Risk factors of hypomineralised second primary molars in a group of Iraqi schoolchildren.
A developmental defect of enamel has been causing growing concern worldwide. This qualitative disruption in mineralisation in permanent teeth has been denominated as molar incisor hypomineralisation (MIH). It is identified visually as an alteration in enamel translucency with a clear border, variable in degree which can be white, yellow or brown in colour [Weerheijm, 2004]. It has been reported as affecting the first permanent molars primarily and occasionally permanent incisors. Demarcated hypomineralised lesions have also been diagnosed in second primary molars [Weerheijm et al., 2003, Lygidakis et al., 2010]. A hypomineralised second primary molar has been defined as idiopathic hypomineralisation of one to four second primary molars [Elfrink et al., 2008].
Demarcated hypomineralisation lesions have been associated with their detrimental role for the affected individuals by causing rapid loss of enamel, encouraging plaque retention and caries development (Leppaniemi et al., 2001, Mahoney 2001, Jalevik and Klingberg, 2002). Investigations into the occurrence of hypomineralised second primary molars revealed that hypomineralisation is a significant dental caries risk factor as defective teeth were associated with a greater prevalence of dental decay in comparison to other primary teeth [Elfrink et al., 2006, 2010].
The majority of the studies involving primary teeth have focused on the prevalence of enamel hypoplasia rather than hypomineralisation. The available clinical studies on the prevalence of the demarcated hypomineralisation defects in primary teeth are scarce and illustrate a wide variation in prevalence rates without specifying individual tooth type [Ghanim et al., 2012]
Demarcated hypomineralisation defects are thought to have a multifactorial aetiology with pathogenesis occurring during the pre-, peri- or post-natal period and disturbing the ameloblasts during the later mineralisation phase of amelogenesis [Jalevik and Noren, 2000]. Crown calcification for the second primary molar begins around the 18th gestational week and completed by the end of the first year of childhood [Kraus and Jordan, 2004].
Mineralisation of this tooth approximates that of the permanent incisors and first permanent molar with these teeth beginning calcification during the third gestational trimester and completion by the end of the third year of childhood [Weerheijm et al., 2003; Kraus and Jordan, 2004]. The possible causes of this developmental defect can be expected to be the same as those anticipated for permanent first molars and incisors, although occurring somewhat earlier in life [Weerheijm et al., 2003]. Accordingly, an insult that takes place pre- or perinatally, concomitant with crown calcification, is more likely to induce a hypomineralisation defect. However, to date, no study has determined the chronological timing of the insult onset and the possible causative factor/s associated with a second primary molar diagnosed with demarcated hypomineralisation lesion. Hence, due to the clinical significance of hypomineralised second primary molars and for the scarcity of information available regarding its aetiological factors, the aims of the present study were to identify the risk factor/s associated with hypomineralised second primary molars in a group of school-aged children in Mosul city, Iraq; and to relate the location of the affected tooth in the dental arches with the timing of an earlier illness/condition occurrence.
Materials and methods
Sample and procedures. The present study was a part of a larger project investigating the prevalence, severity and aetiological factors of demarcated hypomineralisation lesions in the first permanent molars, permanent incisors and the second primary molars. As the present study was focused on the possible causes of hypomineralised second primary molars, information regarding the clinical examination will be described briefly [for further details about the selection of the study participants and the defect prevalence data, see Ghanim et al., 2012]. The sample consisted of cohorts of public school children (7-9 years-old) born in 2000, 2001 and 2002 and residing in the centre of Mosul city, the second largest city in Iraq after the capital Baghdad. The natural content of fluoride in the reticulated water supply is below 0.19 [+ or -] 0.07 ppm/F [Al-Dahan and Al-Rawi, 2006]. Ethical approval from the Human Research Ethics Committee of the University of Melbourne and the Dental College of Mosul University were obtained. Permission from the Education Department of the Neinavha Governorate and the school directors was also obtained. Given that all schools are publicly funded in Iraq [Ahmed et al., 2007] children from different socio-economic classes were included. Fifty-two schools were selected randomly from the schools list (total n=102), equally distributed along the right and left banks of the City Centre. A sample of 1000 potential school children, with equal numbers of both genders and age groups were proposed to be examined for the presence of hypomineralisation defect. A letter of invitation was sent to the potential participants' parents asking if they would allow their children to participate in the study and inviting the mother to participate in a questionnaire-based interview.
