Study of Developmental Defects of Enamel in Young Permanent Maxillary Incisors in 11–13-year-old Indian Children for Occurrence Distribution and Associated Factors
Corresponding Author: Neha Sheoran, Department of Pedodontics and Preventive Dentistry, Sudha Rustagi College of Dental Sciences & Research, Faridabad, Haryana, India, e-mail: firstname.lastname@example.org
Purpose: The aim of present study was to assess the frequency, severity, and distribution of developmental defects of tooth enamel and correlate the etiology with the type of defect in 11–13-year-old Indian children.
Materials and methods: The present study included examination of permanent maxillary incisors in 500 children in the age-group of 11–13 years to examine the occurrence of distribution of developmental defects of tooth enamel.
Materials and methods: Only the buccal surface of four permanent maxillary incisors was examined for enamel defects using modified developmental defects of enamel (DDE) index by Clarkson which recognized three basic types of enamel defects; namely demarcated opacities, diffuse opacities, and hyploplsia. Personnel details, dental history which included dental infection, extraction, trauma, lifetime fluoride, fluoride in water, and medical history were also recorded. Data was coded and analyzed for distribution of developmental defects of tooth enamel by tooth type and gender using Statistical Package for the Social Sciences.
Result: Out of 500, 114 (22.8%) children showed defective enamel in permanent maxillary incisors. Of all enamel defects, diffuse opacities were most prevalent with 48.25% occurrence followed by demarcated opacities 38.5%, hypoplasia 10.52%, and any other defects 1.75%. No significant difference was observed in males and females for the occurrence of developmental enamel defects. The occurrence of dental enamel defect significantly correlated with dental history as well as with medical history (Chi-squared statistical test, p-value = 0.001**).
Conclusion: (1) High fluoride in water accounts for most prevalent diffuse opacity. (2) Demarcated opacities are associated mainly with positive dental history. (3) Hypoplasia of incisors was found to be least prevalent associated with trauma, periapical infections.
How to cite this article: Sheoran N, Garg S, Dhindsa A, et al. Study of Developmental Defects of Enamel in Young Permanent Maxillary Incisors in 11–13-year-old Indian Children for Occurrence Distribution and Associated Factors. Int J Clin Pediatr Dent 2023;16(S-2):S176–S182.
Source of support: Nil
Conflict of interest: None
Keywords: Anterior teeth, Demarcated opacities, Esthetics
Enamel on teeth is not like any other tissue. In vertebrates, it is the toughest tissue due to its high degree of structure and mineralization. Tooth enamel is tough, yet it may nevertheless be affected by developing enamel abnormalities.1 Hypoplasia, defined opacities, diffuse opacities, and discolored enamel are only a few of the clinical manifestations of developmental enamel abnormalities, which may either be qualitative or quantitative in character. Different types of enamel defects are thought to be caused by disturbances occurring at various points in the amelogenesis process.
It is vital to remember that permanent incisors and molars are the first teeth to undergo calcification,2 therefore they’re also the ones most likely to have enamel abnormalities. The hard tissue formation begins at the age of 3–4 months for permanent central incisors and 10–12 months for permanent lateral incisors. Both the incisors complete their enamel formation by the age of 4–5 years. Because of how long teeth develop, several potential causes of enamel abnormalities have time to manifest throughout this time. Diseases and medications, such as tetracycline and fluoride, can also contribute to systemic factors. “These include genetic predisposition, chromosomal abnormalities, congenital defects, inborn errors of metabolism, neonatal disturbances, infectious diseases, neurological disturbances, endocrinopathies, nutritional deficiencies, nephropathies, enteropathies, and liver diseases.” Primary teeth are more vulnerable to trauma and develop periapical osteitis.3
Enamel abnormalities are quite common in today’s societies, with estimates “ranging from 63 to 68% among Caucasians in New Zealand, Ireland, and England to 95–99% among Hong Kong Chinese.4 Children’s teeth affected by fluorosis have been observed to be unattractive in a number of Indian studies. However, there is a lack of research on the incidence of developing enamel abnormalities and their causes in India.5 The purpose of this research was to determine the prevalence, severity, and geographic distribution of dental enamel developmental abnormalities in Indian children aged 11–13, and to connect the etiology of each defect type with its prevalence.”
