Enamel organ

This is the initial stage of tooth development, which occurs at week 8 i.u.. Proliferation of dental lamina occurs, forming small tooth buds which are spherical or ovoid condensations of epithelial cells, now known as the enamel organ.[1] The enamel organ consists of peripherally located, low columnar cells and centrally located polygonal cells. The enamel organ is also surrounded by proliferating mesenchymal cells, which results in the condensation of two distinct areas:[2]

1. The dental papilla: below the enamel organ
2. The tooth sac: ectomesenchymal condensation of the area surrounding the tooth bud and dental papilla.

Both the dental papilla and the tooth sac are not structurally defined in the bud stage, and will become more defined in subsequent stages (Cap and Bell stages). The interaction and signalling between the enamel organ and the surrounding mesenchymal cells play an important role in the later stages of tooth development.[2] Each dental arch will have 10 tooth buds, accounting for 20 primary teeth.

The cap stage occurs in week 9-10 i.u.[1] Unequal proliferation of cells during this stage, invaginating into the ectomesenchyme tissue, leads to the formation of the cap-shaped enamel organ. The ectomesenchyme tissue also invaginates superficially to shape the primitive dental pulp. Differentiation of cells occurs at this stage to make different tissue layers; external enamel epithelium, stratum intermedium, stellate reticulum, internal enamel epithelium, dental papilla, and dental follicle. The external enamel epithelium, a layer of simple cuboidal epithelium, has a protective role during tooth development.[1] The stellate reticulum, the innermost layer of the enamel organ, gathers GAGs between cells. The internal enamel epithelium will form enamel during the Bell Stage

There is uneven growth of enamel organ in this phase, and the epithelial cap deepens.[3] The cap shape of the enamel organ assumes a bell shape as the undersurface of the cap deepens.[3] Foldings of the internal enamel epithelium (done by the growing papilla cells) maps out the occlusal pattern of the tooth crown. The process is known as morphodifferentiation. The pressure exerted by the dental papilla cells has been shown to be opposed equally by the pressure from the fluid in the stellate reticulum (present in the enamel organ).[3]

The folding of the enamel organ is caused by different rates of mitosis and difference in cell differentiation times, causing different crown shapes in each tooth.

This stage is the apposition stage (formation of dental hard tissues), also characterised by the commencement of root formation and mineralisation. The area between the internal enamel epithelium and odontoblasts outline the future dentinoenamel junction. Formation of dentine (dentinogenesis) precedes enamel formation (amelogenesis). It occurs first as along the future dentinoenamel junction in the region of future cusps and proceeds pulpally and apically. Cells of the internal enamel epithelium become pre-ameloblasts and release inductive factors which encourage the differentiation of odontoblasts from the mesenchymal cells of the dental papilla.[1] This can be seen in the figure (marked A). The odontoblasts lay down dentine (see pale blue band). After the first layer of dentine is formed, this induces ameloblasts (B) to lay down enamel (red region) over the dentine in the future incisal and cuspal areas. Amelogenesis will then follow. The cervical portion of the enamel organ then gives rise to the Hertwig Epithelial Root Sheath (HERS)-  this outlines the future root and also is responsible for the size, shape, length and the number of roots.

Odontomes are considered to be developmental anomalies resulting from the growth of completely differentiated epithelial and mesenchymal cells that give rise to ameloblasts and odontoblasts.[10] Histologically, they are composed of different dental tissues including enamel, dentine, cementum[11] and in some cases, pulp tissue, therefore if the enamel organ is not arranged in its proper fashion, an odontome may form.[12] Odontomes are categorised as either:

Compound

this malformation is anatomically like a normal tooth, and has dental tissues (enamel, dentine, cementum) placed in an orderly fashion. These are more frequent than complex odontomes.[12][13]

Complex

this malformation results in dental tissues being arranged in a disorderly fashion, forming an irregular mass.[12][13]

Odontomes are rare entities and usually asymptomatic; they are often incidental findings on routine dental radiographic examinations.[14][15] The complex odontome appears as an irregular mass of calcified material surrounded by a thin radiolucent area with smooth periphery, and the compound type shows calcified structures resembling teeth in the centre of a well-defined radiolucent lesion.

Some factors related to the development of odontomes are:

• Changes in genetic components responsible for tooth development
• Trauma at primary dentine period
• Inherited conditions such as Gardner's Syndrome
• Infection
• Inflammation
• Hyperactivity of odontoblasts.[12][15]

The first reported case of an odontome erupting in the oral cavity was in 1980.[15]

Dens Invaginatus is a dental anomaly which means that the affected tooth (dilated odontome) contains a cavity that is completely or partially lined by enamel, radiographically resembling a tooth within a tooth (dens in dente).[16]

There is a lack of consensus on the aetiology of dens invaginatus. It is suggested that dens invaginatus arises because during odontogenesis, there is proliferation and ingrowth of the cells of the enamel organ into the dental papilla during development.[17]  

Another proposed theory is that the distortion of the enamel organ during tooth development and subsequent protrusion of a part of the enamel organ will lead to the formation of an enamel-lined channel ending at the cingulum or occasionally at the incisal tip.[18]

Histologically, there are differences in the structure and composition between the external and internal enamel in dens invaginatus. The internal enamel exhibits atypical and more complex rod shapes and its surface has the typical honeycomb pattern but no perikymata.[19]

The invagination can be:

• Coronal type: slight pitting involving the enamel organ infolding into the dental papilla
• Radicular type: occupying most of the crown and root involving invagination of Hertwig's epithelial root sheath, lined with cementum.[20]

Dens invaginatus has a clinical importance as teeth affected with dens invaginatus are predisposed to developing pulpal disease. The invagination allows entry of irritants into an area which is separated from pulpal tissue by only a thin layer of enamel and dentine and extra preventative measures are advised to prevent dental caries.[21]

Coeliac disease in children is thought to be underdiagnosed because it may initially be asymptomatic. Studies have shown that enamel defect of permanent and deciduous or primary teeth may suggest the presence of undiagnosed coeliac disease in children and adults.[22][23][24] Coeliac disease-related enamel defects are most commonly associated with incisors and first molar teeth, and are characterised by symmetrical distribution of enamel defects on the same tooth in all 4 quadrants.[22][25] This is a distinct characteristic of enamel defects in coeliac disease that cannot be seen in other enamel defects.

Enamel defects in coeliac disease occur due to an interference in tooth formation by amelogenin. Amelogenin is a proline-rich enamel protein that plays a major role in mineralisation and organisation of tooth crystals.[26][27] Disruption to this process cause alterations in the tooth surface. Patients with coeliac disease produce high levels of circulating IgG and IgA antigliadin antibodies (AGA) in order to get rid of protein gliadin, which is toxic to these patients. However, due to the structural similarities between amelogenin and gliadin, AGA may interfere with amelogenin which lead to improper formation of enamel.[26] Furthermore, because IgG can be transported across the placenta, the amelogenesis process is disturbed from the intrauterine period to adolescence.[25]

Gliadins are highly hydrophobic proteins in wheat gluten. The antibodies are produced to interact with this protein. Therefore, a gluten-free diet may lead to normalisation of tooth development as circulating antibodies for enamel defect may decrease.[28]