Eur Arch Paediatr Dent DOI 10.1007/s40368-014-0170-8
ORIGINAL SCIENTIFIC ARTICLE
A comparison of the presentation of molar incisor hypomineralisation in two communities with different fluoride exposure R. Balmer • K. J. Toumba • T. Munyombwe • M. S. Duggal
Received: 29 July 2014 / Accepted: 17 December 2014 Ó European Academy of Paediatric Dentistry 2015
Abstract Aim To compare the clinical presentation of two cohorts of children diagnosed with molar incisor hypomineralisation (MIH) and living in areas of low and high background fluoridation. Methods The study population comprised 12-year-old children participating in the 2008–2009 National Dental Epidemiological Programme in five regions in Northern England. Participating dentists were trained and calibrated in the use of the modified Developmental Defects of Enamel Index. Children were examined at school under direct vision with the aid of a dental mirror. First permanent molars and incisors were recorded for the presence and type of enamel defects greater than 2 mm. A diagnosis of MIH was ascribed to any child with a demarcated defect in any first permanent molar. Risk ratios for the occurrence of demarcated, diffuse and hypoplastic defects were generated for MIH children in the fluoridated and non-fluoridated area. Results 3,233 children were examined. The prevalence of MIH in the fluoridated community was 11 % and in the non-fluoridated community was 17.5 %. Incisors in children with MIH were at greater risk of having demarcated defects (risk ratio 4.0, 3.6–4.5) and diffuse defects (risk ratio 2.2, 2.0–2.5). Molars in children with MIH were at greater risk of diffuse defects (risk ratio 4.4, 3.8–5.0). The teeth of children with MIH living in the fluoridated area were at greater risk of demarcated defects for both incisors
R. Balmer (&) K. J. Toumba T. Munyombwe M. S. Duggal Department of Child Dental Health, Leeds Dental Institute, University of Leeds, Clarendon Way, Leeds LS2 9LU, UK e-mail: [email protected]
(risk ratio 1.6, 1.3–2.0) and molars (risk ratio 1.3, 1.2–1.5) relative to the teeth of MIH children living in the nonfluoridated area. Conclusions Children with MIH were at increased risk of both diffuse and demarcated defects in their incisors. Children with MIH living in the fluoridated area were at increased risk of diffuse and demarcated defects relative to MIH children living in the non-fluoridated area. Keywords Molar incisor hypomineralisation Enamel defects Fluoride
Introduction Molar incisor hypomineralisation (MIH) has been defined as enamel hypomineralisation of systemic origin of 1–4 permanent first molars frequently associated with affected incisors (Weerheijm 2003). The classical defect is a demarcated one which, particularly in the posterior teeth, can breakdown under post eruptive occlusal forces. The aetiology is likely to be secondary to ameloblast damage in the transition phase (early maturation phase) which results in yellow/brown, porous lesions. Fluoride also causes damage during the maturation phase, probably by inhibition of protein degradation resulting in failure of the enamel to mineralise fully. In these cases the lesion is diffuse and confined to the subsurface area. The two conditions of fluorosis and MIH are normally considered distinct in terms of both the pathogenesis and presentation. Most studies examining enamel defects in fluoridated areas have demonstrated increased diffuse defects but no increase in demarcated defects (Cutress et al. 1985; Clarkson and O’Mullane 1989; Kanagaratnam et al. 2009; Milsom and Mitropoulos 1990).
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The overall prevalence of MIH has been reported at 2.3–40 %. In 2003 Koch compared the prevalence of MIHtype lesions in children with and without high background exposure to fluoride (Koch 2003). This study found a generally low level of children with the MIH-type lesion and no difference according to fluoride exposure. It concluded that fluoride was not an aetiological factor in MIH. No other studies have specifically compared MIH with regard to background fluoride levels although a study in Brazil did note that the prevalence of MIH in the urban fluoridated (0.7 ppm) area was lower than in the nonfluoridated rural area with rates of 17.8 and 24.9 %, respectively (Da Costa-Silva et al. 2010). A similar pattern emerged in Finland in a study whose aim was to measure MIH prevalence secondary to local dioxin contamination (Holtta et al. 2001). In this study, MIH prevalence was 5.6 % in the fluoridated town compared to a prevalence of 14.2 % in the non-fluoridated area. The authors attributed this difference to the possibility that diffuse lesions in the fluoridated area had masked the presence of MIH. It is interesting to note that of the other prevalence studies in the literature, the two with the lowest reported rates were also the only studies to be carried out in areas of raised fluoridation levels. Cho et al. (2008) reported a prevalence of only 2.8 % in Hong Kong which was fluoridated to a level of 0.5 ppm. A further study by Fteita et al. (2006) in an area of Libya with fluoridation 0.4 ppm had a MIH prevalence rate of 2.9 %. Although these previous studies reported on specific prevalence of MIH, there have been no published studies which have examined the impact of fluoridation on the presentation of MIH. The aim of this study therefore was to compare the clinical presentation of two cohorts of children diagnosed with MIH and living in areas of low and high background fluoridation. This analysis formed one aspect of a study which examined overall prevalence of MIH in a number of areas in Northern England against key demographic indicators (Balmer et al. 2012).
good to excellent kappa scores. The index chosen was the modified Developmental Defects of Enamel (mDDE) (1992) which scored tooth surfaces of index teeth (first permanent molars and incisors) for the presence of demarcated, diffuse or hypoplastic defects or combinations of these three. Only defects larger than 2 mm were recorded. Combination defects were broken down to the presence or absence of each of the components. For instance code 5, demarcated and diffuse, was broken down into the presence of both codes 1 (demarcated defect) and 2 (diffuse defect). Therefore, a tooth surface was coded for the absence or presence of each of the three basic defects. For posterior teeth, this therefore resulted in each posterior tooth being scored for the presence or absence of a demarcated defect, a hypoplastic defect and a diffuse defect for any of the three index surfaces. For example, a molar tooth with a combined hypoplastic and demarcated defect (code 6) on the occlusal surface and a diffuse defect only (code 2) on the buccal surface would score positive for all three basic defects. Diagnosis of MIH was attributed to any participant who recorded a demarcated defect on any of the permanent molars. In effect they were considered to have MIH if any first permanent molar tooth surface had a demarcated defect either in isolation or in combination with another defect. In cases, where all first permanent molars were absent MIH diagnosis was judged if any demarcated defects were noted on the incisors. If some of the first permanent molars were missing and the remainder had no defects, MIH diagnosis was also attributed based on the presence of defects in the anterior teeth. Current residential postcode for each child was correlated with information from NHS North East (2011). This identified those children who resided in areas which had had the fluoride level of their water supply adjusted to one part per million. Postcode was also used to obtain an index of multiple deprivation (IMD) score and quintile as described in a previous publication (Balmer et al. 2012).
Materials and methods Statistics Materials and methods for sample selection, training and calibration of examiners and for data collection and analysis have been provided in detail in a previous publication (Balmer et al. 2012). In summary, the sample consisted of 12-year-old children in the North of England participating in the NHS National Dental Epidemiological Programme (2008). The specific areas covered were Newcastle which has an artificially fluoridated water supply and North Yorkshire, Hull, Bradford and Airedale which are not artificially fluoridated. Training and calibration of examiners were carried out using clinical photographs which yielded
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Data were entered into IBM SPSS Statistics version 20 which was used to generate the results of independent t tests for overall comparison of numbers of defects in the two communities. A binary logistic regression model was used to account for the effect of fluoridation, gender and deprivation on the occurrence of MIH. Risk ratios were calculated in StataSE version 12 by analysing number of teeth exposed to one of the two risk factors (fluoridation or presence of MIH) against number of teeth with the presence or absence of each of the three basic defects.