MATERIALS AND METHODS
The current research was conducted at M.M. College of Dental Sciences and Research at the Department of Pedodontics and Preventive Dentistry in Ambala, Haryana, India. The study looked at the prevalence of developmental abnormalities in tooth enamel by examining 500 children’s permanent maxillary incisors between the ages of 11 and 13. The Ethics Committee of Maharishi Markandeshwar University in Ambala, Haryana, India, gave its stamp of approval to this research.
Initial screening of schools was done before to finally examine 500 children from a homogeneous group of the population for the study. For the needed age range of 11–13 years old, researchers chose three local schools for their prevalence study. The letters of permission were obtained from the relevant school administrations. The student’s age was verified by both the official birth certificate and the student’s school records.
The preformed patient assessment form 1 to be filled by parents was explained and distributed to children. In case of any difficulty to children, help was provided to them by the examiner.
The patient assessment form 1 consisted of the following:
Personnel details: Information on the individual’s parents, including their names, ages, genders, addresses, telephone numbers, birthdates, places of birth, occupations, and annual household incomes.
Dental history: This included dental infection, extraction, trauma, lifetime fluoride, and fluoride in water. The address and place of birth of children were taken into consideration to know the levels of fluoride in water in the area where the child resided.
Medical history: This included metabolic diseases, genetic defects, drugs, and childhood illness.
The forms were collected the next day and visual and digital examination was carried out with plane mouth and explorer. The research was conducted on school premises with permission from the respective principals. The kids were given comfy chairs to sit on while being inspected by a doctor, and they were all given the benefit of natural light. Only four permanent maxillary incisors had their buccal surfaces checked for enamel flaws. Clarkson6 created “the developmental defects of enamel (DDE) index (Fig. 1), which distinguished between three primary forms of enamel defects (demarcated opacities, diffuse opacities, and hypoplasia”; see Figure 22222222). This index served as the basis for the diagnostic criteria used here. The findings were recorded on the patient assessment form 2. The defect was recorded in which the numerator denoted the type of defect and the denominator denoted the extent of the defect. All 500 children were photographed using a Sony (DSC H-10) camera and further stored as JPEJ files on PC. The aim to ascertain the frequency, severity, and distribution of enamel defects and their etiology was completed.
Data Transfer and Statistical Analysis
The input was coded and input into a computer. Descriptive statistics were used to analyze the data (cross-tabulation and frequency distribution). Using the statistical tool “Statistical Package for the Social Sciences”, we were able to determine the frequency of tooth enamel developmental abnormalities in relation to tooth type and gender.
A total of 500 children (192 females and 308 males) aged 11–13 were examined for developmental enamel defects.
Distribution of Developmental Enamel Defects in Children
Out of 500, 114 (22.8%) children showed defective enamel in permanent maxillary incisors and 386 (77.2%) children were without enamel defects. Of all enamel defects diffuse opacities (code 3, 4, 5, 6) were most prevalent with 48.25% occurrence followed by demarcated opacities (code 1, 2) 38.5%. Only a very few children presented with hypoplasia (code 7, 8) (10.52%), and any other defects (code 9) (1.75%) (Table 1).