Inclusion criteria: Children and their mothers who were lifelong residents in Mosul City and of Arabic ethnic background.
Exclusion criteria: Children whose mothers were not able to attend the interview.
Systemic health questionnaire-based interview. Based on a previous UK study [Whatling and Fearne, 2008] a questionnaire was developed with 63 items regarding pregnancy and childhood history for the first three years of age. The questionnaire was validated in advance in terms of applicability and repeatability on 12 mothers of children from a public primary school and not included in this study. The questions were drawn from the available literature related to the possible systemic causative factors of hypomineralisation defects in first permanent molars, permanent incisors and second primary molar teeth. In the questionnaire, potential aetiological factors were divided into three chronological phases: pre-natal, peri-natal and post-natal time periods. Assessment of the relevant health history used either an open question method or multiple choice questions:
Pre-natal phase (from 0 to 36-38 weeks in utero): pregnancy type, classified as "single" or "multiple"; maternal illness during pregnancy; medications taken and the number of ultrasound scans taken in each gestational trimester, classified as "none" "1-3 times" "> 3 times".
Peri-natal phase (from birth to 28 days after birth): Gestational age of the baby at birth, classified as "preterm birth, <37 weeks" and "full-term birth, [greater than or equal to] 37 weeks"; maternal age at delivery, subsequently classified into three categories "<20 years", "20-40 years", ">40 years"; delivery type "vaginal", "caesarian"; delivery complications; birth weight, classified as "low, <2.5 kg" "normal, [greater than or equal to] 2.5 kg" and neonatal complications.
Post-natal phase (from 29 days to 4 years of age): duration of breastfeeding following birth, categorised as "up-to the 1st six months", "up-to the 1st year", "up-to the 2nd year" "more than 2 years"; immunisation history; illnesses "acute" "chronic"; allergies; operations under general anaesthesia and antibiotic usage during that period.
Additional information on a child's birth sequence in their family, soy intake (that may change calcium availability) in the form of infant soy-extract formula, family history of enamel defects and mother's employment status at the time of pregnancy was also obtained. Interviews were performed face-to-face with the child's mother, taking an average of 20-25 minutes to complete, and responses recorded using a semi-structured proforma. To reduce administrative disruptions and enhance compliance, no attempt was made to review the written medical records of the child or mother. The interview was carried out first, followed by the dental examination and both were conducted at the school by a single trained, calibrated examiner (AG).
Examination criteria and clinical diagnosis. As there was no available national system for the purpose of diagnosing demarcated hypomineralisation defects in the second primary molar, the lesions were diagnosed by visual examination for MIH-characteristic hypomineralisation. Demarcated opacities, post-eruptive enamel loss, atypical restorations and missing teeth presumably due to demarcated lesions, were recorded using criteria adapted from the European Academy of Paediatric Dentistry criteria for diagnosing MIH in first permanent molars and permanent incisors [Weerheijm et al., 2003].
The sampling included similar numbers in each age and gender group. Prior to the clinical examination, participating children were given a toothbrush and toothpaste to brush their teeth thoroughly. The buccal, occlusal and lingual/ palatal surfaces of the second primary molar were evaluated for demarcated hypomineralisation lesions by visual examination. The teeth were dried using sterile cotton-rolls and examined with the aid of a transillumination light source (Denlite; Miltex Inc., York, PA, USA) with a disposable mirror-head [for further details about the study setting and the clinical examination, see Ghanim et al., 2012].