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Results The total 12-year-old population of all the regions was 21,986. Of these 4,795 were invited to participate in the survey of whom 3,233 (67.4 %) were examined. 852 children were absent on the day of the examination, 636 declined examination, and for 74 children, the reason for non-examination was not recorded. Of the 3,233 examined 518 were diagnosed with molar incisor hypomineralisation, with a prevalence rate of 16.02 % (95 % CI 14.77–17.33 %). Table 1 shows the difference in MIH prevalence between the fluoridated and non-fluoridated areas. Prevalence rate in the fluoridated area was 11 % and was lower than that of the non-fluoridated area (17.5 %). Chi squared test indicated a significant difference (v2 = 18.2, p \ 0.001). Area of residence (fluoridated vs non-fluoridated), gender and deprivation (by original IMD score) were entered into a binary multiple logistic regression model with occurrence of MIH as the outcome. The result is shown in Table 2. In this model area of residence was no longer significant (p = 0.186) whereas IMD score remained significant (p = 0.023). The number, type and distribution of teeth with specific defects in children with MIH residing in the fluoridated area were compared with children with MIH in the nonfluoridated area. Independent samples t tests were used to analyse these data and a summary is shown in Table 3. Further detailed analyses were carried out by calculation of risk ratios for the occurrence of specific defects in teeth according to the presence of MIH and fluoridation.
children living in a fluoridated area. As expected, the risk ratios for the incisors of children with MIH (relative to those without MIH) were high regardless of whether those children were living in a fluoridated area or not (6.5 and 3.6, respectively). For those children with MIH and living in a fluoridated area, the risk ratio of an incisor having a demarcated defect relative to children with MIH and living in a non-fluoridated area was 1.6 (95 % CI 1.3––2.0). In addition, the risk ratio for a molar in MIH children in the fluoridated area having a demarcated defect relative to children in the non-fluoridated area was 1.3 (95 % CI 1.2–1.5). Deprivation and area of residence for MIH children only were entered into two binary logistic Poisson regression models with the presence of demarcated defects in anterior teeth and the presence of demarcated defects in posterior teeth as the outcomes. The odds ratio for an incisor tooth having a demarcated defect in a MIH child in the fluoridated area was 1.73 (95 % CI 1.33–2.25) relative to a MIH child in the non-fluoridated area. The odds ratio for a molar tooth having a demarcated defect was 1.30 (95 % CI 1.07–1.57). In both of these models the effect of socioeconomic status was insignificant. Therefore, in this study, living in the fluoridated area increased the chance of children with MIH having demarcated defects in incisors and molars even after accounting for socioeconomic differences of the two communities. Fluoridation, however, had no impact in terms of demarcated defects on all children overall in the study or on those children who did not have MIH (risk ratios of 1.0 and 0.9, respectively).
Demarcated defects Table 4 summarises the risk ratios for the presence of demarcated defects on the teeth of children with MIH and of Table 1 Prevalence of MIH in fluoridated and non-fluoridated areas Area
Total examined
Fluoridated Non-fluoridated
Number with MIH
Percentage with MIH (95 % CI)
726
80
11.0 (8.8–13.5)
2,507
438
17.5 (16.0–19.0)
CI confidence interval Table 2 Logistic regression demonstrating impact of fluoridation, gender and IMD score on the occurrence of MIH p value
Odds ratio
95 % CI for odds ratio
Fluoridated area
0.186
1.264
0.893–1.789
Gender
0.595
1.059
0.856–1.310
IMD score
0.023
0.992
0.986–0.999
IMD index of multiple deprivation, CI confidence interval
Diffuse defects Tables 5 and 6 summarise the risk ratios for the presence of diffuse defects on the teeth of children with MIH and of children living in fluoridated areas. Table 5 shows the risk of teeth in MIH children (relative to non-MIH children) having a diffuse defect according to area of residence. It demonstrated that, regardless of the area in which the children lived and of which teeth were being examined (incisors or FPMs) and teeth of MIH children were at increased risk of diffuse defects. Therefore, in this study, MIH was a risk factor for diffuse defects independent of background fluoridation. Table 6 shows the risk of teeth in children in fluoridated area (relative to living in a non-fluoridated area) having a diffuse defect according to the presence of MIH. As would be expected, for both anterior and posterior teeth, the risk is increased in the fluoridated area regardless of whether the children had MIH or not.
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Eur Arch Paediatr Dent Table 3 Summary of the prevalence of different defects in MIH cases in fluoridated and non-fluoridated areas
Demarcated incisors
N (fluoridated)
Mean number/case fluoridated (SD)
N (non-fluoridated)
Mean number/case non-fluoridated (SD)
p value
109
1.36 (1.37)
356
0.81 (1.16)
\0.001* \0.001*
Demarcated/missing FPMs
187
2.34 (1.02)
782
1.79 (0.97)
Diffuse incisors
126
1.58 (2.78)
246
0.56 (1.3)
0.002*
Diffuse FPMs
83
1.04 (1.55)
211
0.48 (0.97)
0.003*
Hypoplastic incisors
10
0.13 (0.4)
32
0.07 (0.34)
0.286
Hypoplastic FPMs
47
0.59 (0.9)
192
0.44 (0.83)
0.143
SD standard deviation, N number of defective teeth * Significant p \ 0.05, independent samples t test
Table 4 The risk ratios of teeth having demarcated defects in children with MIH and children resident in fluoridated area Teeth
Test
Incisors
MIH vs non-MIH
Fluoridated vs non-fluoridated
First permanent molarsa a
Fluoridated vs Non-fluoridated
Control
Risk ratio
95 % confidence interval
p value
All areas
4.0
3.6–4.5
\0.001
Fluoridated areas only
6.5
5.1–8.3
\0.001
Non-fluoridated areas only
3.6
3.1–4.0
\0.001
All children MIH group only
1.0 1.6
0.9–1.2 1.3–2.0
0.824 \0.001
Non-MIH group only
0.9
0.8–1.1
0.371
MIH group only
1.3
1.2–1.5
\0.001
Includes all demarcated and missing first permanent molars
Table 5 The risk ratio of teeth having diffuse defects in children with MIH relative to children without MIH by area Teeth
Test
Control
Incisors
MIH vs non-MIH
All areas Fluoridated areas only Non-fluoridated areas only All areas
First permanent molars
MIH vs non-MIH
Risk ratio
95 % confidence interval
p value
2.2
2.0–2.5
\0.001
2.5
2.0–2.9
\0.001
2.5
2.1–2.9
\0.001
4.4
3.8–5.0
\0.001
Fluoridated areas only
2.9
2.3–3.6
\0.001
Non-fluoridated areas only
6.0
5.0–7.3
\0.001
Table 6 The risk ratio of teeth having diffuse defects in children living in a fluoridated area relative to a non-fluoridated area by the presence of MIH Teeth
Test
Incisors
Fluoridated vs non-fluoridated
First permanent molars
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Fluoridated vs non-fluoridated
Control
Risk ratio
95 % confidence interval
p value
All children
2.6
2.3–2.9
\0.001
MIH group only
2.8
2.3–3.4
\0.001
Non-MIH group only
2.8
2.5–3.2
\0.001
All children
3.0
2.6–3.5
\0.001
MIH group only
2.2
1.8–2.8
\0.001
Non-MIH group only
4.7
3.9–5.7
\0.001
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Hypoplastic defects Tables 7 and 8 summarise the risk ratios for the presence of hypoplastic defects for children with MIH and for children living in the fluoridated area. Table 7 shows the risk of teeth in MIH children (relative to non-MIH children) having a hypoplastic defect according to area of residence in the study. This shows that regardless of area of residence, teeth of children with MIH had a much higher risk of hypoplastic defects. The risk ratios for FPMs were very large, again regardless of background fluoridation. The total numbers in these calculations however were relatively small (Table 3) which is reflected in the very large confidence intervals. Table 8 shows the risk of teeth in children in the fluoridated area (relative to living in the non-fluoridated area) having a hypoplastic defect according to the presence of MIH. It shows that there was very little impact of fluoride on the presence or absence of hypoplastic teeth apart from the FPMs of children with MIH. In this case for children in the fluoridated area, there was an increased risk which only just reached significance (risk ratio 1.4, 95 % CI 1.03–1.86).
