|Year : 2016 | Volume
| Issue : 1 | Page : 4-11
|Association between enamel hypoplasia and dental caries in primary second molars and permanent first molars: A 3-year follow-up study
Sakeenabi Basha1, Roshan Noor Mohamed2, Hiremath Shivalinga Swamy3
1 Department of Preventive and Community Dentistry, College of Dental Sciences, Davangere, Karnataka, India
2 Department of Pediatric Dentistry, College of Dental Sciences, Davangere, Karnataka, India
3 Department of Public Health Dentistry, Oxford College of Dental Sciences, Bengaluru, Karnataka, India
Click here for correspondence address and email
|Date of Web Publication||22-Jan-2016|
| Abstract|| |
Context: Enamel hypoplasia is a defect caused by disturbances during enamel formation. These defects in the enamel present important clinical significance as they predispose a tooth to dental caries. Aim: The aim of this study was to assess the longitudinal relationships between enamel hypoplasia and caries experience of primary second molars and permanent first molars. Materials and Methods: The study sample consisted of 765 subjects who underwent dental examinations at both ages 6 and 9 by the calibrated examiner. Primary second molars and permanent first molars were scored for the presence of enamel hypoplasia for each participant. Caries presence and number of decayed and filled surfaces (dfs and DFS) were determined at ages 6 and 9. The relationships between enamel hypoplasia and caries experience were assessed using multivariable regression models. Results: At the tooth level, 2.8% and 3.5% of children had hypoplasia on primary second molars and permanent first molars respectively. Multivariable logistic regression analyses showed that children with enamel hypoplasia were at a significantly higher risk of caries at both ages 6 (odds ratio, OR = 5.27 for primary second molars and OR = 3.21 for permanent first molars) and age 9 (OR = 3.45 for primary second molars and OR = 4.57 for permanent first molars), and that a statistically significant association was seen with caries incidence (OR = 2.08 for primary second molars and OR = 2.87 for permanent first molars). Conclusion: Enamel hypoplasia appears to be a significant risk factor for caries in both primary second molars and permanent first molars and should be considered in caries risk assessment.
Keywords: Caries, enamel hypoplasia, permanent first molars, primary second molars
|How to cite this article:|
Basha S, Mohamed RN, Swamy HS. Association between enamel hypoplasia and dental caries in primary second molars and permanent first molars: A 3-year follow-up study. Ann Trop Med Public Health 2016;9:4-11
|How to cite this URL:|
Basha S, Mohamed RN, Swamy HS. Association between enamel hypoplasia and dental caries in primary second molars and permanent first molars: A 3-year follow-up study. Ann Trop Med Public Health [serial online] 2016 [cited 2020 Jan 29];9:4-11. Available from: http://www.atmph.org/text.asp?2016/9/1/4/168719
| Introduction|| |
Developmental enamel defects are disturbances during enamel formation and may manifest as enamel hypoplasia or opacities. Enamel hypoplasia is defined as a defect of enamel matrix formation with reduced or altered amounts of enamel caused by an insult to the ameloblast cells.  Clinically, the enamel hypoplasia is visually and morphologically identified by various irregularities, such as pits, grooves, or the absence of enamel structure, over the tooth surfaces. These defects in the enamel are of high clinical significance as they are responsible for esthetic problems, dental sensitivity, and also a predisposition to dental caries.  Defective enamel sites may provide a suitable local environment for adhesion and colonization of cariogenic bacteria, and the bacteria may remain at the base of the defect, in contact with exposed dentin; thus, dental caries on these defective sites may develop more rapidly.  Defective enamel has a higher acid solubility than normal enamel and is more susceptible to carious attack.  Most epidemiological studies show that the frequency of appearance of these defects is on the rise in practically all populations, with a prevalence of 23-52% in the primary dentition depending on the population studied, teeth examined, and diagnostic criteria used, ,[18.104.22.168.9] and the results of the few published studies have shown that the prevalence of enamel defects in permanent dentition varies 20-77%. ,,,,, The association between enamel hypoplasia and dental caries has been reported in several cross-sectional studies ,,, and a few longitudinal studies. ,,, Enamel defects such as enamel hypoplasia appear to be a significant, reliable risk marker or predictor of dental caries; however, most of the previous studies have mainly been conducted on primary dentition. ,,,,, Consequently, the risk factors causing caries were not minimized in primary dentition.  Therefore, a well-designed, prospective, longitudinal study that can take multiple important factors into consideration for both primary and permanent teeth is needed. The aim of the present study was to assess the longitudinal relationships between enamel hypoplasia and caries experience in primary second molars and permanent first molars after stratifying and adjusting for important confounders such as gender, socioeconomic status (SES), childhood illness, birth weight, dietary factors, and oral hygiene.
