ORIGINAL RESEARCH


https://doi.org/10.5005/jp-journals-10015-2344
World Journal of Dentistry
Volume 15 | Issue 1 | Year 2024

Prenatal, Natal, and Postnatal Risk Factors Associated with Molar Incisor Hypomineralization: Case–control Study


Malini Venugopal1https://orcid.org/0000-0002-2485-1809, Nishna Thankappan2, Vennila Chandran3, Rohith Radhakrishna4, Niveditha Kartha5, Lekshmi Anand6, Krupa R Robert7, Gopika MS Nair8

1–8Department of Pediatric and Preventive Dentistry, Amrita School of Dentistry, Amrita Institute of Medical Sciences (AIMS), Amrita Vishwa Vidyapeetham, Kochi, Kerala, India

Corresponding Author: Malini Venugopal, Department of Pediatric and Preventive Dentistry, Amrita School of Dentistry, Amrita Institute of Medical Sciences (AIMS), Amrita Vishwa Vidyapeetham, Kochi, Kerala, India, Phone: +91 7559064198, e-mail: mailtomalu85@gmail.com

Received: 05 December 2023; Accepted: 06 January 2024; Published on: 20 February 2024

ABSTRACT

Aim: The aim of the study is to investigate the association of molar-incisor hypomineralization (MIH) with prenatal, natal, and postnatal factors among children aged 7–12 years.

Materials and methods: It is a case–control study. The participants were first examined for the diagnosis of MIH as per European Academy of Paediatric Dentistry (EAPD) criteria 2003. A structured closed-ended questionnaire including potential etiological factors during prenatal, natal, and postnatal periods was constructed. A face-to-face interview was conducted with the mother, and the mother answered yes/no. Proposed risk factors were collected from exhaustive literature reviews.

Results: Prenatal risk factors were found to have a strong correlation with MIH. Among these, hypertension, chickenpox, and excessive consumption of medications showed a strong correlation. Thyroid, excessive vomiting, and abortion also showed a positive correlation. Low birth weight among natal factors, pneumonia, tonsillitis, prolonged breastfeeding, and multiple hospital admissions among postnatal factors were shown to have a strong correlation with MIH.

Conclusion: In the present study, the presence of prenatal and postnatal risk factors was significantly associated with a higher risk of developing MIH. A significantly higher prevalence of MIH was seen in children belonging to the lower middle socioeconomic section of the study population.

Clinical significance: It’s important to identify MIH groups at risk to reach an early diagnosis so that prevention can be initiated as soon as possible. MIH-affected teeth are 10 times more prone to treatment needs than normal counterparts. Awareness among pediatricians and gynecologists is highly recommended as adequate care for pregnant women and children during the first years of life is the key to the prevention of MIH. The dental follow-up of children who are exposed to risk factors during the perinatal stages is suggested for the timely diagnosis, preventive therapies, and treatment of MIH.

How to cite this article: Venugopal M, Thankappan N, Chandran V, et al. Prenatal, Natal, and Postnatal Risk Factors Associated with Molar Incisor Hypomineralization: Case–control Study. World J Dent 2024;15(1):36–43.

Source of support: Nil

Conflict of interest: None

How to cite this article: Venugopal M, Thankappan N, Chandran V, et al. Prenatal, Natal, and Postnatal Risk Factors Associated with Molar Incisor Hypomineralization: Case–control Study. World J Dent 2024;15(1):36–43.

Keywords: Molar Incisor hypomineralization, Perinatal history, Risk factors

INTRODUCTION

Molar-incisor hypomineralization (MIH) is defined as a specific developmental dental enamel defect affecting at least one first permanent molar with the involvement of permanent incisors.1,2 Amelogenesis is a complex process genetically controlled and largely influenced by environmental factors, and ameloblasts are chiefly responsible for enamel formation and mineralization during the process of amelogenesis. Any adverse impacts during the period of amelogenesis might lead to compromised mineralization of enamel, resulting in hypomineralization.3

The mineralization of the first permanent molar begins before birth and is completed around four years of age and is closely followed by the development of the upper central incisor. Hence, the cause of abnormal enamel formation must be present in this particular period. Maxillary lateral incisor, mandibular central, and lateral incisor are less involved; the difference in developmental timetable partly explains this. The explanation of the probable etiology of MIH needs a thorough knowledge of risk factors during prenatal, natal, and postnatal periods. A variety of risk factors are reported in the literature for the occurrence of MIH, like viral infections, episodes of high fever, hypertension, medications, stress during pregnancy, consumption of alcohol, and smoking during the prenatal period. Premature birth, underweight, cesarean section, hypoxic conditions, and other complications during pregnancy were considered as natal factors. Postnatal factors shown were early childhood illnesses like pyrexia, chicken pox, asthma, ear infections, antibiotics, and asthmatic drugs.4,5

MIH can be visualized as an abnormality in the translucency of the tooth. The defect in MIH is shown as a demarcated opaque area on the MIH-affected tooth surface, which is clearly distinguished from surrounding sound enamel. The color of the enamel varies from creamy white till yellowish brown.6 The dental enamel of teeth affected by MIH is porous and soft clinically due to the presence of disorganized and weakly attached prisms, which also favors greater microbial proliferation and, consequently, when associated with other factors, results in the establishment of dental caries. MIH results in atypical cavities requiring extensive restorative treatment.

