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RESEARCH REPORTS |
1 Faculty of Dentistry, University of Otago, PO Box 647, Dunedin, New Zealand;
2 Discipline of Dental Public Health and Epidemiology, Department of Oral Sciences, Faculty of Dentistry, University of Otago, Dunedin, New Zealand; and
3 Department of Preventive and Social Medicine, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand;
* corresponding author, jonathan.broadbent{at}stonebow.otago.ac.nz
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMETHODSRESULTSDISCUSSIONREFERENCES |
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KEY WORDS: caries • enamel defect • longitudinal study
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONREFERENCES |
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A 1992 UK study of enamel defects found a greater prevalence of enamel defects among Asian children than in others. The authors noted that ‘previous local studies’ had found more primary caries in Asian children, and an etiological link between caries and enamel defects was suggested; however, no effort was made to confirm this (Elley and Charlton, 1993). In a second UK study, children of about age 12 with no enamel defects in permanent teeth were found to have a mean DMFS of 2.7, while those having only demarcated opacities had 3.4, those with only diffuse defects had 1.6, and those with a combination had 2.4. The authors speculated that, since children with caries by age 12 are likely to have had caries in their primary teeth, caries in the primary dentition may cause local conditions resulting in demarcated opacities in permanent teeth; the lower mean DMFS among those with diffuse defects was believed to be associated with fluoride exposure (Ellwood and O’Mullane, 1994).
A study in China recently drew attention back to this possible association between caries in primary teeth and enamel defects in permanent successors. Some 452 children living in the non-fluoridated region of Conghua (Southern China) were examined for caries in the primary teeth between the ages of three and six. A total of 388 of these children had at least two examinations during this period, and, of these, 250 participated in a follow-up study of enamel defects at about 12 years of age. All erupted surfaces of the teeth of succession were examined for enamel defects at this age. Where the primary precursor of a permanent tooth had been carious, there was greater prevalence of demarcated opacities, and hypoplasia was greater, than where there had been no caries [7.5 vs. 3.8% and 1.9 vs. 0.4%, respectively (Lo et al., 2003)].
Furthermore, experimental studies have shown an association of artificially induced inflammation of the periapical tissues of primary teeth with defects of formation of permanent teeth (including hypoplasia) in monkeys (Kaplan et al., 1967; Winter and Kramer, 1972; Valderhaug, 1974) and dogs (Binns and Escobar, 1967), and these have been supported by human autopsy reports (Morningstar, 1937; Bauer, 1946).
It can be difficult to establish the etiology of enamel defects (Suckling et al., 1987). Demarcated opacities and hypoplastic defects of enamel tend to be isolated and of a sporadic distribution; thus, a local cause would be most plausible. In contrast, diffuse opacities more frequently affect multiple teeth which have undergone enamel secretion and maturation during the same period; thus, a systemic cause (such as consumption of fluoridated water) is more likely. The close approximation of the buccal surface of a developing permanent incisor with the root end of its precursor means that insult to a developing permanent tooth (by caries-associated periapical inflammation of the primary tooth) may interfere with the normal process of enamel matrix deposition or mineralization, thus resulting in a demarcated opacity or hypoplastic defect. A further possibility is that early extraction of a primary tooth may cause trauma to the developing permanent tooth, thus damaging the enamel matrix and resulting in a defect of enamel. Since carious teeth are more likely to be extracted than non-carious primary teeth, this could result in a higher likelihood of enamel defects in the permanent successors of such teeth. Alternatively, a carious primary tooth might be more likely to be a target for topical fluoride application by a dentist; this high concentration of locally applied fluoride might result in a fluorotic defect of enamel.
The aim of this study was to test the hypothesis that dental caries in primary teeth is a risk factor for enamel defects in their permanent successors.
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METHODS |
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONREFERENCES |
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Most of the age-five dental examinations were conducted within four to six weeks of the Study members’ fifth birthdays. Diagnosis and recording of dental caries were made according to the World Health Organization criteria (1977). The age-nine examinations for enamel defects were conducted within three months of each child’s ninth birthday. A tooth was considered present when more than half the clinical crown had erupted; scoring of enamel defects was according to the FDI Index of Developmental Defects of Dental Enamel.
Because children are in the mixed-dentition stage at age nine, the permanent canines and premolars have not normally erupted. For this reason, such teeth were excluded from the analysis; also excluded were first molar teeth (since these are accessional teeth) and lower incisors (since their incidence of caries and prevalence of enamel defects are relatively low). The analysis of enamel defects was limited to the buccal surfaces of the maxillary incisors, since these teeth are usually erupted by the age of nine, and the buccal surfaces are the most important esthetically.
It was not possible to determine whether missing primary teeth were missing due to caries, trauma, or early exfoliation. Detailed information was available on trauma to the primary teeth. Where a tooth had a history of trauma and was missing at age five, a dummy variable was created designated ‘Missing at five, trauma’. Where a tooth had a history of trauma but was not missing at age five, a dummy variable was created labeled ‘Trauma, not missing at five’. Where a tooth did not have a history of trauma but was missing by age five (e.g., due to extraction or early exfoliation), a dummy variable was created designated ‘Missing at five (not trauma)’.
The socio-economic status (SES) of the Study members’ families was measured on the basis of the parents’ self-reported occupational status. Occupation was scaled into one of six categories (6 = unskilled laborer, 1 = professional) on the basis of the educational levels and income associated with that occupation in data from the New Zealand census (Irving and Elley, 1977; Elley and Irving, 1985). For the purposes of the multivariate analysis, dummy variables were created. Scores ‘5’ and ‘6’ (Low SES) formed the reference category; ‘3’ and ‘4’ were the ‘Medium SES’ category, and scores ‘1’ and ‘2’ comprised the ‘High SES’ category.