Discussion Recently, the majority of prevalence studies into MIH have used the European Academy of Paediatric Dentistry (EAPD) Index which was proposed in 2003 and which was
aimed specifically at the identification of MIH (Weerheijm et al. 2003). Jalevik (2010) has suggested that the EAPD index should be the default index for all prevalence studies although there is no published validation of the index for the recording of MIH as a condition. However, by definition, the EAPD index only included demarcated defects therefore making it impossible to consider the relationship of other types of defects with MIH. One of the aims of this study was to consider the presentation of MIH in a community with high levels of background fluoride, and it was therefore important to also examine diffuse and hypoplastic defects and the way in which these related to demarcated defects and to each other. The index of choice was therefore the mDDE Index which had been validated (Clarkson and O’Mullane 1989) and therefore, given appropriate training and calibration, could be relied upon to be a true reflection of the presentation of disease in the communities studied. In the EAPD judgement criteria (Weerheijm et al. 2003), diagnosis of MIH is based on identification of the category of ‘‘demarcated opacity’’ in a first permanent molar and the application of that to the definition of MIH by ‘‘the presence of demarcated defects in a first permanent molar’’. In this study, the index used examined for ‘‘demarcated defects’’ as defined by mDDE. If these were present in a first permanent molar a diagnosis of MIH was attributed. This process is similar to a number of other studies that have used mDDE (Jalevik et al. 2001; Weerheijm et al. 2001; Zagdwon et al. 2002) for the
Table 7 The risk ratio of teeth having hypoplastic defects in children with MIH relative to children without MIH by area Teeth
Test
Control
Incisors
MIH vs non-MIH
All areas
First permanent molars
MIH vs non-MIH
Risk ratio
95 % confidence interval
p value
2.6
1.8–3.8
\0.001
Fluoridated areas only
5.0
2.3–11.0
\0.001
Non-fluoridated areas only
2.2
1.5–3.4
\0.001
All areas
24.5
18.2–32.9
\0.001
Fluoridated areas only
49.0
23.5–103.0
\0.001
Non-fluoridated areas only
21.0
15.2–29.1
\0.001
Table 8 The risk ratio of teeth having hypoplastic defects in children living in a fluoridated area relative to a non-fluoridated area by the presence of MIH Teeth
Test
Incisors
Fluoridated vs non-fluoridated
First permanent molars
Fluoridated vs non-fluoridated
Control
Risk ratio
95 % confidence interval
p value
All children
0.9
0.6–1.4
0.621
MIH group only
1.8
0.8–3.4
0.133
Non-MIH group only
0.8
0.4–1.3
0.352
All children
0.8
0.6–1.1
0.123
MIH group only
1.4
1.03–1.86
0.035
Non-MIH group only
0.6
0.3–1.2
0.154
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identification of MIH. Given that in both indices the key condition (demarcated defects) has the same definition it is reasonable to conclude that those children having a demarcated defect in a first permanent molar identified using mDDE satisfied the EAPD criteria (Weerheijm et al. 2003) for a diagnosis of MIH. Of interest was the finding that in this present study children were less likely to have MIH in the fluoridated area, but those that did were more severely affected. One of the confounding factors however was that children in the fluoridated area were more deprived than other areas and in this cohort deprivation was inversely proportional to the prevalence of MIH (Balmer et al. 2012). Logistic regression analysis using original IMD score, fluoridation level and gender showed that it was the IMD score (p = 0.023) that was the most likely reason for this difference. To consider the impact that background fluoridation had on the clinical presentation of MIH, MIH children were considered as a specific subgroup. Those children with MIH living in the fluoridated area were compared to those children with MIH living in the non-fluoridated area. Initial independent t tests simply examined if there were differences between the groups according to the mean number of teeth per case affected by each specific defect. This showed that children with MIH from the fluoridated area presented with increased numbers of teeth that had demarcated and diffuse defects although there was no difference in the number of hypoplastic teeth. To explore this in more detail risk ratios were calculated taking into account the presence of MIH and the background fluoridation levels. As would be expected MIH carried higher risk for the presence of demarcated defects in incisors regardless of area of residence. In addition, for children overall and for children without MIH, fluoridation had no increased risk of having an anterior tooth with a demarcated defect. This is consistent with most epidemiological studies which have shown that demarcated defects are unaffected by fluoride (Cutress et al. 1985; Suckling et al. 1987; Clarkson and O’Mullane 1989; Milsom and Mitropoulos 1990; Kanagaratnam et al. 2009). Fluoridation did however increase the risk of both anterior and posterior demarcated defects for children with MIH. So although fluoride, both in this study and in the majority of other studies, has not normally increased the risk of a demarcated defect, there was an increase in the presence of MIH. It could be argued that one possible explanation is simply that the examiners were mistaking diffuse for demarcated defects in this area. It should be noted however that the kappa scores for all examiners were good to very excellent. In addition, children without MIH in the fluoridated area had no increased risk of demarcated defects relative to similar children in the non-fluoridated area. Finally, if diffuse defects were being mistaken for
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demarcated ones the prevalence of MIH itself would be higher in the fluoridated area which was not the case. The results of this study suggest that fluoride may act to increase the severity of MIH when it does occur. Clearly fluoridation does not increase the likelihood of a traumatic physiological event; however, it may act by making ameloblasts more vulnerable to that event. This, in combination with an individual who is susceptible, could lead to an increased number of demarcated defects in that individual. Recent evidence has suggested that a low pH environment during the maturation stage encourages fluoride uptake in the form of hydrogen fluoride by ameloblasts, thereby causing impairment of function (Sharma et al. 2010) and ultimately cell death (Sierant and Bartlett 2012). Maturation of enamel takes place in a fairly narrow pH range of 6–7.4. Even at the lower pH of 6 it has been demonstrated that there can be significant influx of fluoride ions into the ameloblast. Therefore, tissue hypoxia (secondary to physiological insult) causing small decreases in environmental pH could result in significantly increased uptake of fluoride ion into ameloblasts with subsequent toxic effects. If this happened at an early enough stage of maturation then ameloblast damage or death could lead to the demarcated lesions seen in MIH. Whilst demarcated defects are considered to be the characteristic lesion of MIH, diffuse defects are not thought to be related to this condition and indeed the EAPD index has specifically excluded them (Weerheijm et al. 2003). This was based on the fact that diffuse lesions are associated with fluorosis and that fluoride was shown not to influence the occurrence of MIH (Koch 2003). It has meant, however, that none of the prevalence studies which have exclusively used this index have examined for diffuse defects. Of the few that have, the prevalence of diffuse lesions is generally low (Jalevik et al. 2001; Calderara et al. 2005; Fteita et al. 2006). Of note in this study is the increase in diffuse defects in MIH children. This increase is consistent regardless of fluoridated or non-fluoridated area and is a characteristic of MIH children that has not previously been reported. In clinical terms diffuse defects have not been traditionally associated with MIH although their presence may explain the success that some authors have reported in the use of microabrasion type techniques for anterior MIH defects (Wong and Winter 2002; Wright 2002). The mechanisms for the formation of diffuse and demarcated defects have generally been regarded as distinct. Ameloblasts are particularly vulnerable to systemic insult in the early and late maturation phases (Suga 1989). Defects of the early maturation phase have been linked with the classical demarcated defect (Jalevik and Noren 2000). Disruption of ameloblasts in the late maturation phase causes disturbance of matrix degradation (Suga 1989)
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which is similar to the mechanism that has been proposed for fluorosis. Recently, it has been suggested that the influence of fluoride in inhibiting protein degradation during maturation is more likely to be attributable to direct damage to the ameloblast as opposed to fluoride binding either to the proteins or proteases (Sierant and Bartlett 2012). In this case systemic insult to ameloblasts could result in defects which are similar in nature to diffuse ones. Certainly diffuse defects have been produced in animal studies in response to such chronic challenges as metabolic and respiratory acidosis and hypoxia (Whitford and AngmarMansson 1995), and many epidemiological studies have demonstrated the presence of diffuse defects in low fluoride areas (Suckling et al. 1987; Milsom and Mitropoulos 1990; Kanagaratnam et al. 2009). Hong et al. (2005) examined specifically for diffuse defects using the Fluorosis Risk Index (Pendrys 1990) and reported a risk ratio of 2.04 for its occurrence in relation to amoxicillin use at 3–6 months, a factor that has been implicated in the aetiology of MIH. Arrow (2009) demonstrated diffuse defects related to prematurity (odds ratio 2.75) and to general medical intervention secondary to medical problems (odds ratio 2.4), again, both factors that are normally linked with the occurrence of demarcated defects. There was clearly an extremely large increase in risk for MIH children having hypoplastic defects in the FPMs regardless of the area in which they lived and it is very likely that this reflected posteruptive breakdown. There was a marginally increased risk of hypoplasia in children with MIH living in a fluoridated area compared to children with MIH in a non-fluoridated area.