| Materials and Methods|| |
The investigation was conducted in Davangere, Karnataka, India between June 2008 and June 2011. Six (6)-year-old schoolchildren in primary schools were included in the study. The children were participants of an ongoing study, where children were examined for association between caries and Body Mass Index.  The study population consisted of 765 (376 boys and 389 girls), 6-year-old schoolchildren. All the participants were residents of communities with low natural fluoride content (<0.3 mg/L) in the drinking water. Ethical clearance was taken from the Ethics Committee of Government Dental College, Bengaluru, Karnataka, India. Written informed consent was taken from all participants' parents. The baseline dental examination was conducted in the period of June-July 2008. Three years later, in June 2011, the same group of children (n = 732, 359 boys and 373 girls) was reexamined.
All children received a semistructured questionnaire to be answered by their parents. The returned questionnaires were utilized to obtain information regarding demographic data, children's beverage intakes, general health/illness, oral health behaviors (tooth-brushing frequency and use of fluoridated toothpaste), and birth weight was also obtained. Sugar consumption was considered present if the children consumed snacks (cookies, candies, chocolate), fruit juice, non-diet or other sugar-containing drinks. No quantification was done on the amount of sugar consumed per day. Tooth-brushing frequency was dichotomized as "once a day or less," (≤1/day) versus "more than once a day" (≥2/day). The reliability of the questionnaire was assessed by asking 20 subjects to complete it twice with a 2-week interval. Cronbach's alpha was used as a measure of reliability (α = 0.75).
SES was assessed according to Prasad's classification  using per capita family income, and the children were classified into one of the three clusters: Upper class, middle class, and lower class.
Both baseline and follow-up dental examinations were conducted under the same conditions, in classroom settings with natural light and standard mouth mirrors and WHO probes. The sterilization of instruments was done by autoclave method. The same examiner examined all children. All teeth were examined for both enamel hypoplasia and caries, but only the primary second molars and permanent first molars were used for these analyses, as they were the most consistently present for both the examinations at ages 6 and 9. Person-level hypoplasia and caries were defined as present whenever any of the primary second molars/permanent first molars exhibited hypoplasia or caries. Teeth were evaluated for the presence of enamel hypoplasia without being dried. The presence or absence of enamel hypoplasia was recorded separately for each tooth. Deficiencies in enamel formation, such as pits and linear grooves, were recorded as enamel hypoplasia, while localized opacities that were white, yellow, or brownish in color were recorded as demarcated opacities.  Diagnosis of dental caries [decayed-missing-filled tooth (dmft and DMFT)] was established according to the World Health Organization (WHO) guidelines.  Frank cavitation and visual caries in interproximal surfaces were recorded. In this report, caries experience was considered in two ways. First, caries presence was defined as having any decayed (cavitated and noncavitated lesions) and/or filled surfaces on primary second molars (yes/no), and permanent first molars (yes/no). Second, the number of decayed (cavitated and noncavitated lesions) and/or filled surfaces (dfs/DFS) were calculated on primary second molars and permanent first molars. These caries measures were calculated for both age 6 and 9 exams. Caries incidence was computed as the percentage of subjects with new caries, and caries increments as increases in dfs/DFS. Initial caries were diagnosed after air-drying the tooth. Fissure opacity/change in translucency after air drying (5 s) was recorded as initial caries.