Univariate statistics were computed, and bivariate analyses were undertaken. The level of significance was set at P < 0.05; we used the 
2 test to test for significance of observed associations. Multivariate analysis was conducted in Intercooled Stata 8.0 (Stata Corporation, College Station, TX 77840, USA, 2003) by generalized estimating equations, with independent working matrices and robust standard errors.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONREFERENCES |
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). A total of 616 permanent maxillary incisors (25.7%) had enamel defects (Table 2). Diffuse opacities were the most commonly observed defect and were most prevalent in the central incisors. Demarcated opacities were the next most common and were most prevalent in the central incisors. Hypoplastic defects were the least prevalent and showed no difference by tooth type.
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). Before adjustment for potential confounding factors, a permanent tooth with a carious predecessor had 2.3 times the odds of having a demarcated opacity compared with a permanent tooth with a sound predecessor.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONREFERENCES |
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This study has found that if caries occurs in a primary tooth, the successor tooth is more than twice as likely to have a demarcated enamel defect. In the case of early tooth loss (for reasons other than trauma, e.g., extraction due to caries/abscess), the permanent successor tooth was five times more likely to have a demarcated defect.
No significant relationship was observed between caries in the primary incisors and the presence of diffuse opacities in the permanent incisors. However, an association was found between diffuse defects of enamel and exposure to fluoridated water supplies. Analysis of these data supports the idea that diffuse enamel defects are related to systemic causes. Other significant findings were the high odds ratios relating tooth loss due to trauma to both hypoplasia and the ‘other/combination’ defects.
One problem with secondary analyses is that there is no control over the data which are collected. Unfortunately, data on sources of fluoride exposure other than water fluoridation were not collected. Also, the reasons for missing teeth at age five were not recorded; hence, some teeth that were missing due to caries (i.e., extracted) were designated as non-carious. However, these teeth were accounted for by the use of the dummy variable ‘missing teeth (not related to trauma)’. The high odds ratio for this variable relating to demarcated opacities supports the study hypothesis, since such teeth are more likely to have had severe caries with periapical abscesses.
This study supports the hypothesis that caries in a primary tooth will increase the odds of the succeeding permanent tooth having a demarcated defect, with the risk more than doubling. The precise mechanism for this process is unclear as yet, but it may be related to the presence of periapical infection. An interesting perspective on these findings is that perhaps fluoridation of municipal water supplies (at optimal levels) could indirectly lead to a decrease in the rate of demarcated defects.
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ACKNOWLEDGMENTS |
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Received April 29, 2004; Last revision November 7, 2004; Accepted December 31, 2004
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REFERENCES |
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Binns WH Jr, Escobar A (1967). Defects in permanent teeth following pulp exposure of primary teeth. J Dent Child 34:4–14.[Medline]
Elley KM, Charlton J (1993). Prevalence of dental enamel defects in 6, 7 and 8-year-old children resident in West Bromwich, Sandwell, UK. Community Dent Health 10:11–21.[Medline]
Elley WB, Irving JC (1985). The Elley-Irving socio-economic index 1981 census revision. NZ J Educ Stud 20:115–128.
Ellwood RP, O’Mullane DM (1994). Association between dental enamel opacities and dental caries in a north Wales population. Caries Res 28:383–387.[ISI][Medline]
Evans RW, Beck DJ, Brown RH (1980). Dental health of 5-year-old children: a report from the Dunedin Multidisciplinary Child Development Study. NZ Dent J 76:179–186.
Irving JC, Elley WB (1977). A socio-economic index for the female labour force in New Zealand. NZ J Educ Stud 12:154–163.
Kaplan NL, Zach L, Goldsmith ED (1967). Effects of pulpal exposure in the primary dentition on the succedaneous teeth. J Dent Child 34:237–242.[Medline]
Lo EC, Zheng CG, King NM (2003). Relationship between the presence of demarcated opacities and hypoplasia in permanent teeth and caries in their primary predecessors. Caries Res 37:456–461.[ISI][Medline]
McCormick J, Filostrat DJ (1967). Injury to the teeth of succession by abscess of the temporary teeth. J Dent Child 34:501–504.[Medline]
Morningstar CH (1937). Effect of infection of the deciduous molar on the permanent tooth germ. J Am Dent Assoc 24:786–791.
Niswander JD, Sujaku C (1962). Relationship of enamel defects of permanent teeth to retention of deciduous tooth fragments. J Dent Res 41:808–814.
Silva PA, Stanton WR (1996). From child to adult: the Dunedin Multidisciplinary Health and Development Study. Auckland: Oxford University Press.
Suckling GW, Brown RH, Herbison GP (1985). The prevalence of developmental defects of enamel in 696 nine-year-old New Zealand children participating in a health and development study. Community Dent Health 2:303–313.[Medline]
Suckling GW, Herbison GP, Brown RH (1987). Etiological factors influencing the prevalence of developmental defects of dental enamel in nine-year-old New Zealand children participating in a health and development study. J Dent Res 66:1466–1469.
Turner JG (1906). Effects of abscess arising from temporary teeth. Br J Dent Sci 49:562–564.
Turner JG (1912). Two cases of hypoplasia of enamel. Br J Dent Sci 55:227–228.
Valderhaug J (1974). Periapical inflammation in primary teeth and its effect on the permanent successors. Int J Oral Surg 3:171–182.[ISI][Medline]
Winter GB, Kramer IR (1972). Changes in periodontal membrane, bone and permanent teeth following experimental pulpal injury in deciduous molar teeth of monkeys (Macaca irus). Arch Oral Biol 17:1771–1779.[ISI][Medline]
World Health Organization (1977). Oral health surveys. Basic methods. 2nd ed. Geneva: World Health Organization.
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