The MIH-affected tooth is fragile and can fracture easily due to reduced hardness and elastic modulus. Severely affected molars undergo fracture soon after their eruption into the oral cavity due to masticatory forces, which is classified as posteruption breakdown.7

There is sensitivity, in most cases, to cold, heat, or mechanical trauma, and brushing is usually painful, due to which the child becomes reluctant to carry out appropriate oral hygiene practices and to undergo dental procedures. They also develop dental phobias and present with behavioral problems, which become difficult to manage clinically.8 Therapeutic interventions become very challenging among pediatric patients with MIH. Affected incisors, particularly the maxillary teeth, are another major concern due to their unesthetic appearance, which worries parents and the child. MIH tends to negatively impact the child’s self-oral perception and the perception of the family regarding their child’s oral health.9 Therefore, MIH is regarded as the most challenging dental disease worldwide, creating a major treatment burden.

The prevalence of MIH varies widely, ranging from 2.8 to 40.2%.10,11 In Kerala, studies conducted in 2019 and 2020 showed the prevalence of MIH among children ranging from 4 to 23.6.%.12,13 With increasing prevalence, a thorough insight into the risk factors is necessary, which will help in early diagnosis, planning preventive strategies, and minimizing the need for extensive treatment procedures. To date, there are no conclusive data regarding the etiology of MIH. The number of studies in the southern part of India is limited. Hence, owing to the cultural and demographic differences, the current study aimed to investigate the association of MIH with prenatal, natal, and postnatal risk factors and the mother’s demographic background among 7–12 years children in the Kerala population and to compare these with an age-matched control selected from the same population.

MATERIALS AND METHODS

A case–control study was carried out at the Department of Pediatrics and Preventive Dentistry in a tertiary health care center in Kerala. The period of the study was from August 2022 to January 2023. Institutional Ethical Committee approval ECASM-AIMS-2022-154A was obtained. Informed consent was collected from the child’s mother before the start of the study.

Study Population

Healthy children, both boys and girls, between the age group of 7 and 12 years, visiting the outpatient department of pediatric and preventive dentistry in a tertiary health care center in Kerala, were selected for the study as cases as well as controls to avoid selection bias. Based on the Odds ratio of etiological factors contributing to MIH in comparison with the control group, observed from an existing literature14 and with 80% power and 95% confidence, the minimum sample size came to 127. The minimum sample size for each case in the study was 127, and an equal number of control samples were also taken.

Children having hypomineralized defects with demarcated borders on any of the permanent first molars were considered as cases as per European Academy of Paediatric Dentistry (EAPD) criteria 2003 for MIH.15 The involvement of incisors was not necessary. At least one of the incisors and all four molars should be erupted to be included in the study. In case of any doubt regarding the presence of MIH, the child was excluded from the final sample. Children with fluorosis, enamel hypoplasia, and amelogenesis imperfecta and parents who declined consent were excluded from the study. For the selection of the control group, children included were within the same age group and visiting the same tertiary health care center but without MIH. Children with fluorosis, enamel hypoplasia, amelogenesis imperfecta, and parents who declined consent were excluded from the study.

Questionnaire

Prior to the study, multiple and comprehensive calibrations were carried out by the principal investigator and coinvestigator. The investigators specialized in pediatric dentistry and were well-trained in the recognition of cases with MIH. Children diagnosed with MIH were further examined by an expert to rule out any bias. One single sheet, a structured questionnaire consisting of 38 close-ended questions which included potential etiological factors during prenatal (11 questions), natal (seven questions), and postnatal period till the first 4 years of life (15 questions), according to the timing of MIH occurrence were asked to the child’s mother. Questions about sociodemographic status (five questions) were also added based on the modified Kuppuswamy scale16 (Table 1). Socioeconomic status was calculated based on cumulative scores of education of the head of the family (scores ranging from 1 to 7), occupation of the head of the family (scores ranging from 1 to 10), and total per capita family income per month (scores ranging from 1 to 12). Based on the total score, gradation was done into socioeconomic classes: upper (score 26–29), upper middle (score 16–25), middle lower (score 11–15), lower upper (score 5–10), and lower (score <5).