The intraexaminer calibration was performed with respect to the diagnostic criteria of enamel hypoplasia and dental caries. There was a significant correlation with the Kappa value of 0.83 at age 6 and 0.85 at age 9 for hypoplasia, and 0.96 at age 6 and 0.97 at age 9 for dental caries.
Descriptive summary statistics were obtained for all demographic and outcome variables. Difference in proportion was tested using chi-square tests. Difference in means was tested using the t-test. Multivariable regression models were developed for caries at the tooth level using enamel hypoplasia as the explanatory factor, after controlling for other potentially important factors. These other potential predictors included gender, childhood illness (yes/no), birth weight, SES (upper, middle and lower), dietary habits (sugar exposure yes/no), daily tooth-brushing frequency, type of dentifrice used (fluoridated/nonfluoridated), and previous (age 6) dfs/DFS (for age 6-9 increment models only). For these other potential predictors, bivariate associations with caries at ages 6 and 9 were assessed using simple logistic regression for prevalence data (percentage of subjects with caries) and Spearman correlations for count data (dfs/DFS) at the person level (not tooth level). Those variables that were significant at α = 0.10 were used in backward elimination multivariable models, and the final model included variables that were jointly significant at α = 0.05, plus hypoplasia. Because caries data for individual teeth within the same subject are correlated, statistical methods must account for the correlation between teeth within a subject. A subject-level hypoplasia score was defined as the mean number of primary teeth/permanent teeth with hypoplasia and was used to assess the between-subject effects of hypoplasia. A within-subject hypoplasia score for each tooth was also defined using contrasts between tooth-level scores (0.1) and person-level averages. For example, a subject having one tooth with hypoplasia (out of four primary second molars and four permanent first molars) would have four within-subject hypoplasia scores (0.75, -0.25, -0.25, and -0.25) for each tooth. Use of the within-subject hypoplasia score in regression models gives insight into differences between hypoplastic teeth vs nonhypoplastic teeth within the same subject. Logistic generalized estimating equation models (GEE) were used for binary outcomes (yes/no), and negative binomial GEE models for count outcomes (dfs and DFS). Odds ratios (OR) and confidence intervals (CI) were calculated. Analysis was done using the Statistical Package for Social Science version 17 (SPSS Inc., Chicago, IL, USA). All statistical tests were two-sided, and the significance level was set at P < 0.05.
| Results|| |
[Table 1] shows that at the tooth level, 2.8% and 3.5% of children had hypoplasia on primary second molars and permanent first molars respectively at the age of 6 years. Sixteen percent (16%) of children had caries at age 6 (mean dfs 0.39); 26.4% had caries at age 9 (mean dfs 0.41); 10.3% developed new carious lesions from ages 6 to 9 (mean dfs 0.03) on primary second molars; 5.8% of children had caries at age 6 (mean DFS 0.08);, 14.6% had caries at age 9 (mean DFS 0.29); and 11.7% developed new carious lesions from ages 6 to 9 (mean DFS 0.22) on permanent first molars. The caries and enamel hypoplasia distributions for individual molars (55, 65, 75, 85, 16, 26, 36, and 46) are also included in [Table 1].
|Table 1: Distribution of enamel hypoplasia and dental caries in primary second molars and permanent first molars|
Click here to view
[Table 2] presents the subject level distribution of enamel hypoplasia according to variables studied. Statistically significant difference was seen with the gender with boys (57.8%) presented with more hypoplasia compared to girls (42.2%).
|Table 2: Subject level distribution of enamel hypoplasia according to variables studied|
Click here to view
The bivariate relationships between enamel hypoplasia (age 6 exam) and caries experience of primary second molars and permanent first molars at ages 6 and 9, and incidence from age 6 to 9 are presented in [Table 3]. Children with enamel hypoplasia had more caries than those without enamel hypoplasia for both prevalence/presence and dfs/DFS at both ages 6 and 9 at both the person and tooth levels. The results were statistically significant.
