The enamel organ, also known as the dental organ, is a cellular aggregation seen in a developing tooth and it lies above the dental papilla.

At the end of week 7 i.u., localised proliferations of cells in the dental laminae form round and oval swellings known as tooth buds, which will eventually develop into mesenchymal cells and surround the enamel organ. Each epithelial swelling and the surrounding mesenchymal cells form a tooth germ.

Tooth germs are the primitive structure of teeth; their formation is in three distinct stages: bud stage, cap stage, bell stage.

The stages are based on the degree of development of enamel organ. Oral epithelium forms the tooth enamel while the ectomesenchyme forms the pulp and dentine of the tooth. The ectomesenchyme lies deep to the oral epithelium.

Bud Stage

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. and cell signaling between cells in the dental extracellular matrix/enamel matrix play a role.

The shape of the enamel layer covering the crown is determined by five growth parameters:

  1. The appositional growth rate
  2. Duration of appositional growth (at the cusp tip)
  3. Ameloblast extension rate
  4. Duration of ameloblast extension
  5. Spreading rate of appositional termination.

The appositional growth mechanism establishes the thickness of the enamel layer and it is determined by ribbon-like carbonate apatite crystals which are present in the rods (or prisms) and interrods. They are produced by the ameloblast in the bell stage of tooth development. As the crystals are long and closely packed, the thickness depends on the abundance of the crystals in the tooth. Crown shape or morphology is determined by the epithelial-mesenchymal interaction, which occurs at the dentinoenamel junction (DEJ).

Firstly, the pre-ameloblasts differentiate from the inner enamel epithelia on the dentine surface covering the pulp horn. A wave of ameloblasts will then differentiate from the cusp tip and move through the inner enamel epithelia down the slope of the mineralised dentine surface. The differentiation will extend down the slope of the dentine surface and reaches its limit, where the inner epithelium is fused with the outer enamel epithelium to form Hertwig's epithelial root sheath. Enamel mineral will increase daily (apposition growth) during the secretory stage of amelogenesis (enamel formation). Ultimately, the secretory stage will end and they will transition into maturation stage ameloblasts. These ameloblasts will move down to the enamel surface of the tooth and the shape of the crown and tooth is then established.

Abnormalities

Odontomes

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. Histologically, they are composed of different dental tissues including enamel, dentine, cementum and in some cases, pulp tissue, therefore if the enamel organ is not arranged in its proper fashion, an odontome may form. 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.

; Complex: this malformation results in dental tissues being arranged in a disorderly fashion, forming an irregular mass. 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.

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.

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.

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.

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.

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.

Enamel Defect and Coeliac Disease

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. 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. 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. 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.

See also

  • Ameloblast
  • Tooth
  • Tooth development
  • Tooth enamel

References