Table 1: Questionnaire about socioeconomic background and potential etiological factors
Sociodemographic details
Maternal age during pregnancy In years
Gender of the child Boy/girl
Birth order First/second/third 
Consanguineous marriage Yes/no
Socioeconomic status modified Kuppuswamy scale (2022) Occupation/education/income
Prenatal history
Anemia/malnutrition Yes/no
Diabetes Yes/no
Hypertension Yes/no
Frequent episodes of fever (more than three episodes) Yes/no
Renal deficiency Yes/no
Thyroid/parathyroid Yes/no
Chickenpox Yes/no
Excessive vomiting Yes/no
Prolonged consumption of medicines Yes/no
Abortion Yes/no
Intrauterine growth retardation Yes/no
Natal history
Type of birth Yes/no
Prolonged/complicated delivery
(respiratory distress and birth asphyxia)
Yes/no
Preterm delivery specified (before 37 weeks of pregnancy) Yes/no
Hemorrhage
(detachment during delivery)
Yes/no
Cyanosis Yes/no
Twins Yes/no
Low birth weight (<2.5 kgs) Yes/no
Postnatal history
Otitis media Yes/no
Fever Yes/no
Chickenpox Yes/no
Kidney disease Yes/no
Allergy asthma Yes/no
Pneumonia Yes/no
Seizures–afebrile Yes/no
Exanthematous diseases (incubator) Yes/no
Bronchitis Yes/no
Tonsillitis Yes/no
Urinary tract infections Yes/no
Gastrointestinal tract (GIT) disorders Yes/no
Neonatal jaundice Yes/no
Hospital admission Yes/no
Duration of hospital admission Less than seven times/more than seven times

The questionnaire was prepared both in English and Malayalam (local Language). The proposed questionnaire for the risk factors was prepared based on thorough research of existing literature reviews.14,17 Questionnaires were validated by an expert committee consisting of experienced pediatric dentists, and their suggestions were used to refine the questionnaire. Questions about smoking and drinking during pregnancy were not included owing to the negligence of these habits among the population considered. A pilot study was conducted among 30 subjects visiting the hospital to ensure the questionnaire’s reliability. The questionnaires were filled by a single examiner using face-to-face interviews with the mother to decrease the risk of bias in recording risk factors. The mother answered the questions as yes/no. The questions were easily understood by the mothers regardless of their educational status. There was no need to bring any changes to the questionnaire after the pretest. The maximum time taken to complete the questionnaire was 5 minutes.

The examination was carried out in the dental chair. Any gross debris, if present, was removed using sterilized cotton gauze. During examination, teeth were kept wet to rule out opacities due to the effect of drying. It was a participant-blinded study, and MIH diagnosis was not disclosed to mothers before filling out questionnaires.

Statistical Details

The analysis was done using IBM Statistical Package for the Social Sciences, version 20 for Windows. Categorical data was presented as numbers and percentages. The Chi-squared test was used to test the statistical significance of the association of all prenatal, natal, and postnatal factors with MIH. Multivariate binary logistic regression analysis was used to identify the predictor of MIH. A p-value of <0.05 was considered statistically significant.

RESULTS

A total of 254 children in the age group of 7–12 years who visited the outpatient department of the Department of Pediatric and Preventive Dentistry were enrolled in the current study. The study group consisted of 127 children with MIH, and the control group consisted of 127 children without MIH. Out of the total 254 samples, 129 (50.8%) were girls and 125 (49.2%) were boys. The difference in gender was not significant in the present study. Among the total sample, 95 (37.4%) belonged to the upper class, 82 (32.3%) belonged to the upper middle class, and 77 (30.3%) belonged to the lower middle class. Table 2 describes the baseline characteristics of sociodemographic, prenatal, natal, and postnatal factors.

Table 2: Baseline characteristics of potential risk factors during the prenatal, natal, and postnatal period
Variables Frequency (%)
Anemia/malnutrition (present) 13 (5.1%)
Diabetes (present) 23 (9.1%)
Hypertension (present) 13 (5.1%)
Fever (more than three episodes) (present) 16 (6.3%)
Renal deficiency (present) 1 (0.4%)
Thyroid/parathyroid (present) 20 (7.9%)
Chicken pox (present) 17 (6.7%)
Excessive vomiting (present) 52 (20.5%)
Prolonged medicine consumption (present) 21 (8.3%)
Abortion (present) 27 (10.6%)
Vitamin D deficiency (present) 13 (5.1%)
Intrauterine growth retardation (present) 4 (1.6%)
Type of birth (cesarean) 119 (46.9%)
Prolonged/complicated delivery (present) 20 (7.9%)
Preterm delivery (present) 21 (8.3%)
Hemorrhage (present) 5 (2.0%)
Cyanosis (present) 3 (1.2%)
Twins (present) 4 (1.6%)
Low birth weight (<2.5 kg) (present) 37 (14.6%)
Otitis media (present) 12 (4.7%)
Frequent episodes of fever (present) 36 (14.2%)
Chicken pox (present) 14 (5.5%)
Kidney disease (present) 3 (1.2%)
Allergy asthma (present) 32 (12.6%)
Pneumonia (present) 13 (5.1%)
Seizures—afebrile (present) 7 (2.8%)
Exanthematous diseases (present) 8 (3.1%)
Bronchitis (present) 12 (4.7%)
Tonsillitis (present) 21 (8.3%)
Urinary tract infections (present) 8 (3.1%)
GIT disorders (present) 7 (2.8%)
Neonatal jaundice (present) 14 (5.5%)
Bottle-feeding (present) 49 (19.3%)
Duration of hospital admission (less than seven times) 55 (21.7%)