|Table 3: Bivariate associations between dental caries and enamel hypoplasia of primary second molars and permanent first molars|
Click here to view
Screening for other important potential predictors for caries levels (yes/no at age 6, age 9 and age 6-9 increment) used simple logistic regression (at the person level) and examined bivariate associations with gender, age, childhood illness, birth weight, SES (three levels), type of dentifrice used (fluoridated/non fluoridated), Sugar consumption (yes/no), and daily tooth brushing frequency. Spearman correlations were used to examine the bivariate associations of these same potential risk factors with caries counts (dfs and DFS) for age 6, age 9 and age 6-9 increments. Variables having associations with P < 0.05 are listed in the footnotes to [Table 4] and [Table 5], and were used in backward elimination GEE procedures.
|Table 4: Tooth level logistic generalized estimating equation (GEE) models for caries (yes/no) using backward elimination method|
Click here to view
|Table 5: Tooth level negative binomial generalized estimating equation (GEE) models of caries dfs and DFS counts and important predictor variables using backward elimination|
Click here to view
Final GEE models in caries presence/incidence and counts/increments included all variables that remained jointly significant (P < 0.05), plus hypoplasia, and are detailed in [Table 4] and [Table 5], respectively. Logistic GEE models predicting caries (yes/no) at age 6 and 9, and any new caries from age 6 to 9, were fitted using the aforementioned selected predictors, along with hypoplasia, and final models are presented in [Table 4]. The models were developed for repeated measures or clustered data. After controlling for the other important predictor variables, children with enamel hypoplasia had a significantly higher risk of caries (see "between-subject" hypoplasia variable) at both age 6 (OR = 5.27 for primary second molars and OR = 3.21 for permanent first molars, P < 0.01) and age 9 (OR = 3.45 for, primary second molars and OR = 4.57 for permanent first molars, P < 0.01), and a statistically significant association was seen with caries incidence (OR = 2.08 for primary second molars P = 0.04 and OR = 2.87 for permanent first molars, P < 0.01). "Within-subject" hypoplasia was not a significant factor in any of the models in the primary second molars, indicating that, for a given subject, the caries risk for hypoplastic and nonhypoplastic teeth was comparable. In relation to the permanent first molars, within-subject hypoplasia showed statistically significant association with DFS at age 6 (OR = 2.71, P = 0.03) and at age 9 (OR = 2.97, P = 0.04). However, no significant relation was seen with DFS increments from age 6 to 9.
Repeated-measure negative binomial GEE models were constructed to predict the number of decayed and filled surfaces (dfs and DFS) at age 6, age 9 and age 6-9 dfs and DFS increment [Table 5]. Between-subject hypoplasia was a statistically significant predictor for dfs and DFS at age 6 (parameter estimate = 1.29, P < 0.01 for primary second molars, and parameter estimate = 1.03, P = 0.04 for permanent first molars), age 9 (parameter estimate = 1.17, P < 0.01 for primary second molars, and parameter estimate = 1.98, P < 0.01 for permanent first molars), and age 6-9 caries increment (parameter estimate = 1.12, P < 0.01 for primary second molars, and parameter estimate = 0.78, P = 0.04 for permanent first molars).
| Discussion|| |
This prospective study examined the risk of dental caries on primary second molars and permanent first molars associated with enamel hypoplasia in schoolchildren of ages 6 to 9 years. The primary second molars were the teeth most consistently present at both examinations, and limiting to this teeth type helped to reduce the confounding effects of differential caries rates on different primary tooth types (canines had much lower caries rates). Therefore, although some of the total caries experience would be missed due to many primary teeth not being included, the confounding effect of differing caries rates would be avoided.
Most of the previous studies that assessed the association of enamel hypoplasia with dental caries have mainly been conducted on primary dentition. ,,,,,, Consequently, the risk factors causing caries were not minimized in the primary dentition. Direct clinical examination of newly erupted teeth like permanent first molars would provide a more reliable result; therefore, permanent first molars were also included in the present investigation.
