Introduction

Molar–incisor hypomineralization (MIH) is a developmental defect of the human dentition that primarily affects the enamel of the first permanent molars and can involve the incisors. Typically, the second permanent molars and premolars are not involved. This condition has been recognized since around 1970 and has been described using a variety of terms (e.g., cheese molars, idiopathic hypomineralization of enamel) (Weerheijm et al., 2001a). The term MIH was accepted by leaders in the field that convened at the European Academy of Pediatric Dentistry in 2000, and this continues to the name most used to describe this condition (Weerheijm et al., 2001b). The clinical characteristics vary from case to case and between teeth in the same individual. The more severely affected the first permanent molars, the more likely it is that there will be incisor involvement. The defects vary from small well-demarcated areas of color change to extensive hypomineralization that includes the entire dental crown. Affected teeth form with a normal thickness of enamel and the abnormal areas of enamel having a decreased mineral content and increased protein and water content. Thus, the defects are not hypoplastic in that the full thickness of enamel develops. Once the tooth begins to erupt and come into function, rapid enamel loss can make the crowns appear hypoplastic, but this is typically the result of enamel fracturing, wear, and dental caries. Discoloration of the involved areas is a result of the decreased mineral content and increased protein and water content that change the optical character of the hypomineralized enamel (Fagrell, 2011). The enamel color changes range from white opaque lesions to a creamy yellow or brown. The more severe the level of hypomineralization, the more likely the tooth is to have early loss of enamel. Early enamel loss is often associated with the development and progression of dental caries that can lead to rapid deterioration of the clinical crown (Figure 12.1) and pulpal involvement if left untreated. The degree of hypersensitivity associated with these defects varies but can be quite pronounced and appears to be frequently associated with the severity of hypomineralization and enamel loss. Hypersensitivity and difficulty anesthetizing the affected molars can add to the challenge of treating individuals with MIH (William et al., 2006).

Prevalence and etiology

The prevalence of MIH ranges from about 3–40% in the population, making it relatively common and a condition that will challenge clinicians on a regular basis (Jalevik, 2010). The first permanent molar is the permanent tooth most likely to develop dental caries, and hypomineralized molars are at increased risk for developing dental caries. Caries development can obscure the presence of enamel hypomineralization that likely contributes to the carious involvement in at least some first permanent molars. The first permanent molars begin to form in utero and typically start to mineralize just before or shortly after birth (first permanent molars of girls tend to form earlier than those of boys). The enamel of the permanent first molars and permanent incisors does not fully mineralize until the age of 3–5 years. Having enamel hypomineralization in the primary dentition increases the odds that the individual will have MIH in the permanent dentition (Elfrink et al., 2012).

Attempts to identify the etiology of MIH have largely focused on categorizing environmental insults that might be associated with the condition. Maternal health, premature birth, infant health, use of antibiotics, and a number of other conditions have been associated with MIH in several studies (Whatling and Fearne, 2008; Laisi et al., 2009; Alaluusua, 2010). Most of the associated environmental stressors associated with MIH appear to occur in the first year of life (Fagrell et al., 2013). Although there were initially thought to be associations and possible toxins associated with breast feeding (dioxins), subsequent studies do not support an association of MIH with breastfeeding (Laisi et al., 2008).

Studies evaluating the environmental influences associated with MIH have not ruled out the potential contribution of hereditary factors as being potentially participating in the cause of MIH. Indeed one genetic locus has been associated with MIH, and there are families with a history of MIH in multiple generations and in multiple siblings (Kuhnisch et al., 2013). These findings all suggest that there is at least some genetic component contributing to MIH. This appears entirely reasonable, given that we know enamel formation is highly regulated at the molecular level and involves the expression of thousands of genes (Jeremias et al., 2013). Just as genetics contributes significantly to an individual’s risk for developing dental caries, it is probable that multiple genetic variations are at play in defining one’s risk for developing MIH and making them more susceptible to environmental insults.

Diagnosis of molar–incisor hypomineralization

Diagnosing MIH can be difficult, and clinicians may confuse MIH with other developmental defects of enamel such as fluorosis or amelogenesis imperfecta (a group of hereditary conditions that cause a variety of enamel defects). There are hundreds of environmental and genetic conditions that are known to affect enamel formation, and so making a definitive diagnosis can be challenging. The diagnosis of MIH can be further complicated if the tooth begins to decay as the tooth is erupting, thereby destroying the affected crown structure. It is, however, important to accurately diagnosis MIH so that the different approaches for managing the condition can be implemented to achieve optimal treatment outcomes. There often will not be family history of enamel defects such as can occur in cases of amelogenesis imperfecta. The hypomineralization defect is primarily limited to the first permanent molars and incisors, whereas most of the teeth of both the primary and permanent dentitions are involved in amelogenesis imperfecta. With fluorosis the primary dentition is typically not affected, but all the permanent teeth tend to be involved, and the enamel defects are more uniformly distributed than it appears with MIH (e.g., all four first permanent molars and incisors will be similarly affected).

Clinical evaluation for the presence of MIH ideally involves examining the four first permanent molars and eight permanent incisors and is often best accomplished in an 8-year-old child (Weerheijm et al., 2003). The examination should be performed when the teeth are clean and moist. They are examined for the presence of demarcated changes in enamel color and translucency (opacities) and areas of enamel loss that most often occur in the affected molars. A severity scale has been developed to classify MIH as mild, moderate, or severe at the tooth level, meaning that one tooth may be mild, and another tooth in the same patient may be severe, and seeing this amount of variability is a common occurrence (Table 12.1) (Mathu-Muju & Wright, 2006). Enamel color changes are caused by changes in the enamel composition (amount of mineral and protein) and structure. Enamel that is yellow brown tends to have less mineral compared to white opacities and is more likely to succumb to enamel loss. These yellow-brown areas tend to lack the shiny reflective surfaces of normal enamel and have a more ground glass and slightly rough appearance indicative of a decreased mineral content. Clinically assessing these characteristics is helpful in determining prognosis for an individual tooth and the likelihood that it will break down over time as a result of enamel loss. These clinical attributes are also helpful in selecting appropriate treatment approaches and optimizing therapeutic success.