MIH must be differentiated from other structural disorders as part of its identification. In addition to the understanding the key features, which are essential for an accurate diagnosis, a patient’s medical history is mandatory to distinguish acquired, environmental, or genetic causes. The following sections present the various differential diagnostic entities to be excluded.
Developmental enamel defects occur due to dys-function of the ameloblasts during tooth development as a result of various influences. They always have irreversible consequences, as remodeling processes can no longer take place in the hard tooth tissue they form.
Disruption of the ameloblasts during the enamel formation phase causes a structural defect in the composition of the enamel matrix. Quantitative or morphological defects are the consequence. A disruption during enamel maturation, on the other hand, causes defects in the developing crystal structure. Morphologically normal, but structurally or qualitatively defective enamel results.
The earlier and the longer the disruption affects the tooth, the more prominent the later appearance of the anomaly.1
Basically, a differentiation can be made between quantitative and qualitative defects (Table 7-1).2 Opacities are qualitative defects. Demarcated and diffuse forms can be classified (Fig 7-1). Demarcated opacities can be white, yellow, or brown, and show a clear border to the adjacent normal tooth hard tissue. Diffuse forms appear linear, irregularly distributed over the tooth surface or directly neighbouring. Qualitative defects may fracture after eruption of the tooth at the surface due to the microporosities they contain.
Qualitative defects (opacities)
Quantitative defects (hypoplasia)
Quantitative defects manifest themselves as hypoplasia. They develop as a consequence of deficient enamel matrix formation and are thus already present pre-eruptively. In the hypoplastic areas, the enamel is too thin. Single or multiple, flat or deep pits or grooves occur. Furthermore, enamel may be completely absent in certain areas of the tooth crown (Fig 7-2). Figure 7-3 shows the difference between qualitative and quantitative enamel defects in the form of hypomineralization and hypoplasia.
Künzel3 subdivided the origin of developmental enamel disorders into the following three main groups:
- exogenously caused, and
- endogenous structural anomalies.
Genetic structural disorders are hereditary. They occur in generalized form in both, the primary and permanent dentition. All teeth are affected in the same way. There are comparable alterations of the teeth in the family. Examples are amelogenesis imperfecta and dentinogenesis imperfecta.
Exogenously caused defects can be induced by inflammatory, traumatic, or radiation-physical noxae on individual tooth germs. Inflammatory disorders include periapical periodontitis of primary teeth or osteomyelitic processes in infancy and childhood, which may subsequently negatively influence the development of permanent teeth. Traumatic effects in the primary dentition, eg, as intrusion injuries, can also damage the subsequent tooth germ. Exogenously caused structural disorders are characterized by a solitary, asymmetrical, predominantly unilateral occurrence in individual teeth or tooth groups.
Endogenously induced structural disorders are consequences of a temporary deficiency or a direct functional impairment/damage of the tooth-forming cells. These disorders can occur pre-, peri-, and postnatally. Thus, the primary and permanent dentition may be affected, but usually the permanent teeth are involved. Endogenously caused structural disorders are always seen in teeth or tooth groups that mineralize simultaneously during the exposure to the noxious agent. They are thus restricted to a certain developmental phase. A solitary, unilateral occurrence is excluded. Molar incisor hypomineralization can be assigned to this group of structural disorders.
Figure 7-4 shows a scheme of the different forms with their typical occurence pattern in the dentition.
MIH must be differentiated from amelogenesis imperfecta, dental fluorosis, and other endogenous and exogenous structural disorders.
Amelogenesis imperfecta (AI) is an inherited disorder.4 The prevalence ranges from 1:718 to 1:14,000, depending on the population studied. The genetic defect disturbs the differentiation or function of the ameloblasts. This results in the formation of chemically, quantitatively, and/or structurally abnormal enamel. The dentin structure is normal in this case.
AI exists in isolation or associated with other abnormalities or syndromes. However, the non-syndromal forms are most common.5,6 The mode of inheritance is autosomal dominant, autosomal recessive, or X-linked. Sporadic appearance is also possible.