MOLAR INCISOR HYPOPLASIA

Linda Greenwall

INTRODUCTION

Molar incisor hypoplasia (MIH) is a condition that affects the incisors and molar teeth. It has a varied prevalence of 2.8–25%. However, a recent systematic review has reported a wide variation in defect prevalence (2.4–40.2%, mean around 18%) (Jälevik et al. 2010). Some of the prevalence may be masked by the presence of caries (Shubna and Hegde 2013).

It seems to be more prevalent and is noticed as the permanent teeth are erupting. It was first documented in the 1970s (Willmott et al. 2008). In 2001 this enamel defect was given a new name (MIH) with the definition of a “systemic hypomineralization” that affects one or more permanent first molars with or without permanent incisor involvement (Weerheijm and Merjare 2003). The appearance can range from mild to extreme and can be distressing for children and parents as they become aware of white areas and patches on the new teeth as they erupt. The purpose of this chapter is to elaborate on the condition and offer options for treatment.

Hypocalcification often appears as white spots on the teeth. Affected teeth have demarcated enamel opacities that can range from brown to yellow to white and orange. Its occurrence is common; white spots can vary in prevalence from 10–19% (Kellerhof and Lussi 2004). It is normally related to the central incisors and the first permanent molars. One or all four first permanent molars can be affected, with different degrees of hypomineralized enamel occurring within the same dentition (Sahlstrand et al. 2013). Because the lesion is normally located at the incisal part of the tooth, this can sometimes help with the etiologic assessment.

VARIED TERMINOLOGY

There are numerous terms associated with this condition. Some of the terms include idiopathic enamel hypomineralization in the permanent first molars, idiopathic enamel opacities in the permanent first molars, nonfluoride enamel hypomineralization in the permanent first molars, nonendemic mottling of enamel in the permanent first molars (Kellerhof and Lussi 2004).

PRESENTATION OF THE LESIONS

The lesions normally become apparent at the time of eruption of the permanent teeth. The molar teeth are worse affected than the incisor teeth.

AGE OF DIAGNOSIS

Diagnosis is normally made as the permanent teeth erupt at ages 6–8 (Jedeon et al. 2013).

APPEARANCE OF THE LESIONS

These lesions often are referred to as “cheese molars” owing to the consistency and appearance of the lesions on the molar teeth. Normally, the molar teeth are more severely affected than the incisors. The lesions are more extensive in the upper jaw than in the lower jaw.

ETIOLOGY OF THE LESIONS

There are several explanations as to the cause of the lesions. One is that they arise as a result of a systemic cause at around the time of birth. Another explanation for the variations in expressivity of MIH may be that they result from differences in the start of mineralization between homologue teeth at the time of the incident (Shalstrandt 2013). However, it is often difficult to calculate or assess the exact cause owing to the variation and multitude of causes. Diverse environmental conditions, such as medication (amoxicillin), hypoxia, hypocalcemia, dioxins, polychlorinated biphenyls, and prolonged breast-feeding, have been associated with MIH (Alaluusua 2010).

•  Prenatal causes (Shubna and Hegde 2013)—MIH occurring after the following:

•  High maternal fever.

•  Maternal calcium deficiency.

•  Maternal antibiotics.

•  Perinatal causes—factors causing defective ameloblast activity (Lygidakis et al. 2008):

•  Cesarean section.

•  Prolonged complicated delivery.

•  Premature birth.

•  Birth of twins.

•  Hypoxia.

•  Low birth weight.

•  Hemorrhage.

•  Detachment during delivery.

•  Other birth complications following oxygen deficiency.

•  Postnatal causes

•  Congenital.

•  Hereditary-genetic factors.

•  Trauma.

•  Calcium deficiency.

•  Dioxins in the mother’s milk.

•  Prolonged breastfeeding (Alaluusua 2010).

•  Environmental pollutants such as exposure to bisphenol A (BPA; Jedeon et al. 2013).

•  Fever precipitating pneumonia, upper respiratory tract infection, otitis media, tonsillitis.

•  Exanthematous childhood fever (e.g., chickenpox).

•  Celiac disease.

•  Gastrointestinal disease (Shubna and Hegde 2013).

•  Early ear, nose, and throat surgery or tonsillectomy.

•  Antibiotics, especially amoxicillin.

•  Renal insufficiency.

•  Other systemic disease and unknown factors.

Some studies show a relation between uptake of dioxins via mother’s milk after prolonged breastfeeding and developmental defects of the child’s teeth.

Because the ameloblasts are very sensitive to oxygen supply, complications involving oxygen shortages during birth or respiratory diseases such as asthma or bronchitis and pneumonia are discussed as further etiologic factors.

Renal insufficiency, hypoparathyroidism, diarrhea, malabsorption and malnutrition, and high-fever diseases can be other reasons for the occurrence of these defects.

MICROSCOPIC STUDIES

The effect of environmental pollutants on amelogenesis was studied in rats in an experimental model to create MIH (Jedeon et al. 2013). The enamel that was exposed to BPA showed an abnormal accumulation of exogenous albumin in the maturation stage of the enamel. The BPA exerts its effects on amelogenesis by disrupting normal protein removal from the enamel matrix. Interestingly, in 100-day-old rats, erupting incisor enamel was normal, suggesting that amelogenesis is sensitive to MIH-causing agents only during a specific time window during development (as reported for human MIH) (Jedeon et al. 2013). MIH affects those teeth that are undergoing mineralization around the time of birth; it is clear that the enamel-forming ameloblasts are sensitive to the causative agent(s) responsible for MIH only during this specific time window. The enamel in MIH is rough and has a protective layer. This rough layer can be removed by a hypochlorite rinse or the use of hydrochloric acid in the form of microabrasion (6.6–10% hydrochloric acid) or resin infiltration using 15% hydrochloric acid first. It has been suggested that reduced Klk4 gene expression in the presence of mineral- bound albumin and enamel matrix proteins in the early maturation stage could inhibit enamel crystal growth, leading to hypomineralization. The nature of this organic material is unclear at present, but its sensitivity to hydrolysis by hypochlorite suggests it may be protein-aceous (Jedeon et al. 2013).