Calibration. Training and calibration sessions in diagnosing hypomineralised second primary molars, using photographs adopted from a previous study [Elfrink et al., 2008] were undertaken by the first author. Using kappa statistics, the intra-observer agreement for hypomineralisation defect was reasonably high (0.80).
Data analysis. The information from each participant was transferred onto code sheets and data entered into PASW statistics (version 18.0, SPSS Inc, Chicago, IL, USA). In order to determine variations from the non-hypomineralisation-defect-affected subjects the sample was dichotomised into: those diagnosed with hypomineralisation in their second primary molars (HSPM) (referred to as "HSPM-affected group") and those who were "non-HSPM-affected" (considered the control). Chi-square ([chi square]) statistics were used for testing the location of the affected tooth in the dental arches as well as the differences between the study groups in relation to the chronological time point of the potential risk factor.
To better understand the relationship between the independent variables and the hypomineralised defect, a continuous iterative process was applied using the KnowledgeSEEKER[R] software program (ANGOSS Software Corp.; Toronto, Canada) [First MARK Technologies, 1990]. This corresponds to a multivariate stepwise decision making procedure, which chooses combinations of independent variables that best split groups based on the statistical significance. The method also allows the identification of combinations of exploratory factors and non-linear relationships between them and the outcome variable [First MARK Technologies, 1990; Biggs et al., 1991]. Several alternative models were tested and the one that explained a larger proportion of the variance was considered as final.
In general, KnowledgeSEEKER[R] divides data sets into new, identical subsets of data (nodes) [Biggs et al., 1991]. At each node, all predictor variables are expected to further split the node. The node of best division is based on the selection of that variable which produces the highest level of significance. The process continues until no more significant splits can be established [Biggs et al., 1991]. To decide if the relationship between the outcome variable and the independent variable was significant, the significance level was set at 0.20 (exploration level) that resulted in a "bushy" decision tree. In the next step, in order to eliminate association patterns that may be revealed by chance, the resulting tree was "pruned back" until the significance level of the lowest branch was lower than 0.05 [McKenzie et al., 1993].
The reliability of the protocol used to diagnose hypomineralised defects was determined. A set of 40 intra-oral photographs of affected teeth were scored and the readings were compared with their clinically examined counterparts. Cohen's kappa was calculated and revealed excellent value (0.96) for both inter- and intra-observer agreements.
Population and defect prevalence. Of the 1,000 invitation letters distributed, 823 were returned consenting to the interview and child's oral examination achieving a response rate of 82.3%. The nine year-old group produced the highest rate of response (91.8%), whereas the seven year-old group had the lowest rate of response (70.5%). Males comprised 57.2% of the participant subjects. Of the 823 subjects, 14 did not have a second primary molar present at the time of examination leaving a final sample size of 809. Fifty three children (6.6%) were diagnosed with at least one hypomineralised second primary molar, and were designated as the HSPM-affected group. To avoid confounding the results by the outcomes of hypomineralised permanent dentition, children who had demarcated hypomineralisation lesions in first permanent molars and/or permanent incisors were excluded from the analysis (n=132, this figure also included those children who did not have a second primary molar present at the time of examination). Therefore, possible causative factors for hypomineralised second primary molar were assessed in 691 subjects categorised as the HSPM-affected group (53; 7.7%) and non-HSPM-affected group (638; 92.3%).
Distribution of the demarcated hypomineralisation defect by its type, affected tooth/surface and timing of the possible causative factor. Eighty-three teeth were affected by hypomineralisation lesions. Demarcated opacities were the most frequent defect type (71.0%). Opacities with post-eruptive enamel loss were second most prevalent (21.6%). Maxillary molars were the teeth most frequently affected by hypomineralisation, irrespective of the insult period (69.9% vs 30.1%); however, out of six missing second primary molars (presumably extracted as a result of hypomineralisation as a primary cause, with subsequent caries lesions), five were from the mandible. No atypical restorations were observed.