In the present study, the overall incidence of caries was higher for hypoplastic permanent first molars (11.7%) compared to hypoplastic primary second molars (10.3%). This might suggest that, for subjects exhibiting enamel hypoplasia, the risk of developing caries is not similar in the primary and permanent teeth. This would be similar to the study conducted by Vahid et al.,  where it was shown that hypoplastic permanent teeth were more susceptible to carious attack than the primary teeth. The increased incidence and increment of caries in the first permanent molars in the present study indicates that structural defects in enamel make it more soluble, resulting in a faster breakdown in the pattern of enamel rods. This, in turn, facilitates the presence of dental caries even before other risk factors could even gain enough time for enamel destruction.
In the present study, the results of the bivariate analyses indicated that enamel hypoplasia was significantly associated with dental caries in primary second molars and permanent first molars. The trend was generally consistent at all levels of bivariate analysis, at both the person and tooth levels for age 6 findings, to a lesser degree for age 9 in primary second molars, and to a higher degree for age 9 in permanent first molars. Theoretically, considering the pathogenesis, teeth with enamel hypoplasia should have a higher risk of dental caries because hypoplastic enamel surfaces have reduced thickness of enamel and may provide a more suitable local environment for adhesion and colonization of cariogenic bacteria,  and are more acid-soluble. ,
The results of the present study were somewhat consistent with previous studies, which suggested that enamel hypoplasia increases the risk of dental caries in the affected teeth. ,,,,,,, The study by Li et al.  showed that enamel hypoplasia was a stronger predictor of caries than the individual's parental income or the country of residence. The authors also found that the higher the defect score, the more caries was experienced by the children. Rodrigues and Shiham,  on the other hand, found a weaker association between enamel hypoplasia and caries in primary teeth. They found that while enamel hypoplasia was significantly related to caries increment, the effect disappeared after controlling for sociodemographic and socioeconomic variables, although this weaker association between enamel hypoplasia and caries could be due to the fact that relatively few children in the study had hypoplasia. From the results of multivariable regression analyses in the present study, the between-subject effect from enamel hypoplasia was consistently significant in all the models for both primary second molars and permanent first molars [Table 4]. This indicates that subjects with hypoplasia are more at risk for caries at ages 6 and 9, and also likely to have more surfaces affected by caries [Table 5]. However, the within-subject effect from enamel hypoplasia was not consistently significant in primary second molars. This might suggest that, for subjects exhibiting enamel hypoplasia, the risk for developing caries is similar for all teeth. Also, the weaker effects of hypoplasia on caries increments may indicate that hypoplasia has a stronger early influence (seen in age-6 caries experience, with a carryover effect on the age-9 caries experience), but that the effect may not continue to put subjects at an increased risk for caries many years after eruption. The majority of earlier investigations have been performed on primary dentition, ,,,,,, and there is a lack with regard to the information on hypoplastic permanent molars.  The present study shows that the hypoplastic permanent first molars (between subject, OR = 4.57) suffer more from carious attack than the primary second molars (between subject, OR = 3.45) at age 9, and this may be attributed to the fact that as the individual's age advances, a greater number of permanent first molars are exposed to the oral cavity, increasing their susceptibility to carious attack. A case-control study conducted by Vahid et al.  showed that hypoplastic permanent first molars were 4× more susceptible to carious attack compared to those without hypoplasia.