Sociodemographic Details

The distribution of MIH did not differ between boys and girls. The birth order also showed no statistically significant difference in the occurrence of MIH between cases and control. Maternal age showed a positive correlation with MIH. The maximum number of cases was seen in the maternal age group between 26 and 32 (55.1 vs 38.6%, p-value of <0.001). The lower middle class (37 vs 29.9%, p-value of <0.022) showed significantly higher cases than the upper class. Table 3 shows a univariate analysis of associates of sociodemographic details.

Table 3: Risk factors analysis between study and control group (univariate analysis of associates of all variables)
Variables Group p-value
Cases Controls
Gender Male 64 61 0.707
Female 63 66
Birth order First 74 63 0.340
Second 42 53
Third 11 11
Maternal age 18–25 42 78 <0.001
26–32 70 49
≥33 15 0
Socioeconomic status Upper class 38 57 0.022
Upper middle 42 40
Lower middle 47 30
Consanguineous marriage Yes 2 0 0.478
No 125 127
Anemia/malnutrition Yes 9 4 0.155
No 118 123
Diabetes Yes 12 11 0.827
No 115 116
Hypertension Yes 11 2 0.010
No 116 125
Fever (more than three episodes) Yes 16 0 <0.001
No 111 127
Renal deficiency Yes 1 0 1.000
No 126 127
Thyroid/parathyroid Yes 16 4 0.005
No 111 123
Chicken pox Yes 15 2 0.001
No 112 125
Excessive vomiting Yes 33 19 0.029
No 94 108
Prolonged medicine consumption Yes 19 2 <0.001
No 108 125
Abortion Yes 22 5 0.001
No 105 122
Vitamin D deficiency Yes 7 6 0.776
No 120 121
Intrauterine growth retardation Yes 2 2 1.000
No 125 125
Type of birth Natural 70 65 0.530
Cesarean 57 62
Prolonged/complicated delivery Yes 14 6 0.062
No 113 121
Preterm delivery Yes 7 14 0.111
No 120 113
Hemorrhage Yes 1 4 0.175
No 126 123
Cyanosis Yes 3 0 0.245
No 124 127
Twins Yes 4 0 0.131
No 123 127
Low birth weight (<2.5 kg) Yes 27 10 0.004
No 100 117
Otitis media Yes 123 119 0.237
No 4 8
Frequent episodes of fever Yes 22 14 0.150
No 105 113
Chickenpox Yes 10 4 0.099
No 117 123
Kidney disease Yes 2 1 1.000
No 125 126
Allergy asthma Yes 18 14 0.449
No 109 113
Pneumonia Yes 10 3 0.046
No 117 124
Seizures—afebrile Yes 4 3 1.000
No 123 124
Exanthematous disease Yes 5 3 0.719
No 122 124
Bronchitis Yes 9 3 0.076
No 118 124
Tonsillitis Yes 17 4 0.003
No 110 123
Urinary tract infections Yes 2 6 0.281
No 125 121
GIT disorders Yes 4 3 1.000
No 123 124
Neonatal jaundice Yes 8 6 0.582
No 119 121
Bottle-feeding Yes 35 14 0.001
No 92 113
Duration of hospital admission More than seven times 36 19 0.010
Less than seven times 91 108

Prenatal Period

Of the various prenatal risk factors examined, univariate regression analysis showed hypertension (8.7 vs 1.6%, p < 0.010) and prolonged consumption of medications during pregnancy (15.0 vs 1.6%, p < 0.029) and chickenpox (15 vs 2%, p < 0.001) were found to be very high in the MIH group. Abortion (17.3 vs 3.9%, p < 0.001), thyroid (12.6 vs 3.1%, p < 0.005), and excessive vomiting (26.0 vs 15%, p < 0.001) were found to be statistically significant in the MIH group. Frequent episodes of fever (more than three times) were also found to be statistically significant in the study group (p < 0.001) (Table 3).