[FIGURE 1 OMITTED]
The occlusal surface of the second primary molar was the site most commonly (16 lesions) affected by post-eruptive breakdown (PEB), 11 lesions were located on the lingual/ palatal and five on the buccal surfaces. Whereas the buccal surface was the most common site for opacities (22 lesions) only 15 lesions were found on the lingual/palatal and eight on the occlusal surfaces. No significant differences existed between opacities and PEB by their distribution on tooth surface.
Right and left maxillary molars were frequently associated with all different timings of the illness onset (69.9%), followed by the mandibular right molar (20.3%), whereas the affected contralateral molar was the least reported (9.8%).
No statistically significant difference was found between the location of the affected tooth in the dental arches and any chronological period of the health problem onset (Figure1).
Distribution of the study groups by timing of the putative risk factor. Amongst the HSPM-affected group, 94.3% reported health-related history, compared with 44.2% in the non-affected group ([chi square] (1) = 24.81, p<0.001) (Table 1). Perinatal events were the most frequently observed (45.3%), followed by pre-natal (24.5%) and post-natal (9.4%). Health events in more than one chronological period were found in 15.1% of the total HSPM cases. In contrast, amongst nonHSPM-affected children reported health events were mainly during the combined peri- and post-natal periods (21.9%).
[FIGURE 2 OMITTED]
A significant difference existed between the study groups in the time from when possible risk factors occurred (x2 (3) = 65.95, p<0.001).
Distribution of HSPM-affected children by possible risk factors. The analysis of the questionnaire-based interview indicated that of the 95 investigated variables, 19 were significant potential risk factors (p<0.05). These included conditions related to gestational illnesses, delivery complications, neonatal complications, acute childhood illness, birth weight and duration of breast feeding. The prevalence of hypomineralised defects was higher in children whose mothers had complications at birth compared with those who did not (14.6% vs. 6.7%) ([chi square] (1) = 6.37, p<0.02). Of those children whose mothers reported maternal peri-natal complications, the individuals who had experienced neonatal complications had a greater prevalence of defects than those unaffected (33.3% vs. 5.5%) ([chi square] (1) = 11.27, p<0.01). Additionally, the timing of the pre-natal complications reported by the mothers was important in this group. Significantly more children were affected by the defect if their mothers had experienced illnesses during the second or third gestational trimester compared with those children whose mothers had illnesses during the first trimester (80% vs. 22.7%) ([chi square] (1) = 6.01, p<0.02). On the other hand, of those children whose mothers did not report delivery complications, the prevalence of hypomineralised defects was significantly higher in those who had a history of acute illness including chest infection other than pneumonia and unexplained high fever (38.5%) compared to those who had a history of ear infection, tonsillitis or pneumonia (5.3%) ([chi square] (1) = 43.55, p<0.001). Important findings were revealed in the group of children with a low prevalence of acute illness. Of this group, the children who were born with low birth weight had higher defect prevalence than those born at normal weight (10.9%, 2.8%, respectively) ([chi square] (1) = 16.68, p<0.001). Furthermore, those children with low birth weight and breast-fed up to six months or less had a higher defect prevalence than those children who were breast-fed for a longer period (25.8%, 7.9%, respectively) ([chi square] (1) = 8.49, p<0.01).
No significant associations were found between HSPM and child's chronic illnesses, antibiotics usage, soy-extract intake, immunisation history, mother's occupation (70% were housewives), mother's age at birth, medications taken during pregnancy, gestational age at delivery and family history of enamel defects.