Conclusion Children with MIH had more diffuse defects. In addition, fluoridation increased the chances of demarcated defects appearing in MIH children and marginally increased the chances of hypoplastic defects. The study supports the view that, in terms of type and mechanism of enamel damage, there may be a relationship between fluoride toxicity and the aetiology which leads to the occurrence of demarcated defects. Conflict of interest of interest.
The authors declare that they have no conflict
References Arrow P. Risk factors in the occurrence of enamel defects of the first permanent molars among schoolchildren in Western Australia. Commun Dent Oral Epidemiol. 2009;37:405–15.
Balmer R, Toumba J, Godson J, Duggal M. The prevalence of molar incisor hypomineralisation in Northern England and its relationship to socioeconomic status and water fluoridation. Int J Pediatr Dent. 2012;22:250–7. Calderara PC, Gerthoux PM, Mocarelli P, et al. The prevalence of molar incisor hypomineralisation (MIH) in a group of Italian school children. Eur J Paediatr Dent. 2005;6:79–83. Cho S-Y, Ki Y, Chu V. Molar incisor hypomineralization in Hong Kong Chinese children. Int J Pediatr Dent. 2008;18:348–52. Clarkson J, O’mullane D. A modified DDE Index for use in epidemiological studies of enamel defects. J Dent Res. 1989;68:445–50. Commission on Oral Health Research and Epidemiology. A review of the developmental defects of enamel index (DDE Index). Report of an FDI working group. Int Dent J. 1992;42:411–26. Cutress TW, Suckling GW, Pearce EI, Ball ME. Defects of tooth enamel in children in fluoridated and non-fluoridated water areas of the Auckland region. NZ Dent J. 1985;81:12–9. Da Costa-Silva CM, Jeremias F, De Souza JF, et al. Molar incisor hypomineralization: prevalence, severity and clinical consequences in Brazilian children. Int J Pediatr Dent. 2010;20:426–34. Fteita D, Ali A, Alaluusua S. Molar-incisor hypomineralization (MIH) in a group of school-aged children in Benghazi, Libya. Eur Arch Paediatr Dent Off J Eur Acad Paediatr Dent. 2006;7:92–5. Holtta P, Kiviranta H, Leppaniemi A, et al. Developmental dental defects in children who reside by a river polluted by dioxins and furans. Arch Environ Health. 2001;56:522–8. Hong L, Levy SM, Warren JJ, et al. Association of amoxicillin use during early childhood with developmental tooth enamel defects. Arch Pediatr Adolesc Med. 2005;159:943–8. Jalevik B, Noren JG. Enamel hypomineralization of permanent first molars: a morphological study and survey of possible aetiological factors. Int J Pediatr Dent. 2000;10:278–89. Jalevik B, Klingberg G, Barregard L, Noren JG. The prevalence of demarcated opacities in permanent first molars in a group of Swedish children. Acta Odontol Scand. 2001;59:255–60. Jalevik B. Prevalence and diagnosis of molar-incisor-hypomineralisation (MIH): a systematic review. EurArch Paediatr Dent Off J Eur Acad Paediatr Dent. 2010;11:59–64. Kanagaratnam S, Schluter P, Durward C, Mahood R, Mackay T. Enamel defects and dental caries in 9-year-old children living in fluoridated and nonfluoridated areas of Auckland, New Zealand. Commun Dent Oral Epidemiol. 2009;37:250–9. Koch G. Prevalence of enamel mineralisation disturbances in an area with 1–1.2 ppm F in drinking water. Review and summary of a report published in Sweden in 1981. Eur J Paediatr Dent. 2003;4:127–8. Milsom K, Mitropoulos CM. Enamel defects in 8-year-old children in fluoridated and non-fluoridated parts of Cheshire. Caries Res. 1990;24:286–9. NHS Dental Epidemiological Oral Health Survey of 12 year old children in England 2008/2009 National Protocol. 2008. Available http://www.nwph.net/dentalhealth/survey-results-12.aspx. Accessed June 2013. NHS North East—Dentistry. The Strategic Health Authority for the North East (Online). 2011. Available http://www.northeast.nhs. uk/news-centre/news-packs/38187E9CB86249E483B739F0EB73 1E56.aspx. Accessed June 2013. Pendrys DG. The fluorosis risk index: a method for investigating risk factors. J Public Health Dent. 1990;50:291–8. Sharma R, Tsuchiya M, Skobe Z, Tannous BA, Bartlett JD. The acid test of fluoride: how pH modulates toxicity. PLoS One. 2010;5:e10895 (electronic resource).
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Eur Arch Paediatr Dent Sierant ML, Bartlett JD. Stress Response pathways in ameloblasts: implications for amelogenesis and dental fluorosis. Cells. 2012;1:631–45. Suckling GW, Herbison GP, Brown RH. Etiological factors influencing the prevalence of developmental defects of dental enamel in 9-year-old New Zealand children participating in a health and development study. J Dent Res. 1987;66:1466–9. Suga S. Enamel hypomineralization viewed from the pattern of progressive mineralization of human and monkey developing enamel. Adv Dent Res. 1989;3:188–98. Weerheijm KL, Jalevik B, Alaluusua S. Molar-incisor hypomineralisation. Caries Res. 2001;35(5):390–1. 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;4:110–3.
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Weerheijm KL. Molar incisor hypomineralisation (MIH). Eur J Paediatr Dent. 2003;4:114–20. Whitford GM, Angmar-Mansson B. Fluorosis-like effects of acidosis, but not NH4?, on rat incisor enamel. Caries Res. 1995;29:20–5. Wong FSL, Winter GB. Effectiveness of microabrasion technique for improvement of dental aesthetics. Br Dent J. 2002;193:155–8. Wright JT. The etch-bleach-seal technique for managing stained enamel defects in young permanent incisors. Pediatr Dent. 2002;24:249–52. Zagdwon AM, Toumba KJ, Curzon ME. The prevalence of developmental enamel defects in permanent molars in a group of English school children. Eur J Paediatr Dent. 2002;3(2):91–6.