Despite the dramatic decline in dental caries experience over the last several decades in Western countries, dental caries remains a significant health problem in India. The prevalence of dental caries varies in the range of 33.7-90% in the child population and is increasing at an alarming rate. ,, Extensive evidence indicates that dental caries is a communicable, infectious disease  that involves many environmental and host factors and the interactions among these factors.  This supports a paradigm shift from a surgical model that focuses mainly on removing the carious tooth structure, followed by replacement with a restorative material to a biological/medical model in which the individual's overall and site-specific susceptibility are assessed, and interventions can be individualized to prevent and control this infection.  Therefore, in the contemporary management of dental caries with this medical model, caries risk assessment plays a crucial role.  Unfortunately, there is no simple, valid, and reliable caries risk assessment model currently available. Previous caries experience and/or untreated (active) lesions are the best predictors for future caries development.  However, these predictors are post-disease and do not serve well for early detection and primary prevention of the disease. As a result, they might not be as useful to a practitioner trying to control and prevent caries at the earliest stages in susceptible patients. In this study, after controlling for other potential factors, multivariable regression models suggested that enamel hypoplasia is a good predictor. Enamel hypoplasia might not only itself render the tooth more prone to caries development but also be, in part, a proxy indicator for substandard nutrition and/or childhood infection. All of these negative early-life experiences during enamel formation might manifest collectively as enamel hypoplasia. These sorts of events will put a child at higher risk for dental caries. Together with other information, such as SES, birth weight of the child, childhood illness, sugar consumption, and tooth-brushing frequency, a risk assessment model that considers enamel hypoplasia data could allow better prediction of early caries risk, particularly at the tooth level. Enamel hypoplasia might have good potential to serve as a predictor of caries experience because the teeth could be examined for hypoplasia right after the eruption but before carious lesions develop. Thus, early intervention measures could be applied with at-risk children to prevent early caries stages. The results from this study indicate that enamel hypoplasia is a significant predictor for dental caries in childhood. However, several limitations of the study must be recognized. Several important factors related to dental caries, such as oral bacteria and plaque levels, were not included in the analysis. Diagnosis of dental caries was based on visual examination, and no radiographs were used, which might have led to underestimation of the overall caries experience; other types of enamel defects were not included in the analysis. In addition, the number of children who were diagnosed with hypoplasia (only 51) was small, and even a small change in diagnosis reliability could have had an impact on the results. Within its limitations, this prospective, longitudinal study provided evidence that enamel hypoplasia could be a clinically meaningful predictor of dental caries. More studies are needed to better understand the role of enamel hypoplasia in caries development, including studies of longer duration, with larger, more diverse samples, and assessment of other important factors related to dental caries. Further studies are needed to understand the factors related to the time-dependent effects of enamel hypoplasia on caries presence at ages 6 and 9.
| References|| |
Suckling GW. Development effects of enamel-historical and present day perspectives of their pathogenesis. Adv Dent Res 1989;3:87-94.
Seow WK, Ford D, Kazoullis S, Newman B, Holcombe T. Comparison of enamel defects in the primary and permanent dentitions of children from a low-fluoride District in Australia. Pediatr Dent 2011;33:207-12.
Li Y, Navia JM, Bian JY. Caries experience in deciduous dentition of rural Chinese children 3-5 years old in relation to the presence or absence of enamel hypoplasia. Caries Res 1996;30:8-15.
Zheng S, Deng H, Gao X. Studies on developmental enamel defects in the primary dentition of children with histories of low birth weight and prematurity and their susceptibility to dental caries. Zhonghua Kou Qiang Yi Xue Za Zhi 1998;33:270-2.
Slayton RL, Warren JJ, Kanellis MJ, Levy SM, Islam M. Prevalence of enamel hypoplasia and isolated opacities in the primary dentition. Pediatr Dent 2001;23:32-6.
Lunardelli SE, Peres MA. Prevalence and distribution of developmental enamel defects in the primary dentition of pre-school children. Braz Oral Res 2005;19:144-9.
Farsi N. Developmental enamel defects and their association with dental caries in preschoolers in Jeddah, Saudi Arabia. Oral Health Prev Dent 2010;8:85-92.
Montero MJ, Douglass JM, Mathieu GM. Prevalence of dental caries and enamel defects in Connecticut Head Start children. Pediatr Dent 2003;25:235-9.
Chaves AM, Rosenblatt A, Oliveira OF. Enamel defects and its relation to life course events in primary dentition of Brazilian children: A longitudinal study. Community Dent Health 2007;24:31-6.