MIH is indicative of some adverse event(s) occurring during early childhood that affect enamel development (Jedeon et al. 2013). In humans the adverse event normally occurs from birth to 5 months of age (Robinson et al. 1995). There is some evidence that excessive BPA administered to the newborn may be the cause of the MIH. It has been argued, based on the use of a physiologically based pharmacokinetic modeling approach, that human newborns exhibit plasma BPA concentration 11 times greater than that found in adults, whereas at 3 months of age the ratio has decreased to 2 (Edginton and Ritter 2009).

A scoring or classification system may be used to define the type of white lesion present. There are a few different such systems.

CLASSIFICATION SYSTEM—JEDEON ET AL. 2013

Type 0 = Enamel defect free.

Type 1 = One third of tooth surface or less affected; with or without enamel breakdown.

Type 2 = Two thirds of tooth surface affected.

Type 3 = Total tooth surface affected; enamel breakdown.

Type b = With enamel breakdown.

Defective enamel can be a locus of lowered resistance for caries. Histologically there are areas of porosity of varying degrees. Pathogenically, these factors contribute to pre-eruptive disturbance of mineralization involving albumin and, in patients with posteruptive breakdown, subsequent protein adsorption on the exposed hydroxyapatite matrix.

CLASSIFICATION OF THE CONDITION—ALALUUSUA 2010

1.  Mild: color change only.

2.  Moderate loss of enamel only.

3.  Severe loss of enamel in association with affected dentin.

Classification is essential because it will help in planning treatment and esthetic options, as follows:

1.  Mild: preventive approaches, varnish and fissure sealing, resin infiltration of the molar teeth.

2.  Moderate: whitening of anterior teeth, composite restoration on molar teeth.

3.  Severe: treatment with glass ionomers or composites for the molar defects, whitening of the anterior defects followed by resin infiltration.

MANAGEMENT STRATEGY

EXAMINATION CRITERIA

An explorer is used to check the roughness and consistency of the enamel surface. On the labial surface of the incisors, differentiation is made between white spot lesions, which may appear at the gingival margin, and MIH lesions, which occur in the incisal tip of the center of the tooth. White spot lesions are normally present over plaque associated with poor oral hygiene or around previous orthodontic braces. On the molar teeth, some severe effects are associated with dental caries. These severely affected teeth are called “cheese molars.”

DIAGNOSIS

Early diagnosis is essential for appropriate treatment and to prevent deterioration of the condition in the child. The diagnosis is normally made based on the appearance of the lesions when the permanent teeth erupt (Table 11.1). The differential diagnosis includes enamel hypoplasia, fluorosis, and amelogenesis imperfecta. Rapid breakdown of tooth structure may occur, giving rise to acute symptoms and complicated treatment (Daly and Waldron 2009). There is often rapid breakdown of the first permanent molars from the stage of eruption at around 6 years; thus early detection and treatment are imperative.

Diagnosis can be made using gene evaluation; there are 11 different types of genes involved in enamel matrix formation. Saliva can be collected from the patient and his or her parents. These 11 single-nucleotide polymorphism (SNP) markers can be selected in genes involved in enamel formation and genotyped using predesigned TaqMan genotyping assays (these amplifications were made in a GeneAmp PCR System 9700 [Perkin Elmer Applied Biosystems, Foster City, California]) (Ranade et al. 2001).

For a diagnosis to be made, one to four permanent first molars may be affected as well as the upper central incisors, but the lower central incisors also may be affected (Williams et al. 2006).

Diagnosis can also be made from the color of the permanent molar. Yellow-brown defects have lower Knoop hardness values and greater porosity than white defects and normal enamel and indicate a need for quicker intervention.

SIGNS AND SYMPTOMS

Molar teeth with hypocalcification are porous and soft. These affected teeth can be very sensitive to air and cold, warm, and mechanical stimuli. Even tooth brushing may create toothache in these teeth. Children with MIH can have more intense dental sensitivity from temperature variations (Weerheijm et al. 2001), and there is innervation density in the area of the hypoplasia and the subodontoblastic region of hypomineralized teeth compared with sound teeth (Shubna and Hegde 2013).

This is a result of the combination of the chronic pulp inflammation and innervation of the region right under the hypomineralized area (Rodd et al. 2007). Consequently, children with MIH may have hampered anesthetic action, which can affect their behavior (Rodd et al. 2007). The extreme sensitivity that these children experience causes further deterioration of the tooth because the child cannot brush the teeth, which are too sensitive. Older children have more severe manifestations because the tooth continues to deteriorate after eruption (Shubna and Hegde 2013). Bacteria enter these porous areas of the dentin and rapidly break down the enamel (Fagrell et al. 2008). In sections where bacteria were found in the cuspal areas or deeper in the dentin, a zone of reparative dentin was found; and in sections from one tooth, the coronal pulp showed an inflammatory reaction with inflammatory cells. The dentinal tubules with odontoblastic processes were filled with bacteria (Fagrell et al. 2008). The transitional ameloblast is considered most vulnerable, and when these cells do not undergo complete maturation, full-thickness hypomineralization occurs. Enamel maturation involves (1) the removal of acid labile mineral, (2) replacement with more acid-resistant apatite, and (3) an influx of calcium and phosphate ions, increasing the crystal width and thickness (Avery 2002).

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