ORIGINAL SCIENTIFIC ARTICLE
A comparison of the presentation of molar incisor hypomineralisation in two communities with different fluoride exposure R. Balmer • K. J. Toumba • T. Munyombwe • M. S. Duggal
Received: 29 July 2014 / Accepted: 17 December 2014 Ó European Academy of Paediatric Dentistry 2015
Abstract Aim To compare the clinical presentation of two cohorts of children diagnosed with molar incisor hypomineralisation (MIH) and living in areas of low and high background fluoridation. Methods The study population comprised 12-year-old children participating in the 2008–2009 National Dental Epidemiological Programme in five regions in Northern England. Participating dentists were trained and calibrated in the use of the modified Developmental Defects of Enamel Index. Children were examined at school under direct vision with the aid of a dental mirror. First permanent molars and incisors were recorded for the presence and type of enamel defects greater than 2 mm. A diagnosis of MIH was ascribed to any child with a demarcated defect in any first permanent molar. Risk ratios for the occurrence of demarcated, diffuse and hypoplastic defects were generated for MIH children in the fluoridated and non-fluoridated area. Results 3,233 children were examined. The prevalence of MIH in the fluoridated community was 11 % and in the non-fluoridated community was 17.5 %. Incisors in children with MIH were at greater risk of having demarcated defects (risk ratio 4.0, 3.6–4.5) and diffuse defects (risk ratio 2.2, 2.0–2.5). Molars in children with MIH were at greater risk of diffuse defects (risk ratio 4.4, 3.8–5.0). The teeth of children with MIH living in the fluoridated area were at greater risk of demarcated defects for both incisors
R. Balmer (&) K. J. Toumba T. Munyombwe M. S. Duggal Department of Child Dental Health, Leeds Dental Institute, University of Leeds, Clarendon Way, Leeds LS2 9LU, UK e-mail: [email protected]
(risk ratio 1.6, 1.3–2.0) and molars (risk ratio 1.3, 1.2–1.5) relative to the teeth of MIH children living in the nonfluoridated area. Conclusions Children with MIH were at increased risk of both diffuse and demarcated defects in their incisors. Children with MIH living in the fluoridated area were at increased risk of diffuse and demarcated defects relative to MIH children living in the non-fluoridated area. Keywords Molar incisor hypomineralisation Enamel defects Fluoride
Introduction Molar incisor hypomineralisation (MIH) has been defined as enamel hypomineralisation of systemic origin of 1–4 permanent first molars frequently associated with affected incisors (Weerheijm 2003). The classical defect is a demarcated one which, particularly in the posterior teeth, can breakdown under post eruptive occlusal forces. The aetiology is likely to be secondary to ameloblast damage in the transition phase (early maturation phase) which results in yellow/brown, porous lesions. Fluoride also causes damage during the maturation phase, probably by inhibition of protein degradation resulting in failure of the enamel to mineralise fully. In these cases the lesion is diffuse and confined to the subsurface area. The two conditions of fluorosis and MIH are normally considered distinct in terms of both the pathogenesis and presentation. Most studies examining enamel defects in fluoridated areas have demonstrated increased diffuse defects but no increase in demarcated defects (Cutress et al. 1985; Clarkson and O’Mullane 1989; Kanagaratnam et al. 2009; Milsom and Mitropoulos 1990).
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The overall prevalence of MIH has been reported at 2.3–40 %. In 2003 Koch compared the prevalence of MIHtype lesions in children with and without high background exposure to fluoride (Koch 2003). This study found a generally low level of children with the MIH-type lesion and no difference according to fluoride exposure. It concluded that fluoride was not an aetiological factor in MIH. No other studies have specifically compared MIH with regard to background fluoride levels although a study in Brazil did note that the prevalence of MIH in the urban fluoridated (0.7 ppm) area was lower than in the nonfluoridated rural area with rates of 17.8 and 24.9 %, respectively (Da Costa-Silva et al. 2010). A similar pattern emerged in Finland in a study whose aim was to measure MIH prevalence secondary to local dioxin contamination (Holtta et al. 2001). In this study, MIH prevalence was 5.6 % in the fluoridated town compared to a prevalence of 14.2 % in the non-fluoridated area. The authors attributed this difference to the possibility that diffuse lesions in the fluoridated area had masked the presence of MIH. It is interesting to note that of the other prevalence studies in the literature, the two with the lowest reported rates were also the only studies to be carried out in areas of raised fluoridation levels. Cho et al. (2008) reported a prevalence of only 2.8 % in Hong Kong which was fluoridated to a level of 0.5 ppm. A further study by Fteita et al. (2006) in an area of Libya with fluoridation 0.4 ppm had a MIH prevalence rate of 2.9 %. Although these previous studies reported on specific prevalence of MIH, there have been no published studies which have examined the impact of fluoridation on the presentation of MIH. The aim of this study therefore was to compare the clinical presentation of two cohorts of children diagnosed with MIH and living in areas of low and high background fluoridation. This analysis formed one aspect of a study which examined overall prevalence of MIH in a number of areas in Northern England against key demographic indicators (Balmer et al. 2012).
good to excellent kappa scores. The index chosen was the modified Developmental Defects of Enamel (mDDE) (1992) which scored tooth surfaces of index teeth (first permanent molars and incisors) for the presence of demarcated, diffuse or hypoplastic defects or combinations of these three. Only defects larger than 2 mm were recorded. Combination defects were broken down to the presence or absence of each of the components. For instance code 5, demarcated and diffuse, was broken down into the presence of both codes 1 (demarcated defect) and 2 (diffuse defect). Therefore, a tooth surface was coded for the absence or presence of each of the three basic defects. For posterior teeth, this therefore resulted in each posterior tooth being scored for the presence or absence of a demarcated defect, a hypoplastic defect and a diffuse defect for any of the three index surfaces. For example, a molar tooth with a combined hypoplastic and demarcated defect (code 6) on the occlusal surface and a diffuse defect only (code 2) on the buccal surface would score positive for all three basic defects. Diagnosis of MIH was attributed to any participant who recorded a demarcated defect on any of the permanent molars. In effect they were considered to have MIH if any first permanent molar tooth surface had a demarcated defect either in isolation or in combination with another defect. In cases, where all first permanent molars were absent MIH diagnosis was judged if any demarcated defects were noted on the incisors. If some of the first permanent molars were missing and the remainder had no defects, MIH diagnosis was also attributed based on the presence of defects in the anterior teeth. Current residential postcode for each child was correlated with information from NHS North East (2011). This identified those children who resided in areas which had had the fluoride level of their water supply adjusted to one part per million. Postcode was also used to obtain an index of multiple deprivation (IMD) score and quintile as described in a previous publication (Balmer et al. 2012).
Materials and methods Statistics Materials and methods for sample selection, training and calibration of examiners and for data collection and analysis have been provided in detail in a previous publication (Balmer et al. 2012). In summary, the sample consisted of 12-year-old children in the North of England participating in the NHS National Dental Epidemiological Programme (2008). The specific areas covered were Newcastle which has an artificially fluoridated water supply and North Yorkshire, Hull, Bradford and Airedale which are not artificially fluoridated. Training and calibration of examiners were carried out using clinical photographs which yielded
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Data were entered into IBM SPSS Statistics version 20 which was used to generate the results of independent t tests for overall comparison of numbers of defects in the two communities. A binary logistic regression model was used to account for the effect of fluoridation, gender and deprivation on the occurrence of MIH. Risk ratios were calculated in StataSE version 12 by analysing number of teeth exposed to one of the two risk factors (fluoridation or presence of MIH) against number of teeth with the presence or absence of each of the three basic defects.