Natal Period

Among the natal risk factors, univariate regression analysis showed low birth weight (21.3 vs 7.9%, p < 0.004) was found to be statistically significant in the MIH group. Prolonged/complicated delivery (11.0 vs 4.7%) was also shown to be a potential etiological factor (Table 3).

Postnatal Period

During the postnatal period, the univariate regression analysis showed childhood diseases like pneumonia (7.9 vs 2.4%, p > 0.046) and tonsillitis (13.4 vs 3.1%, p > 0.03) were found to be very high in the MIH group. However, prolonged breastfeeding beyond 1 year (27.6 vs 11.0%, p > 0.001) and hospital admission (13.4 vs 3.1%, p > 0.010) were also found to be statistically significant in the study group (Table 3).

Multivariate logistic analysis was done, and the results are tabulated in Table 4. The results showed children whose mothers consumed medications for longer periods during pregnancy [odds ratio (OR) = 6.353], contracted chicken pox during pregnancy (OR = 5.690), or had hypertension during pregnancy (OR = 4.258) were at a very high risk of developing MIH. However, tonsillitis (OR = 4.997), pneumonia (OR = 3.716), abortions (OR = 2.421), thyroid during pregnancy (OR = 2.644), Excessive vomiting (OR = 1.36) were also found to be potential risk factors in the development of MIH. Low birth weight (OR = 2.05), breastfeeding (OR = 1.36), and multiple hospital admissions (OR = 0.618) were also shown to have high risk.

Table 4: Association between the risk factors studied and development of MIH in 7–12-year-old children with MIH (multivariate analysis of variables)
Variables OR (95% confidence interval) p-value
Socioeconomic status (upper class) 1 0.182
Socioeconomic status (upper middle) 1.764 0.110
Socioeconomic status (lower middle) 1.799 0.118
Hypertension (present) 4.258 0.084
Thyroid/parathyroid (present) 2.644 0.132
Chickenpox (present) 5.690 0.033
Excessive vomiting (present) 1.364 0.421
Prolonged medicine consumption (present) 6.353 0.022
Abortion (present) 2.421 0.129
Low birth weight (<2.5 kg) (present) 2.052 0.115
Pneumonia (present) 3.716 0.086
Tonsillitis (present) 4.997 0.010
Bottle-feeding (present) 2.121 0.062
Duration of hospital admission (present) 0.618 0.207
Constant 0.421 0.038

DISCUSSION

Hypomineralized enamel results from amelogenesis disruption during the late maturation stage, which starts in the last trimester and finishes around 3 years postnatal. Therefore, adverse health events during prenatal, perinatal, and postnatal periods may result in a dental structural defect.9 The present study focused on the association between various risk factors for MIH during prenatal, natal, and postnatal periods among children with MIH and children without MIH. For this purpose, 127 children in the age group of 7–12 years with MIH were selected, and the mothers were asked for potential risk factors during the prenatal, natal, and postnatal periods. An equal number of control samples were taken, and history was recorded from their mothers for potential risk factors.

The present study showed children with low birth weight had twice the chance of developing MIH than normal-weight children. Studies reported by Kusku et al., Whatling and Fearne, Arrow, and Aine et al. showed similar results.18,21 The most likely explanation is that the associated immature calcium metabolism can affect ameloblast activity and the formation of immature enamel matrix.21,22

Of the various prenatal factors involved, chickenpox during pregnancy showed a strong correlation with MIH in the present study. Similar results were reported by Koruyucu et al.23 They found that complications during the mother’s pregnancy, like the frequency of diarrhea, asthma, a frequent high fever, chickenpox, and parotitis, can increase the chances of MIH. The reason may be reduced transfer of essential nutrients leading to chronic hypocalcemia due to compromised health conditions.21

Based on current results, excessive vomiting can be considered one of the etiological factors in MIH. The reason may be compromised fluids and electrolytes, as well as nutritional status, occasionally leading to fetal biochemical disturbance, as reported by Basso et al.24

In the present study, prolonged consumption of medications (mainly antibiotics) was found to be significantly associated with MIH. Studies by Whatling and Fearne, Aggarwal et al., Lygidakis et al., and Butera et al. concluded that prescribed medication is a potential etiological factor of MIH.19,22,25,26

On the other hand, a systematic review by Serna et al. showed that prescribed medicine was not significantly connected with MIH.27 However, there are controversies in this context, as either the medications or the disease could be involved in the etiology of the enamel defect.25

The present study also showed an association between MIH and hypertension during pregnancy. Previous studies by Portella et al., Crombie et al., and Elsori and Hammoud suggested that maternal illnesses during pregnancy, such as gestational diabetes, hypocalcemia, hypertension, and preeclampsia, are more frequent in women who present low vitamin D levels.9,28,29 This micronutrient has the main function of maintaining constant plasma calcium concentrations, playing an important role in stimulating the mineralization of tooth enamel.30 Thus, this may be a possible explanation for the association between MIH and some pregnancy health problems.