|Types of opacity||Frequency||Percent|
|Demarcated opacity = 1, 2||44||38.5%|
|Diffuse opacity = 3, 4, 5, 6||55||48.25%|
|Hypoplasia = 7, 8||12||10.52%|
|Any other defect = 9||2||1.75%|
|Both demarcated and diffuse opacities||1||0.87%|
Distribution of Developmental Enamel Defects among Males and Females
Developmental enamel abnormalities occurred at a similar rate in boys (23.4%) and females (21.9%). Although the result for the sexes separately showed that out of 192 females examined 47.62% presented demarcated opacity (code 1, 2), 45.23% presented diffuse opacity (code 3, 4, 5, 6), 4.76% presented hypoplasia (code 7,8), 2.38% had any other defect (code 9), and 2.38% had both demarcated and diffuse opacity. Out of 308 males examined 33.3% presented demarcated opacity (code 1, 2), 50% presented diffuse opacity (code 3, 4, 5, 6), 13.8% presented hypoplasia (code 7, 8), 1.39% had any other defect (code 9) and 1.39% had both demarcated and diffuse opacity (Table 2).
|Type of opacity||Females||Males|
|Demarcated opacity = 1, 2||20||47.62%||24||33.3%|
|Diffuse opacity = 3, 4, 5, 6||19||45.23%||36||50%|
|Hypoplasia = 7, 8||2||4.76%||10||13.8%|
|Any other defect = 9||1||2.38%||1||1.39%|
|Both demarcated and diffuse opacity||1||2.38%||1||1.39%|
Distribution of Type of Developmental Enamel Defect in Four Permanent Incisors
According to Figure 3, enamel flaws were more common in the central incisors of the permanent maxilla than in the lateral incisors of the same tooth type. On the right side of the mouth, diffuse opacities (code 3) affected 6.6% of the maxillary right central incisors, “on the left side of the mouth 6.4%, on the right side of the mouth 2.2% of the maxillary right lateral incisors, and on the left side of the mouth 2.0% of the maxillary left lateral incisors, according to the modified DDE index.” Demarcated opacities (code 1, 2) affected more maxillary right and left central incisors (3.6%) followed by maxillary right lateral incisor (1.8%) and left lateral incisor (1.4%). Also, it was observed that maxillary lateral incisors were not affected by hypoplasia (code 7, 8).
Distribution of Extent of Developmental Enamel Defect in Four Permanent Incisors
While observing the extent of enamel defect on the tooth, at least two-thirds tooth surface was affected in maxillary lateral incisors as compared to maxillary central incisors in which the defect covered one-third of the tooth surface. Left maxillary lateral incisors were more severely affected than right lateral incisors (Fig. 4).
Association between Possible Etiological Factors and Type of Developmental Enamel Defect
The degrees of correlation between potential causes and enamel-developing abnormalities are shown in Figure 5. The occurrence of dental enamel defect significantly correlated with dental history (dental infection, extraction, trauma, high fluoride in water) (Chi-statistical square test, p-value = 0.001**) as well as with medical history (metabolic diseases, genetic defects, drugs, and childhood illness) (Chi-squared statistical test, p-value = 0.001**).
High fluoride in water (54.5%), dental infection (18.2%) and trauma (13.6%) were etiological factors for demarcated opacities (code 1, 2). Further, diffuse opacities (codes 3, 4, 5, 6) were found to be highly associated with high F in water (in 78.2% of cases). Dental infection (41.7%), dental trauma (25%), and both dental infection and extraction (25%) were found to be the most prominent causes for enamel hypoplasia.7,8
Dental experts have a natural curiosity about tooth enamel. Dentists and oral surgeons use their knowledge of tooth development every day to guide their diagnostic and treatment choices with patients. The timing of tooth disturbance is affected by when teeth first erupt. In contrast to other tissues, enamel does not undergo remodeling throughout development, therefore any changes made to the enamel during this time will remain visible on the tooth’s surface indefinitely. In 1941, Sarnat and Schour9 discovered in their dissertation that the “growing tooth is the biological recorder of both health and disease,” lending credence to the aforementioned notion. Research on enamel developmental abnormalities has been conducted for a number of different purposes. Many are made to keep an eye on public health initiatives, such as the addition of fluorides to public water systems or the distribution of fluoride tablets.8,10-15 Other research aims to better understand the variables that contribute to the development of these disorders,8,16-20 and studies are being conducted to do just that. In order to evaluate the magnitude of the clinical problem these defects cause and their etiology, the current study sought to characterize the prevalence, severity, and distribution of enamel defects in permanent maxillary incisors among a homogeneous group of Indian children aged 11–13.
