Association Between Molar-Incisor Hypomineralization and Enamel Hypoplasia

INTRODUCTION

Developmental defects of enamel (DDE) are alterations in the quality and/or quantity of enamel that may affect the shape, hardness and color of teeth, as a result of disturbances during amelogenesis [1]. Different kinds of enamel defects may occur depending on the stage of enamel formation in which the ameloblast has been affected. Quantitative enamel defects result from changes occurring during the stage of matrix formation, whereas qualitative defects result from changes that affect the major part of the mineralization process [2].

Enamel defects may be expressed as hypomineralizations or hypoplasia lesions. Hypomineralized enamel can be seen due to differences in translucency that may be diffuse or demarcated. This enamel looks soft and porous, and for this reason, teeth may undergo irregularly shaped post-eruptive breakdown (PBE) [3]. Enamel hypoplasia is a reduced quantity of enamel thickness that produces smooth, even edges [3].

DDE may affect both primary and permanent teeth, although the etiology is still unclear. The appearance of these lesions seems to be influenced by some conditions, such as dental trauma [3], maternal diseases [4], use of medication [5] and infections in early childhood [5]. However, DDE may be caused not only by environmental and systemic factors, but also by genetic disorders [6].

Based on the hypothesis that the enamel formation process is influenced by genetics, it is fair to assume that genetic variations could be related to alterations in the amelogenesis. Studies suggest there is an association between hypomineralised enamel and genetic variation in enamel formation genes [6]. A similar pattern has been observed for other dental development defects [2]. There is a pattern of association between several types of dental anomalies with genetic origin, such as agenesis, microdontia and tooth transposition [7]. However, the true association between MIH and enamel hypoplasia is still unknown. Thus, given this scenario and considering the scarcity of scientific information on the subject, the aim of this study was to evaluate the association between MH and enamel hypoplasia.

MATERIALS AND METHOD

RESULTS

The final study sample consisted of 311 orthodontic records of patients (158 females and 153 males), with a mean age of 14.6 years (SD=1.92).

DISCUSSION

This study tested the hypothesis that MIH is associated with enamel hypoplasia, based on the premise that some dental anomalies coexist with others in the same patient [13, 14]. To the best of our knowledge, this is the first study to evaluate the possible association between MIH and enamel hypoplasia.

The prevalence of MIH found in this study (35.4%) is twice the rate greater than reported by Zhao et al [15] (14.2%). However, literature shows that higher prevalence rates of MIH have been observed in South America [15]. Ethnic and environmental differences, in addition to variations in diagnostic criteria, can also explain for this great variability [4]. Therefore, the present study used the defined criteria by the EAPD and modified by Ghanim for the diagnosis of MIH [10], with the aim of synchronizing the methods and allowing for worldwide comparison.

With regard to the prevalence of enamel hypoplasia, only 2.2% of subjects presented this enamel defect, which confirms the low prevalence reported previously 0.8% [16] to 7.6% [17]. Higher rates of enamel hypoplasia have been observed in children from developing countries, who suffered from malnutrition and/or low birth weight [18].

The literature shows that the prevalence of developmental defects of enamel varies around 24.4% [19] and 52% [16]. However, it has been suggested that age, sex or race have an influence on the development of some enamel defects. A higher prevalence of DDE in boys was reported by Robles et al in Spain [16], Li et al [20] in an Asian and Farsi [21] in an Arab population [16]. However, Chaves et al [22] did not find any difference in the occurrence of enamel defects in relation to sex. In the present study, the groups were comparable regarding sex, age and race.