In the current study, hypothyroidism in mothers during pregnancy caused MIH in children around three times more than without hypothyroidism. A study by Schwarz et al. showed that levels of thyroid stimulating hormone and T3 are significantly associated with levels of phosphate and calcium, respectively. In light of all of the evidence reported in these studies, the present study suggests that hypothyroidism may also cause the formation of MIH during odontogenesis because of its effects on bone development and calcium balance in the body.31

Abortions were also associated with MIH, according to current results. Similar results were also reported by Mariam et al.17 Portella et al., in their studies on MIH etiology, reported that children whose mothers had health problems during the prenatal period had 40% higher odds of MIH than children whose mothers had no problems during this same period.9

Associations have been made between the presence of polychlorinated dibenzo-dioxins in breast milk and enamel hypomineralization in both clinical and laboratory studies.

In infancy, children can be exposed to these compounds mainly via breastfeeding. Several studies by Alaluusua et al., Fagrell et al., and Jan et al. reported that long breastfeeding with environmental contaminants in the human milk increases the risk for enamel opacities resulting in disturbances of amelogenesis32,35

The present study also showed mothers who breastfed for longer duration had two times more risk of developing MIH than others. However, a study by Crombie et al. did not agree with these findings. They concluded that the role of breastfeeding in the causation of MIH is not significant.28

In another study by Mariam et al., short duration of breastfeeding and early introduction of bottle feed were associated with MIH.17

In the current study, pneumonia during early childhood showed around four times higher chances of developing MIH than others. Similar studies were reported in various other studies by Arrow, Serna et al., and Lygidakis et al.20,27,36 Higher frequency of respiratory problems like pneumonia, tonsillitis which results in multiple hospital admissions, was found to have a strong association with the occurrence of MIH. The reason is oxygen shortage, associated with respiratory diseases, which can affect the ameloblastic activity and the pH formation stage of the enamel matrix, resulting in enamel defects. Similar results were reported in various other studies by Fagrell et al., Lygidakis et al., Ghanim et al.34,36,37

The influence of socioeconomic status on the prevalence of MIH was observed in the present study group. A significantly higher prevalence was seen in children belonging to the lower and upper middle socioeconomic section when compared to the upper middle class. The plausible reason may be reduced nutrition and higher chances of infection during the prenatal and postnatal period, which in turn may affect amelogenesis.17 However, other studies have shown the prevalence of MIH among the upper class.38

In a systematic review and meta-analysis on etiological factors of molar incisor hypomineralization by Juárez-López et al., illnesses during pregnancy, low birth weight, and illnesses during the first years of life were related to the occurrence of MIH, which is similar to the current study.39 However, in another systematic review and meta-analysis by Garot et al., natal and postnatal factors were more associated with molar incisor hypomineralization.40

The precise knowledge about the risk factors of MIH is still lacking. The prevalence of MIH is becoming alarmingly high all over the world. No studies have been reported to date exploring etiological factors associated with MIH among children in the Kerala population. This manuscript strengthens the existing data on potential risk factors associated with MIH and henceforth will guide us to avoid the possible risk factors related to the high occurrence of MIH. Sociodemographic details of the mother will give an insight into the etiological factors related to the specified demographical area of the current study.

Limitations

In the present study, however, history for etiological factors was taken through an interview with the mother. There are high chances of recall bias in this type of study. Many important details regarding the health status of the child as well as the mother during pregnancy could have been missed, which were felt insignificant by the mother.

CONCLUSION

Within the limitations of the study, it can be concluded that the etiology of MIH is multifactorial. Any disturbances during the period of amelogenesis, which corresponds to pregnancy, delivery, and early childhood, can result in hypomineralized enamel. In the present study, the presence of prenatal and postnatal risk factors was significantly associated with a higher risk of developing MIH. A significantly higher prevalence of MIH was seen in children belonging to the lower middle-class socioeconomic section of the study population.