This is the first published study investigating the potential risk factors of hypomineralised second primary molars diagnosed from criteria adapted from those developed for hypomineralised defects in the permanent dentition. The rationale behind adapting MIH evaluation criteria was to allow recording demarcated lesions in their different clinical presentations. If only demarcated opacities were to be considered, then the other clinical presentations as well as their associated risk factors would be underestimated. Although the questionnaire was designed to collect information about second primary molars, first permanent molars and incisors, the present analysis did not include defective permanent teeth. This was to eliminate the probability that risk factors for hypomineralised second primary molars could be biased by those for the permanent dentition. Additionally, the analysis was not based on the childhood developmental age. Therefore, any medical condition of significant risk to MIH that experienced during the post-natal period (for instance) would be inappropriately accounted for a HSPM as well.
In the present study, the lack of a significant association between the location of the affected tooth in the dental arches with the chronological time of the insult onset might be explained by the close approximation in the timing of enamel mineralisation of all second primary molar teeth, or being difficult to know when the insult occurs with precision [Kraus and Jordan, 2004]. The finding that approximately one quarter of HSPM cases correlate to health events experienced during the pre-natal stage of crown mineralisation supports the theory that a causative factor could occur once enamel mineralisation of the second primary molar had begun [Weerheijm et al., 2001; Lygidakis et al., 2010]. However, children with defects related to medical events experienced during the peri-natal period represented approximately half of the total affected cases. There are no appropriate studies with which to compare these data.
There is no information in the literature specific to the possible aetiological factors of demarcated hypomineralised defects in primary teeth, and that which exists utilises different protocols, investigates enamel developmental defects as a whole and does not specify an individual tooth type when reporting putative causative factors [Nation et al., 1987; Li et al., 1995; Rugg-Gunn et al., 1998; Slayton et al., 2001; Lunardelli and Peres, 2006; Chaves et al., 2007; Lin et al., 2011]. One recent study evaluated the prevalence and aetiological factors of enamel defects in primary incisors only [Massoni et al., 2009].
In the present study, it is important to mention that within each chronological period the chance of having demarcated lesions was higher in some health conditions compared to others. For example, in the post-natal period, the chance of demarcated lesions in children who had ear infection, tonsillitis or pneumonia was higher than those who experienced illnesses like chest infections other than pneumonia or unexplained high fever. Also children who breastfed for less than six months after birth were over three times more likely to have the defect than those who breastfed for the first year of childhood. More efforts should be made to lessen the incidence of such health events in an attempt to reduce or prevent the development of hypomineralised lesions. The positive association between the defect and the duration of breastfeeding is an interesting finding.
Following the WHO recommendations breastfeeding for the first six months following birth should be maintained for the role of the immunological and anti-infectious properties of human milk in the reduction of illnesses [WHO, 2002]. Hence, early weaning [i.e. breastfeeding up to 6 months] could be a risk factor by aggravating the child's nutritional deficiencies, contributing to a greater incidence of enamel defects. Alternatively, in the present study, the significant risk effect of up to 12 months nursing period is perplexing. Nonetheless, this risk effect was in association with low birth weight. It is known that breast milk containing calcium and phosphorus is inadequate for preterm infants regardless of the duration of feeding. Shortage of normal mineral stores can be important factor behind enamel developmental defects in children born prematurely [Schanler and Abrams, 1995; Seow, 1996].
Additionally, an important finding was with increasing number of health events reported, the chance of developing the defect increased. For instance, in the group of subjects who experienced neonatal complications and whose mothers reported pregnancy and birth problems, the chance of having the defect was about six times more likely to happen than in those whose mothers had delivery complications only. This signifies the link between the existence of systemic health deterioration and the probability of the defect occurrence. However, the relationship between the duration of a specific illness and demarcated lesions severity was not possible to be assessed as this can be better explored in studies with prospective-longitudinal design.