“The four permanent maxillary incisors were chosen as the index teeth for the current study because” they have been the subject of numerous previous investigations (e.g., Sognnaes and Armstrong,21 Hurme,22 Nevitt et al.,23 Gray,24 Forrest and James,25 Richards,26 Young,27 Moller and Poulsen,28 Suckling,29 Akpata and Jackson,30 Murray and Shaw31 more crucially, from both a public health and esthetics standpoint, the labial surfaces of these teeth were noted by Al-Alousi et al.,11 and Akpata and Jackson.30 It was advantageous to limit the analysis to the four maxillary incisors since images were required for the research and those teeth are always front and center. Digital photos considerably raise the ability to recognize DDE.32 Furthermore, Thylstrup and Fejerskov,33 and King34 postulated that enamel defects appear “to affect the labial surfaces of maxillary incisors more because of the thickness of enamel and rate of deposition of enamel on these teeth occur over a long period of time making them susceptible to etiological agents capable of inducing enamel defect formation.” Results of our study showed 22.8% of children with enamel defects with males 23.38% and females 21.9%. It is comparable to data obtained by other foreign studies done by using the DDE index to grade enamel defects. While studies examining children aged 8–15 in Ireland found a frequency of 9–15% for missing teeth, studies including children aged nine found a prevalence of 20% (Suckling et al.,35 de Liefde and Herbison.36 However, O’ Mullane et al.,37 hypothesized that the occurrence of enamel abnormalities might vary greatly between locations.
In our research, we found that diffuse opacities were the most common form of the defect (48.25%), followed by delimited opacities (38.5%), and then hypoplastic defects (10.52%). Our research shows that increased exposure to fluoride over time is linked to a rise in the prevalence of diffuse opacities.10,38,39 However, there is little evidence to suggest that an overabundance of fluoride is the only cause of diffuse opacity.40 It’s possible that fluoride’s effectiveness may be amplified or mimicked by other etiological variables, such as genetic or dietary ones.41
Wong et al.42 observed the longitudinal effect on DDE for 3 years and found that diffuse opacities fade over time when compared to demarcated and hypoplastic defects because diffuse opacities are superficial and may abrade mechanically or chemically or may remineralize over time.
This study reports a high occurrence of demarcated opacities (38.5%) in examined permanent maxillary incisors. The connection is quite solid. More than twice as likely to develop a defined enamel defect if caries occurs in a primary tooth. The risk of a permanent successor tooth having a defined defect increased by a factor of five in cases of early tooth loss not caused by trauma, such as extraction owing to cavities or abscesses. While the exact mechanism for this phenomenon is unknown at this time, periapical infection may play a role.43
Our research found that the majority of opacities covered less than a third of the tooth’s surface area (54%), with another 23% covering between a third and a half of the tooth’s surface and another 23% covering at least two-thirds of the surface. Areas with twice or more than ideal fluoride levels,37 it is hypothesized, may be distinguishable in large part by the assessment of the number of faults.
Consistently, both maxillary central incisors had a higher tendency to be affected than maxillary lateral incisors. A similar trend has been observed by other investigators (Nevitt et al.,23 Gray,24 Suckling et al.,29 Murray and Shaw,31 Chellappah et al.44 It has been suggested that the duration of calcification for the crowns of permanent maxillary central incisor teeth is longer than that of the lateral incisors thus the teeth would be in a susceptible state to insults for a longer period of time.44
High fluoride in water accounts mainly for the most prevalent diffuse opacity type of enamel defect of incisors in our study group.
Demarcated opacities are associated mainly with positive dental history in the associated region.
Hypoplasia of incisors was found to be least prevalent in our study group and appears to be associated with complete cessation of ameloblast function in case of extreme insults to the cells. For example, cell death, trauma, and periapical infections.
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