ORCID

Malini Venugopal https://orcid.org/0000-0002-2485-1809

REFERENCES

1. Weerheijm KL, Jalevik B, Alaluusua S. Molar-incisor hypomineralisation. Caries Res 2001;35(5):390–391. DOI: 10.1159/000047479

2. Lygidakis NA, Garot E, Somani C, et al. Best clinical practice guidance for clinicians dealing with children presenting with molar-incisor-hypomineralisation (MIH): an updated European Academy of Paediatric Dentistry policy document. Eur Arch Paediatr Dent 2022;23(1):3–21. DOI: 10.1007/s40368-021-00668-5

3. Suga S. Enamel hypomineralisation viewed from pattern of progressive mineralisation of human and monkey developing enamel. Adv Dent Res 1989;3:188–198. DOI: 10.1177/08959374890030021901

4. Jeremias F, Koruyucu M, Küchler EC, et al. Genes expressed in dental enamel development are associated with molar-incisor hypomineralization. Arch Oral Biol 2013;58(10):1434–1442. DOI: 10.1016/j.archoralbio.2013.05.005

5. Fatturi AL, Wambier LM, Chibinski AC, et al. A systematic review and meta-analysis of systemic exposure associated with molar incisor hypomineralization. Community Dent Oral Epidemiol 2019;47(5):407–415. DOI: 10.1111/cdoe.12467

6. Beentjes VE, Weerheijm KL, Groen HJ. Factors involved in the aetiology of molar-incisor hypomineralisation (MIH). Eur J Paediatr Dent 2002;3(1):9–13. PMID: 12871011.

7. Weerheijm KL. Molar incisor hypomineralization (MIH): clinical presentation, aetiology and management. Dent Update 2004;31(1):9–12. DOI: 10.12968/denu.2004.31.1.9

8. Jalevik B, Klingberg GA. Dental treatment, dental fear and behaviour management problems in children with severe enamel hypomineralization of their permanent first molars. Int J Paediatr Dent 2002;12(1):24–32. DOI: 10.1046/j.0960-7439.2001.00318.x

9. Portella PD, Menoncin BLV, de Souza JF, et al. Impact of molar incisor hypomineralization on quality of life in children with early mixed dentition: a hierarchical approach. Int J Paediatr Dent 2019;29(4):496–506. DOI: 10.1111/ipd.12482

10. Elfrink ME, Ghanim A, Manton DJ, et al. Standardised studies on molar incisor hypomineralisation (MIH) and hypomineralised second primary molars (HSPM): a need. Eur Arch Paediatr Dent 2015;16(3):247–255. DOI: 10.1007/s40368-015-0179-7

11. Lopes LB, Machado V, Mascarenhas P, et al. The prevalence of molar-incisor hypomineralization: a systematic review and meta-analysis. Sci Rep 2021;11(1):22405. DOI: 10.1038/s41598-021-01541-7

12. Emmatty TB, Eby A, Joseph MJ, et al. The prevalence of molar incisor hypomineralization of school children in and around Muvattupuzha, Kerala. J Indian Soc Pedod Prev Dent 2020;38(1):14. DOI: 10.4103/JISPPD.JISPPD_152_18

13. Peedikayil FC, Tomy NC, Chandru TP, et al. Molar incisor hypomineralization in North Malabar: an epidemiological study. Dent Med Res 2019;7(2):40.DOI: 10.4103/dmr.dmr_10_19

14. Elzein R, Chouery E, Abdel-Sater F, et al. Molar-incisor hypomineralisation in Lebanon: association with prenatal, natal and postnatal factors. Eur Arch Paediatr Dent 2021;22(2):283–290. DOI: 10.1007/s40368-020-00555-5

15. Weerheijm KL, Duggal M, Mejare I, et al. Judgement criteria for molar incisor hypomineralisation (MIH) in epidemiologic studies: a summary of the European meeting on MIH held in Athens, 2003. Eur J Paediatr Dent 2003;4(3):110–113. PMID: 14529329.

16. Kumar G, Dash P, Patnaik J, et al. Socioeconomic status scale-Modified Kuppuswamy Scale for the year 2022. Int J Comm Dent 2022;10(1):1–6. DOI: 10.56501/intjcommunitydent.v10i1.26

17. Mariam S, Goyal A, Dhareula A, et al. A case-controlled investigation of risk factors associated with molar incisor hypomineralization (MIH) in 8-12 year-old children living in Chandigarh, India. Eur Arch Paediatr Dent 2022;23(1):97–107. DOI: 10.1007/s40368-021-00665-8

18. Kusku OO, Caglar E, Sandalli N. The prevalence and aetiology of molar-incisor hypomineralisation in a group of children in Istanbul. Eur J Paediatr Dent 2008;9(3):139–144. PMID: 18844443.