As the present study represents part of a larger project, associated data analysis revealed that the prevalence of hypomineralised defects in first permanent molars and incisors was higher than that in the second primary molar (18.6% vs. 6.6%) [Ghanim et al., 2011]. With regard to the chronological timing of the insult onset, the lower defect prevalence in the second primary molar compared to that in permanent teeth could be related to the developing embryo being protected in utero, to some extent. The probability of disturbing the micro-environment of the ameloblasts is therefore more likely to happen prior to the completion of crown mineralisation of the second primary molar by the end of the first year of childhood [Noren et al., 1993]. Therefore, the different prevalence estimates is more likely to be due to a similar specific risk factor occurring at a different tooth crown mineralisation time.
In the present study, the majority of the interviewed mothers were housewives. It has been reported that house duties mothers are less likely to be exposed to occupational hazards and their children could be less likely to experience health problems in contrast to worker mothers [Sivakami, 1997; El-Gilany et al., 2008]. Because of the self-selected feature of this study, little information is available about a working mother and her child's systemic health status that may have biased the results. Therefore, occupational hazards should be investigated in future research along with other environmental contaminants. Additionally, in the present study, LBW was a significant risk factor for demarcated lesions, in accordance with earlier studies investigated developmental enamel defects in primary teeth and identified the significant risk of LBW in its different scales [Seow et al., 1984; Fearne et al., 1990; Ferrini et al., 2008]. However, for the present study it was not possible to extrapolate the impact of different types of LBW on the HSPM as child's medical reports were not approached, which deems further research in this area.
The information provided has to be considered within the limitations of the study design. The most obvious shortcoming is the potential for recall bias in asking mothers to report retrospectively on the health history relating to the gestational period and the child's early childhood. Additionally, the sample for the group of interest was relatively small which did not allow for a more detailed analysis to disclose any further effects of the potential factors on the defect development. However, the assumption that MIH and hypomineralised second primary molars have almost the same causes but vary in developmental timing of the insult onset has been supported in this study. Therefore, health promotion intervention programs need to be more comprehensive, encompassing both the mother and her child from early pregnancy to late stage of childhood. Recognition of causative factors for hypomineralised primary molars can allow early intervention to prevent such factors from happening and causing defective permanent molars.
Although the multivariate analytic tool that has been used in this study is known as being robust, it suffers a limitation common to stepwise analysis in that it does not examine the contribution of all variables to prediction [McKenzie et al., 1993]. Present results, therefore, propose that variables not considered in this analysis might add explanatory power to the models. Nonetheless, a step forward has been made through this research in providing a basis for future studies on larger groups of subjects. Further exploration of the potential causation of hypomineralised second primary molars and identification of specific factor/s by conducting high quality prospective research are important goals, with the anticipation that demarcated hypomineralised defects will become preventable once its causes are determined.
No single factor was identified as a predisposing cause of demarcated hypomineralisation lesions but rather several factors of systemic nature have been identified as contributors of the defect. Children with hypomineralised defects were over twice as likely to have medical health problems than their defect-free counterparts. Peri-natal health events represented by neonatal illness of the child were the most frequently reported associative factor. Pre-natal health conditions represented by maternal illness were second in importance as risk factors
We are grateful to all the children and their mothers for participating in the study and the school Principals for their cooperation in performing this study. Special thanks to Professor Tahani Alsandook and Dr Ali Alnuaimi for their support and assistance when collecting data. We should like to acknowledge Dr Elfrink and her coauthors' contribution of the clinical photographs used in the Dutch study and Drs Whatling and Fearne's contribution of the medical health questionnaire used in the British study. The support of the Oral Health CRC, the University of Melbourne and the Education Department of the Neinavha Governorate is acknowledged with gratitude.
Al-Dahan ZA, Al-Rawi BA. Determination of fluoride, zinc and lead ions concentrations in primary teeth and drinking water and dental caries experience. Al-Rafidain Dent J 2006; 6(Spec Iss):23-29.
Ahmed NA, Astrom AN, Skaug N, Petersen PE. Dental caries prevalence and risk factors among 12-year old school children from Baghdad, Iraq: a postwar survey. Int Dent J 2007; 57:36-44.
