1.4.1 Description
In the late bell stage, the tooth germ increases in size, and the hard tissues of the teeth start forming. The process of dentin formation is called dentinogenesis and it always precedes the process of enamel formation, i.e. amelogenesis. It is beyond the scope of this book to go into details of these processes but briefly, under the influence of inner enamel epithelium (which changes into pre‐ameloblasts), the adjacent peripheral cells of dental papilla become odontoblasts. These odontoblasts start secreting of pre‐dentin followed by dentin; this secretion stimulates pre‐ameloblasts to change into ameloblasts which start secreting the enamel matrix (which mineralizes and becomes dental enamel later). While secreting, odontoblasts move away from the secretion area, leaving behind their odontoblastic processes. Similarly, ameloblasts migrate away from dentin while secreting enamel matrix. It should be noted that the formation of these two tissues begins in the area of future cusps/incisal edges and then slopes downward. This is the stage where the commencement of root formation begins as well.
1.4.2 Key Identifying Features
On the histological sections, prominently visible dental hard tissues (enamel and dentin) can be seen. Ameloblasts (on top of the newly formed enamel) and odontoblasts (just below the newly formed dentin) are also evident.
1.4.3 Clinical Significance
The visible development of HERS begins during this stage. The HERS is responsible for determining the shape, size, and number of roots [4]. Disruption to this stage could affect amelogenesis and dentinogenesis, leading to the formation of abnormal enamel and dentin, respectively (or non‐formation) [5].
1.5 Root Formation
Figure 1.10 H and E stained section showing a tooth's root formation (white arrow, odontoblasts; black arrow, dentin).
1.5.1 Description
The tooth root has many important functions including anchorage of the tooth in maxilla/mandible and facilitating provision of blood supply (through apical foramina). The inside of the root is composed of radicular dentin and pulp canals whereas, on the outside, it is covered by a thin calcified layer of cementum. Root formation occurs because of the interaction between HERS, dental papilla, and dental follicle. After crown formation, the cervical loop grows apically as HERS circling dental papilla. The ectomesenchymal cells of dental papilla near the HERS change into odontoblasts and start secreting radicular dentin. The root dentin comes in contact with the dental follicle due to the perforation of HERS which leads to its mesh‐network appearance. This contact changes dental follicular cells into cementoblasts (forming cementum), fibroblasts (forming PDL), and osteoblasts (forming alveolar bone). It should be noted that the HERS only maps the shape of the root and then disintegrates. Its remnants are known as epithelial cell rests of Malassez.
1.5.2 Key Identifying Features
On histological sections, developing root with prominent radicular dentin can be clearly seen just below a complete crown.
1.5.3 Clinical Significance
The HERS is responsible for determining the number of roots by forming a pair of tongue‐shaped extensions that fuse [6]. Root formation plays an important role in tooth eruption. It is believed that with the pressure of the developing root, the crown of the tooth starts moving vertically to erupt in the oral cavity [7]. It should be noted, however, that there is evidence for rootless teeth to erupt [8] suggesting that it is a multifactorial process where root formation has a role, but it is not the only mechanism involved.
1.6 Amelogenesis Imperfecta (AI)
Figure 1.11 Low‐power view of a ground section of a deciduous incisor showing irregular enamel surface (arrows) related to AI.
Figure 1.12 High‐power view of a ground section of a deciduous incisor showing enamel pitting (arrow) related to AI.
1.6.1 Description
Amelogenesis imperfecta (AI) refers to a group of inherited genetic alterations that result in a defective enamel structure. AI is usually not associated with any syndrome or systemic disease. The teeth could appear yellow, brown, or sometimes grey. Several classifications have been suggested in the literature with the most commonly used one dividing AI into hypoplastic, hypomatured, and hypocalcified types. The hypoplastic type has insufficient amount of enamel matrix, the hypomature type has defective maturation of enamel whereas the hypocalcified type shows insufficient calcification of enamel. The genetic abnormalities in AI usually affect amelogenin (AMELX), enamelin (ENAM), kallikrein (KLK4), and matrix metalloproteinase 20 (MMP‐20) genes. AI poses a significant clinical problem affecting the oral hygiene, masticatory function, and quality of life of the patient.
1.6.2 Key Identifying Features
On histological sections, it is difficult to identify the exact type of AI. However, reduced width/length of enamel along with pitting or clefts can be identified (ground sections) in addition to residual uncalcified enamel matrix (decalcified sections).
1.6.3 Clinical Considerations
Hypoplastic type is most common type of AI (60–73%) followed by hypomatured (20–40%) and hypocalcified (7%) types [9]. AI usually affects all the teeth of an individual and the diagnosis usually involves family history and clinical observation [10]. Radiographs reveal less than opaque enamel, especially when the mineralization has been affected [10]. The affected teeth are more prone to dental caries, dentinal sensitivity, and attrition [6]. Treatment options include masking of defective teeth with veneers and extra‐coronal restorations [11].
1.7 Dentinogenesis Imperfecta (DI)
Figure 1.13 H and E stained decalcified section showing DI.
Figure 1.14 H and E stained decalcified section showing DI with a haphazard tubular architecture.
1.7.1 Description
Dentinogenesis imperfecta (DI) is a developmental hereditary condition (autosomal dominant) that affects the developing dentin. The dentin appears opalescent affecting both primary and permanent dentitions. DI can be classified into three main types: type I: DI associated with osteogenesis imperfecta; type II: DI similar to type I but not associated with osteogenesis imperfecta; and type III: initially reported in Brandywine