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Results The total 12-year-old population of all the regions was 21,986. Of these 4,795 were invited to participate in the survey of whom 3,233 (67.4 %) were examined. 852 children were absent on the day of the examination, 636 declined examination, and for 74 children, the reason for non-examination was not recorded. Of the 3,233 examined 518 were diagnosed with molar incisor hypomineralisation, with a prevalence rate of 16.02 % (95 % CI 14.77–17.33 %). Table 1 shows the difference in MIH prevalence between the fluoridated and non-fluoridated areas. Prevalence rate in the fluoridated area was 11 % and was lower than that of the non-fluoridated area (17.5 %). Chi squared test indicated a significant difference (v2 = 18.2, p \ 0.001). Area of residence (fluoridated vs non-fluoridated), gender and deprivation (by original IMD score) were entered into a binary multiple logistic regression model with occurrence of MIH as the outcome. The result is shown in Table 2. In this model area of residence was no longer significant (p = 0.186) whereas IMD score remained significant (p = 0.023). The number, type and distribution of teeth with specific defects in children with MIH residing in the fluoridated area were compared with children with MIH in the nonfluoridated area. Independent samples t tests were used to analyse these data and a summary is shown in Table 3. Further detailed analyses were carried out by calculation of risk ratios for the occurrence of specific defects in teeth according to the presence of MIH and fluoridation.
children living in a fluoridated area. As expected, the risk ratios for the incisors of children with MIH (relative to those without MIH) were high regardless of whether those children were living in a fluoridated area or not (6.5 and 3.6, respectively). For those children with MIH and living in a fluoridated area, the risk ratio of an incisor having a demarcated defect relative to children with MIH and living in a non-fluoridated area was 1.6 (95 % CI 1.3––2.0). In addition, the risk ratio for a molar in MIH children in the fluoridated area having a demarcated defect relative to children in the non-fluoridated area was 1.3 (95 % CI 1.2–1.5). Deprivation and area of residence for MIH children only were entered into two binary logistic Poisson regression models with the presence of demarcated defects in anterior teeth and the presence of demarcated defects in posterior teeth as the outcomes. The odds ratio for an incisor tooth having a demarcated defect in a MIH child in the fluoridated area was 1.73 (95 % CI 1.33–2.25) relative to a MIH child in the non-fluoridated area. The odds ratio for a molar tooth having a demarcated defect was 1.30 (95 % CI 1.07–1.57). In both of these models the effect of socioeconomic status was insignificant. Therefore, in this study, living in the fluoridated area increased the chance of children with MIH having demarcated defects in incisors and molars even after accounting for socioeconomic differences of the two communities. Fluoridation, however, had no impact in terms of demarcated defects on all children overall in the study or on those children who did not have MIH (risk ratios of 1.0 and 0.9, respectively).
Demarcated defects Table 4 summarises the risk ratios for the presence of demarcated defects on the teeth of children with MIH and of Table 1 Prevalence of MIH in fluoridated and non-fluoridated areas Area
Total examined
Fluoridated Non-fluoridated
Number with MIH
Percentage with MIH (95 % CI)
726
80
11.0 (8.8–13.5)
2,507
438
17.5 (16.0–19.0)
CI confidence interval Table 2 Logistic regression demonstrating impact of fluoridation, gender and IMD score on the occurrence of MIH p value
Odds ratio
95 % CI for odds ratio
Fluoridated area
0.186
1.264
0.893–1.789
Gender
0.595
1.059
0.856–1.310
IMD score
0.023
0.992
0.986–0.999
IMD index of multiple deprivation, CI confidence interval
Diffuse defects Tables 5 and 6 summarise the risk ratios for the presence of diffuse defects on the teeth of children with MIH and of children living in fluoridated areas. Table 5 shows the risk of teeth in MIH children (relative to non-MIH children) having a diffuse defect according to area of residence. It demonstrated that, regardless of the area in which the children lived and of which teeth were being examined (incisors or FPMs) and teeth of MIH children were at increased risk of diffuse defects. Therefore, in this study, MIH was a risk factor for diffuse defects independent of background fluoridation. Table 6 shows the risk of teeth in children in fluoridated area (relative to living in a non-fluoridated area) having a diffuse defect according to the presence of MIH. As would be expected, for both anterior and posterior teeth, the risk is increased in the fluoridated area regardless of whether the children had MIH or not.
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Eur Arch Paediatr Dent Table 3 Summary of the prevalence of different defects in MIH cases in fluoridated and non-fluoridated areas
Demarcated incisors
N (fluoridated)
Mean number/case fluoridated (SD)
N (non-fluoridated)
Mean number/case non-fluoridated (SD)
p value
109
1.36 (1.37)
356
0.81 (1.16)
\0.001* \0.001*
Demarcated/missing FPMs
187
2.34 (1.02)
782
1.79 (0.97)
Diffuse incisors
126
1.58 (2.78)
246
0.56 (1.3)
0.002*
Diffuse FPMs
83
1.04 (1.55)
211
0.48 (0.97)
0.003*
Hypoplastic incisors
10
0.13 (0.4)
32
0.07 (0.34)
0.286
Hypoplastic FPMs
47
0.59 (0.9)
192
0.44 (0.83)
0.143
SD standard deviation, N number of defective teeth * Significant p \ 0.05, independent samples t test
Table 4 The risk ratios of teeth having demarcated defects in children with MIH and children resident in fluoridated area Teeth
Test
Incisors
MIH vs non-MIH
Fluoridated vs non-fluoridated
First permanent molarsa a
Fluoridated vs Non-fluoridated
Control
Risk ratio
95 % confidence interval
p value
All areas
4.0
3.6–4.5
\0.001
Fluoridated areas only
6.5
5.1–8.3
\0.001
Non-fluoridated areas only
3.6
3.1–4.0
\0.001
All children MIH group only
1.0 1.6
0.9–1.2 1.3–2.0
0.824 \0.001
Non-MIH group only
0.9
0.8–1.1
0.371
MIH group only
1.3
1.2–1.5
\0.001
Includes all demarcated and missing first permanent molars
Table 5 The risk ratio of teeth having diffuse defects in children with MIH relative to children without MIH by area Teeth
Test
Control
Incisors
MIH vs non-MIH
All areas Fluoridated areas only Non-fluoridated areas only All areas
First permanent molars
MIH vs non-MIH
Risk ratio
95 % confidence interval
p value
2.2
2.0–2.5
\0.001
2.5
2.0–2.9
\0.001
2.5
2.1–2.9
\0.001
4.4
3.8–5.0
\0.001
Fluoridated areas only
2.9
2.3–3.6
\0.001
Non-fluoridated areas only
6.0
5.0–7.3
\0.001
Table 6 The risk ratio of teeth having diffuse defects in children living in a fluoridated area relative to a non-fluoridated area by the presence of MIH Teeth
Test
Incisors
Fluoridated vs non-fluoridated
First permanent molars
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Fluoridated vs non-fluoridated
Control
Risk ratio
95 % confidence interval
p value
All children
2.6
2.3–2.9
\0.001
MIH group only
2.8
2.3–3.4
\0.001
Non-MIH group only
2.8
2.5–3.2
\0.001
All children
3.0
2.6–3.5
\0.001
MIH group only
2.2
1.8–2.8
\0.001
Non-MIH group only
4.7
3.9–5.7
\0.001
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Hypoplastic defects Tables 7 and 8 summarise the risk ratios for the presence of hypoplastic defects for children with MIH and for children living in the fluoridated area. Table 7 shows the risk of teeth in MIH children (relative to non-MIH children) having a hypoplastic defect according to area of residence in the study. This shows that regardless of area of residence, teeth of children with MIH had a much higher risk of hypoplastic defects. The risk ratios for FPMs were very large, again regardless of background fluoridation. The total numbers in these calculations however were relatively small (Table 3) which is reflected in the very large confidence intervals. Table 8 shows the risk of teeth in children in the fluoridated area (relative to living in the non-fluoridated area) having a hypoplastic defect according to the presence of MIH. It shows that there was very little impact of fluoride on the presence or absence of hypoplastic teeth apart from the FPMs of children with MIH. In this case for children in the fluoridated area, there was an increased risk which only just reached significance (risk ratio 1.4, 95 % CI 1.03–1.86).