Biggs D, DeVille, Suen E. A method of choosing muhiway partitions for classification and decision trees. J Appl Stat 1991; 18:49-62.
Chaves AMB, Rosenblatt A, Oliveira OFB. Enamel defects and its relation to life course events in primary dentition of Brazilian children: a longitudinal study. Community Dent Health 2007; 24:31-36.
Elfrink MEC, Veerkamp JSJ, Kalsbeek H. Caries pattern in primary molars in Dutch 5-year old children. Eur J Paediatr Dent 2006; 7:236-240.
Elfrink MEC, Schuller AA, Weerheijm KL, Veerkamp JSJ. Hypomineralised Second Primary Molars: Prevalence Data in Dutch 5-Year-Olds Caries Res 2008; 42:282-285.
Elfrink ME, Schuller AA, Veerkamp JS et al. Factors increasing the caries risk of second primary molars in 5-year-old Dutch children. Int J Paediatr Dent 2010; 20:151-157.
El-Gilany AH, El-Wehady A, El-Hawary A. Maternal employment and maternity care in Al-Hassa, Saudi Arabia. Eur J Contracept Reprod Health Care 2008;13:304-312.
Fearne JM, Bryan EM, Elliman AM, Brook AH, Williams DM. Enamel defects in the primary dentition of children born weighing less than 2000 g. Br Dent J 1990; 168:433-437.
Ferrini FR, Marba ST, Gaviao MB. Oral conditions in very low and extremely low birth weight children. J Dent Child (Chic) 2008; 75:235-242.
First MARK Technologies. KnowledgeSEEKER user's guide. Ottawa; Ontario, 1990.
Ghanim A, Morgan M, Marino R, Bailey D, Manton D. Molar-Incisor Hypomineralisation: prevalence and defect characteristics in Iraqi children. Int J Paediatr Dent 2011; 21:413-421.
Ghanim A, Manton D, Marino R, Morgan M, Bailey D. Prevalence of Demarcated Hypomineralisation Defects in Second Primary Molars in Iraqi Children. Int J Paediatr Dent 2012; doi: 10.1111/j.1365-263X.2012.01223.
Jalevik B, Noren JG. Enamel hypomineralization of permanent first molars: a morphological study and survey of possible aetiological factors. Int J Paediatr Dent 2000; 10:278-289.
Jalevik B, Klingberg G. Dental treatment, dental fear and behaviour management problems in children with severe enamel hypomineralisation of their FPMs. Int J Paediatr Dent 2002; 12:24-32.
Kraus BS, Jordan RE. Development and morphology of the primary teeth. In: McDonald RE, Avery DR, editors. Dentistry for the child and adolescent. 8th ed. St. Louis: The C.V. Mosby Co; 2004. p. 51-58.
Leppaniemi A, Lukinmaa PL, Alaluusua S. Non-fluoride hypomineralizations in the first molars and their impact on the treatment need. Caries Res 2001; 35:36-40.
Li Y, Navia JM, Bian JY: Prevalence and distribution of developmental enamel defects in primary dentition of Chinese children 3-5 years old. Community Dent Oral Epidemiol 1995; 23:72-79.
Lin X, Wu W, Zhang C et al. Prevalence and distribution of developmental enamel defects in children with cerebral palsy in Beijing, China. Int J Paediatr Dent 2011; 21:23-28.
Lunardelli SE, Peres MA. Breast-feeding and other mother-child factors associated with developmental enamel defects in the primary teeth of Brazilian children. J Dent Child 2006; 73:70-78.
Lygidakis NA, Wong F, Jalevik B et al. Best clinical practice guidance for clinicians dealing with children presenting with Molar-Incisor-Hypomineralisation (MIH): An EAPD Policy Document. Eur Arch Paediatr Dent 2010; 11:75-81.
Mahoney EK. The treatment of localised hypoplastic and hypomineralised defects in FPMs. N Z Dent J 2001; 97:101-105.