19. Whatling R, Fearne JM. Molar incisor hypomineralization: a study of aetiological factors in a group of UK children. Int J Paediatr Dent 2008;18(3):155–162. DOI: 10.1111/j.1365-263X.2007.00901.x

20. Arrow P. Prevalence of developmental enamel defects of the first permanent molars among school children in Western Australia. Aus Dent J 2008;53(3):250–259. DOI: 10.1111/j.1834-7819.2008.00057.x

21. Αine L, Backström MC, Mäki R, et al. Enamel defects in primary and permanent teeth of children born prematurely. J Oral Pathol Oral Med 2000;29(8):403–409. DOI: 10.1034/j.1600-0714.2000.290806.x

22. Aggarwal R, Upadhyay M, Deorari AK, et al. Hypocalcemia in the newborn. Indian J Pediatr 2001;68(10):973–975. DOI: 10.1007/BF02722599

23. Koruyucu M, Özel S, Tuna EB. Prevalence and etiology of molar-incisor hypomineralization (MIH) in the city of Istanbul. J Dent Sci 2018;13(4):318–328. DOI: 10.1016/j.jds.2018.05.002

24. Basso AP, Ruschel HC, Gatterman A, et al. Hipomineralização molar-incisivo. Rev Odonto Cienc 2007;22(58):371–376. PMID: 487220.

25. Lygidakis NA, Wong F, Jälevik B, et al. Best clinical practice guidance for clinicians dealing with children presenting with molar-incisor-hypomineralisation (MIH): an EAPD policy document. Eur Arch Paediatr Dent 2010;11(2):75–81. DOI: 10.1007/BF03262716

26. Butera A, Maiorani C, Morandini A, et al. Assessment of genetical, pre, peri and post natal risk factors of deciduous molar hypomineralization (DMH), hypomineralized second primary molar (HSPM) and molar incisor hypomineralization (MIH): a narrative review. Children (Basel) 2021;8(6):432. DOI: 10.3390/children8060432

27. Serna C, Vicente A, Finke C, et al. Drugs related to the etiology of molar incisor hypomineralization: a systematic review. J Am Dent Assoc 2016;147(2):120–130. DOI: 10.1016/j.adaj.2015.08.011

28. Crombie F, Manton D, Kilpatrick N. Aetiology of molar-incisor hypomineralization: a critical review. Int J Paediatr Dent 2009;19(2):73–83. DOI: 10.1111/j.1365-263X.2008.00966.x

29. Elsori DH, Hammoud MS. Vitamin D deficiency in mothers, neonates and children. J Steroid Biochem Mol Biol 2018;175:195–199. DOI: 10.1016/j.jsbmb.2017.01.023

30. van der Tas JT, Elfrink MEC, Heijboer AC, et al. Foetal, neonatal and child vitamin D status and enamel hypomineralization. Community Dent Oral Epidemiol 2018;46(4):343–351. DOI: 10.1111/cdoe.12372

31. Schwarz C, Leichtle AB, Arampatzis S, et al. Thyroid function and serum electrolytes: does an association really exist? Swiss Med Wkly 2012;17:142. DOI: 10.4414/smw.2012.13669

32. Alaluusua S. Aetiology of molar-incisor hypomineralisation: a systematic review. Eur Arch Paediatr Dent 2010;11(2):53–58. DOI: 10.1007/BF03262713

33. Jan J, Vrbic V. Polychlorinated biphenyls cause developmental enamel defects in children. Caries Res 2000;34(6):469–473. DOI: 10.1159/000016625

34. Fagrell TG, Ludvigsson J, Ullbro C, et al. Aetiology of severe demarcated enamel opacities–an evaluation based on prospective medical and social data from 17,000 children. Swed Dent J 2010;35(2):57–67. PMID: 21827015.

35. Alaluusua S, Lukinmaa PL, Koskimies M, et al. Developmental dental defects associated with long breast feeding. Eur J Oral Sci 1996;104(5-6):493–497. DOI: 10.1111/j.1600-0722.1996.tb00131.x

36. Lygidakis NA, Dimou G, Marinou D. Molar-incisor-hypomineralisation (MIH). A retrospective clinical study in Greek children. II. Possible medical aetiological factors. Eur Arch Paediatr Dent 2008;9(4):207–217. DOI: 10.1007/BF03262637

37. Ghanim A, Manton D, Bailey D, et al. Risk factors in the occurrence of molar-incisor hypomineralization amongst a group of Iraqi children. Int J Paediatr Dent 2013;23(3):197–206. DOI: 10.1111/j.1365-263X.2012.01244.x

38. Balmer R, Toumba J, Godson J, et al. The prevalence of molar incisor hypomineralisation in Northern England and its relationship to socioeconomic status and water fluoridation. Int J Paed Dent 2012;20(22):250–257. DOI: 10.1111/j.1365-263X.2011.01189.x

39. Juárez-López MLA, Salazar-Treto LV, Hernández-Monjaraz B, et al. Etiological factors of molar incisor hypomineralization: a systematic review and meta-analysis. Dent J (Basel) 2023;11(5):1–16. DOI: 10.3390/dj11050111

40. Garot E, Rouas P, Somani C, et al. An update of the aetiological factors involved in molar incisor hypomineralisation (MIH): a systematic review and meta-analysis. Eur Arch Paediatr Dent 2022;23(1):23–38. DOI: 10.1007/s40368-021-00646-x

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