Discussion Recently, the majority of prevalence studies into MIH have used the European Academy of Paediatric Dentistry (EAPD) Index which was proposed in 2003 and which was
aimed specifically at the identification of MIH (Weerheijm et al. 2003). Jalevik (2010) has suggested that the EAPD index should be the default index for all prevalence studies although there is no published validation of the index for the recording of MIH as a condition. However, by definition, the EAPD index only included demarcated defects therefore making it impossible to consider the relationship of other types of defects with MIH. One of the aims of this study was to consider the presentation of MIH in a community with high levels of background fluoride, and it was therefore important to also examine diffuse and hypoplastic defects and the way in which these related to demarcated defects and to each other. The index of choice was therefore the mDDE Index which had been validated (Clarkson and O’Mullane 1989) and therefore, given appropriate training and calibration, could be relied upon to be a true reflection of the presentation of disease in the communities studied. In the EAPD judgement criteria (Weerheijm et al. 2003), diagnosis of MIH is based on identification of the category of ‘‘demarcated opacity’’ in a first permanent molar and the application of that to the definition of MIH by ‘‘the presence of demarcated defects in a first permanent molar’’. In this study, the index used examined for ‘‘demarcated defects’’ as defined by mDDE. If these were present in a first permanent molar a diagnosis of MIH was attributed. This process is similar to a number of other studies that have used mDDE (Jalevik et al. 2001; Weerheijm et al. 2001; Zagdwon et al. 2002) for the
Table 7 The risk ratio of teeth having hypoplastic defects in children with MIH relative to children without MIH by area Teeth
Test
Control
Incisors
MIH vs non-MIH
All areas
First permanent molars
MIH vs non-MIH
Risk ratio
95 % confidence interval
p value
2.6
1.8–3.8
\0.001
Fluoridated areas only
5.0
2.3–11.0
\0.001
Non-fluoridated areas only
2.2
1.5–3.4
\0.001
All areas
24.5
18.2–32.9
\0.001
Fluoridated areas only
49.0
23.5–103.0
\0.001
Non-fluoridated areas only
21.0
15.2–29.1
\0.001
Table 8 The risk ratio of teeth having hypoplastic defects in children living in a fluoridated area relative to a non-fluoridated area by the presence of MIH Teeth
Test
Incisors
Fluoridated vs non-fluoridated
First permanent molars
Fluoridated vs non-fluoridated
Control
Risk ratio
95 % confidence interval
p value
All children
0.9
0.6–1.4
0.621
MIH group only
1.8
0.8–3.4
0.133
Non-MIH group only
0.8
0.4–1.3
0.352
All children
0.8
0.6–1.1
0.123
MIH group only
1.4
1.03–1.86
0.035
Non-MIH group only
0.6
0.3–1.2
0.154
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identification of MIH. Given that in both indices the key condition (demarcated defects) has the same definition it is reasonable to conclude that those children having a demarcated defect in a first permanent molar identified using mDDE satisfied the EAPD criteria (Weerheijm et al. 2003) for a diagnosis of MIH. Of interest was the finding that in this present study children were less likely to have MIH in the fluoridated area, but those that did were more severely affected. One of the confounding factors however was that children in the fluoridated area were more deprived than other areas and in this cohort deprivation was inversely proportional to the prevalence of MIH (Balmer et al. 2012). Logistic regression analysis using original IMD score, fluoridation level and gender showed that it was the IMD score (p = 0.023) that was the most likely reason for this difference. To consider the impact that background fluoridation had on the clinical presentation of MIH, MIH children were considered as a specific subgroup. Those children with MIH living in the fluoridated area were compared to those children with MIH living in the non-fluoridated area. Initial independent t tests simply examined if there were differences between the groups according to the mean number of teeth per case affected by each specific defect. This showed that children with MIH from the fluoridated area presented with increased numbers of teeth that had demarcated and diffuse defects although there was no difference in the number of hypoplastic teeth. To explore this in more detail risk ratios were calculated taking into account the presence of MIH and the background fluoridation levels. As would be expected MIH carried higher risk for the presence of demarcated defects in incisors regardless of area of residence. In addition, for children overall and for children without MIH, fluoridation had no increased risk of having an anterior tooth with a demarcated defect. This is consistent with most epidemiological studies which have shown that demarcated defects are unaffected by fluoride (Cutress et al. 1985; Suckling et al. 1987; Clarkson and O’Mullane 1989; Milsom and Mitropoulos 1990; Kanagaratnam et al. 2009). Fluoridation did however increase the risk of both anterior and posterior demarcated defects for children with MIH. So although fluoride, both in this study and in the majority of other studies, has not normally increased the risk of a demarcated defect, there was an increase in the presence of MIH. It could be argued that one possible explanation is simply that the examiners were mistaking diffuse for demarcated defects in this area. It should be noted however that the kappa scores for all examiners were good to very excellent. In addition, children without MIH in the fluoridated area had no increased risk of demarcated defects relative to similar children in the non-fluoridated area. Finally, if diffuse defects were being mistaken for
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demarcated ones the prevalence of MIH itself would be higher in the fluoridated area which was not the case. The results of this study suggest that fluoride may act to increase the severity of MIH when it does occur. Clearly fluoridation does not increase the likelihood of a traumatic physiological event; however, it may act by making ameloblasts more vulnerable to that event. This, in combination with an individual who is susceptible, could lead to an increased number of demarcated defects in that individual. Recent evidence has suggested that a low pH environment during the maturation stage encourages fluoride uptake in the form of hydrogen fluoride by ameloblasts, thereby causing impairment of function (Sharma et al. 2010) and ultimately cell death (Sierant and Bartlett 2012). Maturation of enamel takes place in a fairly narrow pH range of 6–7.4. Even at the lower pH of 6 it has been demonstrated that there can be significant influx of fluoride ions into the ameloblast. Therefore, tissue hypoxia (secondary to physiological insult) causing small decreases in environmental pH could result in significantly increased uptake of fluoride ion into ameloblasts with subsequent toxic effects. If this happened at an early enough stage of maturation then ameloblast damage or death could lead to the demarcated lesions seen in MIH. Whilst demarcated defects are considered to be the characteristic lesion of MIH, diffuse defects are not thought to be related to this condition and indeed the EAPD index has specifically excluded them (Weerheijm et al. 2003). This was based on the fact that diffuse lesions are associated with fluorosis and that fluoride was shown not to influence the occurrence of MIH (Koch 2003). It has meant, however, that none of the prevalence studies which have exclusively used this index have examined for diffuse defects. Of the few that have, the prevalence of diffuse lesions is generally low (Jalevik et al. 2001; Calderara et al. 2005; Fteita et al. 2006). Of note in this study is the increase in diffuse defects in MIH children. This increase is consistent regardless of fluoridated or non-fluoridated area and is a characteristic of MIH children that has not previously been reported. In clinical terms diffuse defects have not been traditionally associated with MIH although their presence may explain the success that some authors have reported in the use of microabrasion type techniques for anterior MIH defects (Wong and Winter 2002; Wright 2002). The mechanisms for the formation of diffuse and demarcated defects have generally been regarded as distinct. Ameloblasts are particularly vulnerable to systemic insult in the early and late maturation phases (Suga 1989). Defects of the early maturation phase have been linked with the classical demarcated defect (Jalevik and Noren 2000). Disruption of ameloblasts in the late maturation phase causes disturbance of matrix degradation (Suga 1989)
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which is similar to the mechanism that has been proposed for fluorosis. Recently, it has been suggested that the influence of fluoride in inhibiting protein degradation during maturation is more likely to be attributable to direct damage to the ameloblast as opposed to fluoride binding either to the proteins or proteases (Sierant and Bartlett 2012). In this case systemic insult to ameloblasts could result in defects which are similar in nature to diffuse ones. Certainly diffuse defects have been produced in animal studies in response to such chronic challenges as metabolic and respiratory acidosis and hypoxia (Whitford and AngmarMansson 1995), and many epidemiological studies have demonstrated the presence of diffuse defects in low fluoride areas (Suckling et al. 1987; Milsom and Mitropoulos 1990; Kanagaratnam et al. 2009). Hong et al. (2005) examined specifically for diffuse defects using the Fluorosis Risk Index (Pendrys 1990) and reported a risk ratio of 2.04 for its occurrence in relation to amoxicillin use at 3–6 months, a factor that has been implicated in the aetiology of MIH. Arrow (2009) demonstrated diffuse defects related to prematurity (odds ratio 2.75) and to general medical intervention secondary to medical problems (odds ratio 2.4), again, both factors that are normally linked with the occurrence of demarcated defects. There was clearly an extremely large increase in risk for MIH children having hypoplastic defects in the FPMs regardless of the area in which they lived and it is very likely that this reflected posteruptive breakdown. There was a marginally increased risk of hypoplasia in children with MIH living in a fluoridated area compared to children with MIH in a non-fluoridated area.
