 Maturation

Maturation is divided into two phases – pre-eruptive and posteruptive enamel maturation. Pre-eruptive enamel maturation involves the transformation of the initially mineralized enamel matrix into a crystalline structure. These processes include several stages: the growth of enamel crystallites; the densification and hardening of the mineralized structure; the selective change in the composition of the enamel matrix and the loss of water; and the cellular activity in the enamel organ associated with these processes.¹ By the time the tooth erupts, the enamel has received about 65–75% by weight of its mineral content. After eruption, minerals of the saliva can penetrate through the micro-gaps of the enamel, strengthening the crystal structure and even closing the pores. After posteruptive maturation, a permanent tooth has up to 98% by weight of minerals. Lifelong ion exchange takes place on the enamel surface.⁵

3.3 Calcification of the permanent tooth germs

Hard tissue formation begins in the bell stage, which the first permanent molars reach around the 24th week of pregnancy. They start enamel formation shortly before birth (approx. 28 weeks). The permanent maxillary central incisors and all mandibular incisors start hard tissue formation in the 3rd to 4th month of life, and the maxillary lateral incisors in the 10th to 12th month after birth.

Tables 3-1 and 3-2 summarize the chronology of the development of the primary and permanent teeth. Figures 3-1 and 3-2 additionally illustrate the mineralization of crowns and roots in the primary and permanent dentition.

Table 3-1 Chronology of the development of primary teeth according to Schour and Massler30

Table 3-2 Chronology of the development of permanent teeth according to Schour and Massler30

Fig 3-1 Mineralization times of crowns and roots in the primary dentition (source: Cornelia Jungwirth, Katrin Bekes).

Fig 3-2 Mineralization times of crowns and roots in the permanent dentition (source: Cornelia Jungwirth, Katrin Bekes).

3.4 Disturbances in amelogenesis

The phases of enamel formation follow the different life cycles of the ameloblasts. This genetically controlled process is sensitive to disturbances in its development. The ameloblasts are differently susceptible in their various phases and react with different consequences to the respective disturbances.

If damage occurs during the secretion phase (eg, genetic influences, direct trauma), less matrix is secreted, and length growth of the crystals is inhibited. Consequently, there may be a reduction in enamel thickness and thus enamel hypoplasia. Disruptions in the transition and maturation phase can lead to pathologically softer or even hypomineralized enamel despite normal thickness growth. The ameloblasts are particularly sensitive in the maturation phase.6

Therefore, MIH is probably caused by disruptions either in the transitional or in the maturation phase. The resulting structural changes and further alterations of the enamel are described next.

If ameloblasts are irreversibly damaged, increased porosities and the formation of yellow-brown opacities occur. Some of the ameloblasts seem to be able to recover from this irritation, with the result that the enamel surface shows less severe color changes. These visually weaker changes are creamy yellow or creamy white and are found mainly in the inner enamel areas.7–9

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