Association studies involving enamel defects have been published [13, 23], even though most of them focused only on MIH and fluorosis. The studies that reported the coexistence between qualitative and quantitative enamel defects are descriptive in nature and do not provide information on the possible correlation between these two conditions [13, 24]. This association may be suggested, since all DDE are caused by complex interactions between genetic, systemic, and environmental factors that affect the structure of enamel during its formation [25]. Our results confirmed that patients with MIH have a higher prevalence of enamel hypoplasia. However, these defects did not affect the same tooth. The ameloblasts that caused the hypoplasic lesion were able to recover before the beginning of the mineralization phase. Furthermore, this same agent was able to damage the cells of other teeth that were in more advanced stages of amelogenesis, leading to hypomineralization lesions.

Amelogenesis is a complex process regulated by ameloblasts that occurs in two phases: secretory and mineralization. Any event that disturbs one of these phases may result in a qualitative or quantitative defect in tooth enamel [3]. Our results suggest that the same threatening agent may affect ameloblasts at different phases of amelogenesis in different teeth. This is because, although the aetiology of MIH and enamel hypoplasia is not fully elucidated yet, there are several studies suggesting that these defects may be the result of the same threatening agents [3, 4].

The reason why only a few teeth are affected by defects is still unknown, however some studies suggest that the period of damage to the enamel may be short lived, meaning that the ameloblasts may be able to recover or just sensitizing [16, 25]. Furthermore, the minimum time period needed to cause abnormal ameloblast function depends on the sensitivity of the ameloblasts to the harming factor and the power of that factor. However, the late secretion and/or early mineralization stages seem to be more sensitive to the appearance of DDE [11].

It is noticeable that, although several systemic factors have been associated with MIH and enamel hypoplasia, it is difficult to isolate the relative contribution of each due to their potential synergistic effects [11]. However, hypomineralized areas in molars may reflect the approximate period in which the insult has happened [3]. The present study has shown that the period of mineralization in which the molar region was affected and the period of enamel secretion in teeth affected by hypoplasia were similar. These results suggest that DDE may have shared the same etiological factor, especially in the first year of life, which the most critical period for enamel defects as it coincides with early mineralization [11].

In addition to environmental and systemic factors, it was suggested that a genetic predisposition would play a role in the development of enamel defects. Genomic research shows that certain genes are directly related to amelogenesis [25]. While other studies evaluating concordance of identical twins have led researchers to suggest an underlying genetic predisposition to the development of enamel hypoplasia and MIH [25, 26].

Studies on dental anomalies pattern reinforce the role of the genetic factor in the emergence of various developmental anomalies [7, 14]. However, only one study evaluated the correlation between enamel defects and other dental anomalies [8]. The author found a greater prevalence of dental anomalies such as agenesis of second premolars, microdontia of maxillary lateral incisors, infraocclusion of primary molars and palatally displaced canine in patients with enamel hypoplasia. This result was credited to the genetic component, so that the same defect in one gene may produces different phenotypes.

Studies suggest that MIH-affected teeth can be explained by the duration and period of the insult during enamel formation [18, 27]. Therefore, injuries in other teeth could be expected in cases of large magnitude insults. This pattern has been previously reported, showing that the risk of incisor involvement seemed to increase with the number of affected molars [28]. Our results showed that MIH lesions increase 12.45-fold the risk of enamel hypoplasia. However, the findings showed that the presence of enamel hypoplasia is not related to race or sex. A similar result was observed in previous studies [29, 30].

The present study has some limitations that must be considered for an adequate interpretation of the results. This is because this work did not assess the possible etiological factors of DDE. Longitudinal researches are needed to elucidate the etiology and the temporal sequencing of the occurrence of defects. Knowledge of the contribution of genetic, systemic and environmental factors in enamel defects will help in the diagnosis and risk assessment of affected children and also in counseling families about associated complications [25].

CONCLUSION

Patients with MIH have a higher prevalence of enamel hypoplasia and these defects seem to be consequences of the same threatening agent acting at different stages of amelogenesis.

ACKNOWLEDGMENTS

This work was carried out with the support of the Coordination for the Improvement of Higher Education Personnel–Brazil (CAPES)–Financing Code 88887.486387/2020-00.