Conclusion Children with MIH had more diffuse defects. In addition, fluoridation increased the chances of demarcated defects appearing in MIH children and marginally increased the chances of hypoplastic defects. The study supports the view that, in terms of type and mechanism of enamel damage, there may be a relationship between fluoride toxicity and the aetiology which leads to the occurrence of demarcated defects. Conflict of interest of interest.
The authors declare that they have no conflict
References Arrow P. Risk factors in the occurrence of enamel defects of the first permanent molars among schoolchildren in Western Australia. Commun Dent Oral Epidemiol. 2009;37:405–15.
Balmer R, Toumba J, Godson J, Duggal M. The prevalence of molar incisor hypomineralisation in Northern England and its relationship to socioeconomic status and water fluoridation. Int J Pediatr Dent. 2012;22:250–7. Calderara PC, Gerthoux PM, Mocarelli P, et al. The prevalence of molar incisor hypomineralisation (MIH) in a group of Italian school children. Eur J Paediatr Dent. 2005;6:79–83. Cho S-Y, Ki Y, Chu V. Molar incisor hypomineralization in Hong Kong Chinese children. Int J Pediatr Dent. 2008;18:348–52. Clarkson J, O’mullane D. A modified DDE Index for use in epidemiological studies of enamel defects. J Dent Res. 1989;68:445–50. Commission on Oral Health Research and Epidemiology. A review of the developmental defects of enamel index (DDE Index). Report of an FDI working group. Int Dent J. 1992;42:411–26. Cutress TW, Suckling GW, Pearce EI, Ball ME. Defects of tooth enamel in children in fluoridated and non-fluoridated water areas of the Auckland region. NZ Dent J. 1985;81:12–9. Da Costa-Silva CM, Jeremias F, De Souza JF, et al. Molar incisor hypomineralization: prevalence, severity and clinical consequences in Brazilian children. Int J Pediatr Dent. 2010;20:426–34. Fteita D, Ali A, Alaluusua S. Molar-incisor hypomineralization (MIH) in a group of school-aged children in Benghazi, Libya. Eur Arch Paediatr Dent Off J Eur Acad Paediatr Dent. 2006;7:92–5. Holtta P, Kiviranta H, Leppaniemi A, et al. Developmental dental defects in children who reside by a river polluted by dioxins and furans. Arch Environ Health. 2001;56:522–8. Hong L, Levy SM, Warren JJ, et al. Association of amoxicillin use during early childhood with developmental tooth enamel defects. Arch Pediatr Adolesc Med. 2005;159:943–8. Jalevik B, Noren JG. Enamel hypomineralization of permanent first molars: a morphological study and survey of possible aetiological factors. Int J Pediatr Dent. 2000;10:278–89. Jalevik B, Klingberg G, Barregard L, Noren JG. The prevalence of demarcated opacities in permanent first molars in a group of Swedish children. Acta Odontol Scand. 2001;59:255–60. Jalevik B. Prevalence and diagnosis of molar-incisor-hypomineralisation (MIH): a systematic review. EurArch Paediatr Dent Off J Eur Acad Paediatr Dent. 2010;11:59–64. Kanagaratnam S, Schluter P, Durward C, Mahood R, Mackay T. Enamel defects and dental caries in 9-year-old children living in fluoridated and nonfluoridated areas of Auckland, New Zealand. Commun Dent Oral Epidemiol. 2009;37:250–9. Koch G. Prevalence of enamel mineralisation disturbances in an area with 1–1.2 ppm F in drinking water. Review and summary of a report published in Sweden in 1981. Eur J Paediatr Dent. 2003;4:127–8. Milsom K, Mitropoulos CM. Enamel defects in 8-year-old children in fluoridated and non-fluoridated parts of Cheshire. Caries Res. 1990;24:286–9. NHS Dental Epidemiological Oral Health Survey of 12 year old children in England 2008/2009 National Protocol. 2008. Available http://www.nwph.net/dentalhealth/survey-results-12.aspx. Accessed June 2013. NHS North East—Dentistry. The Strategic Health Authority for the North East (Online). 2011. Available http://www.northeast.nhs. uk/news-centre/news-packs/38187E9CB86249E483B739F0EB73 1E56.aspx. Accessed June 2013. Pendrys DG. The fluorosis risk index: a method for investigating risk factors. J Public Health Dent. 1990;50:291–8. Sharma R, Tsuchiya M, Skobe Z, Tannous BA, Bartlett JD. The acid test of fluoride: how pH modulates toxicity. PLoS One. 2010;5:e10895 (electronic resource).
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Eur Arch Paediatr Dent Sierant ML, Bartlett JD. Stress Response pathways in ameloblasts: implications for amelogenesis and dental fluorosis. Cells. 2012;1:631–45. Suckling GW, Herbison GP, Brown RH. Etiological factors influencing the prevalence of developmental defects of dental enamel in 9-year-old New Zealand children participating in a health and development study. J Dent Res. 1987;66:1466–9. Suga S. Enamel hypomineralization viewed from the pattern of progressive mineralization of human and monkey developing enamel. Adv Dent Res. 1989;3:188–98. Weerheijm KL, Jalevik B, Alaluusua S. Molar-incisor hypomineralisation. Caries Res. 2001;35(5):390–1. 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;4:110–3.
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Weerheijm KL. Molar incisor hypomineralisation (MIH). Eur J Paediatr Dent. 2003;4:114–20. Whitford GM, Angmar-Mansson B. Fluorosis-like effects of acidosis, but not NH4?, on rat incisor enamel. Caries Res. 1995;29:20–5. Wong FSL, Winter GB. Effectiveness of microabrasion technique for improvement of dental aesthetics. Br Dent J. 2002;193:155–8. Wright JT. The etch-bleach-seal technique for managing stained enamel defects in young permanent incisors. Pediatr Dent. 2002;24:249–52. Zagdwon AM, Toumba KJ, Curzon ME. The prevalence of developmental enamel defects in permanent molars in a group of English school children. Eur J Paediatr Dent. 2002;3(2):91–6.