Arrow P. Prevalence of developmental enamel defects of the first permanent molars among school children in Western Australia. Aust Dent J 2008;53:250-9.
Ford D, Seow WK, Kazoullis S, Holcombe T, Newman B. A controlled study of risk factors for enamel hypoplasia in the permanent dentition. Pediatr Dent 2009;31:382-8.
Tapias-Ledesma MA, Jiménez R, Lamas F, González A, Carrasco P, Gíl de Miguel A. Factors associated with first molar dental enamel defects: A multivariate epidemiological approach. J Dent Child (Chic) 2003;70:215-20.
Arrow P. Risk factors in the occurrence of enamel defects of the first permanent molars among schoolchildren in Western Australia. Community Dent Oral Epidemiol 2009;37:405-15.
Jälevik B, Klingberg G, Barregård L, Norén JG. The prevalence of demarcated opacities in permanent first molars in a group of Swedish children. Acta Odontol Scand 2001;59:255-60.
Daneshkazemi AR, Davari A. Assessment of DMFT and enamel hypoplasia among junior high school children in Iran. J Contemp Dent Pract 2005;6:85-92.
Lai PY, Seow WK, Tudehope DI, Rogers Y. Enamel hypoplasia and dental caries in very-low birthweight children: A case-controlled, longitudinal study. Pediatr Dent 1997;19:42-9.
Hong L, Levy SM, Warren JJ, Broffitt B. Association between enamel hypoplasia and dental caries in primary second molars: A cohort study. Caries Res 2009;43:345-53.
Oliveira AF, Chaves AM, Rosenblatt A. The influence of enamel defects on the development of early childhood caries in a population with low socioeconomic status: A longitudinal study. Caries Res 2006;40:296-302.
Rodrigues CS, Shiham A. The relationships between dietary guidelines, sugar intake and caries in primary teeth in low income Brazilian 3-year-olds: A longitudinal study. Int J Paediatr Dent 2000;10:47-55.
Vahid Golpaygani M, Mehrdad K, Mehrdad A, Ansari G. An evaluation of the rate of dental caries among hypoplastic normal teeth: A case control study. Res J Biological Sci 2009;4:537-41.
Sakeenabi B, Swamy HS, Mohammed RN. Association between obesity, dental caries and socioeconomic status in 6- and 13-year-old school children. Oral Health Prev Dent 2012;10:231-41.
Prasad BG. Social classification of Indian families. J Indian Med Assoc 1968;51:365-6.
World Health Organization. Oral Health Surveys: Basic Methods. 4 th
ed. Geneva: World Health Organization; 1997. p. 34.
David J, Wang NJ, Astrøm AN, Kuriakose S. Dental caries and associated factors in 12- year-old schoolchildren in Thiruvananthapuram, Kerala, India. Int J Peadiatr Dent 2005;15:420-8.
Rao A, Sequeira SP, Peter S. Prevalence of dental caries among school children of Moodbidri. J Indian Soc Pedod Prev Dent 1999;17:45-8.
Shetty NS, Tandon S. Prevalence of dental caries as related to risk factors in schoolchildren of South Kanara. J Indian Soc Pedod Prev Dent 1988;6:30-7.
Caufield PW. Dental caries: An infectious and transmissible disease where have we been and where are we going? N Y State Dent J 2005;71:23-7.
Featherstone JD. The science and practice of caries prevention. J Am Dent Assoc 2000; 131:887-99.
Horowitz AM. A report on the NIH consensus development conference on diagnosis and management of dental caries throughout life. J Dent Res 2004;83:C15-7.
Fontana M, Zero DT. Assessing patients' caries risk. J Am Dent Assoc 2006;137:1231-9.
Department of Community Dentistry, College of Dental Sciences, Davangere - 577 004, Karnataka
Source of Support: None, Conflict of Interest: None
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5]
| Article Access Statistics|
| Viewed||3460 |
| Printed||106 |
| Emailed||0 |
| PDF Downloaded||25 |
| Comments ||[Add] |