Massoni AC, Chaves AM, Rosenblatt A, Sampaio FC, Oliveira AF. Prevalence of enamel defects related to pre-, peri- and postnatal factors in a Brazilian population. Community Dent Health 2009; 26:143-149.
McKenzie DP, McGorry PD, Wallace CS et al. Constructing a minimal diagnostic decision tree. Methods Inf Med 1993; 32:161-166.
Nation WA, Matsson L, Peterson JE. Developmental enamel defects of the primary dentition in a group of Californian children. J Dent Child 1987; 54:330-334.
Noren JG, Ranggard L, Klingberg G, Persson C, Nilsson K. Intubation and mineralization disturbances in the enamel of primary teeth. Acta Odontol Scand 1993; 51:271-275.
Rugg-Gunn AJ, Al-Mohammadi SM, Butler TJ. Malnutrition and developmental defects of enamel in 2- to 6-year-old Saudi boys. Caries Res 1998; 32:181-192.
Schanler RJ, Abrams SA. Postnatal attainment of intrauterine macromineral accretion rates in low birth weight infants fed fortified human milk. J Pediatr 1995; 26:441-447.
Seow WK, Brown JP, Tudehope DI, O'Callagan M. Developmental defects in the primary dentition of very low birth weight infants: adverse effects of laryngoscopy and prolonged endotracheal intubation. Pediatr Dent 1984; 6:28-31.
Seow WK. A study of the development of the permanent dentition in very low birth weight children. Pediatr Dent 1996; 18:379-348.
Sivakami M. Female work participation and child health: an investigation in rural Tamil Nadu, India. Health Transit Rev 1997; 7:21-32.
Slayton RL, Warren JJ, Kanellis MJ, Levy SM, Islam M. Prevalence of enamel hypoplasia and isolated opacities in the primary dentition. Pediatr Dent 2001; 23:32-36.
Weerheijm KL, Jalevik B, Alaluusua S. Molar-Incisor Hypomineralisation. Caries Res 2001; 35: 390-391.
Weerheijm K, 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; 4:110-113.
Weerheijm KL. Molar incisor hypomineralization (MIH): clinical presentation, aetiology and management. Dent Update 2004; 31:9-12.
Whatling R, Fearne JM. Molar incisor hypomineralization: a study of aetiological factors in a group of UK children. Int J Paed Dent 2008; 18:155-234.
World Health Organization. 55th World Health Assembly. Infant and young child nutrition. Geneva, Switzerland: World Health Organization, 2002 (WHA55.25). Internet: http://www.who.int/gb/ebwha/pdf_files/WHA55/ewha5525.pdf (Accessed by 5 December 2010).
A.M. Ghanim, M.V. Morgan, R.J. Marino, D.L. Bailey, D.J. Manton
Oral Health CRC, Melbourne Dental School, The University of Melbourne, Parkville Victoria, Australia.
Postal address: Professor D.J. Manton, Paediatric Dentistry, Melbourne Dental School, The University of Melbourne, Melbourne, Victoria, 3010, Australia.
Table 1. Distribution of the timing of the potential risk factor in both HSPM-affected and non-affected groups in a group of Iraqi children. Developmental HSPM- Non-HSPM- Total period of a affected affected health N (%) N (%) history (1) No health history 3 (5.7) 356 (55.8) 359 Pre-natal 13 (24.5) 26 (4.1) 39 Peri-natal 24 (45.3) 33 (5.2) 57 Post-natal 5 (9.4) 83 (13.0) 88 Peri- and post-natal 8 (15.1) 140 (21.9) 148 Total 53 638 691 (1) Subjects were categorised according to the developmental period a health condition was experienced into the following: Those with health events experienced only in utero until 36-38 weeks of foetus development (i.e. pre-natal developmental period). Those with health events experienced only during delivery and including the neonatal period (between the 7th day and 28th days of life) (i.e. prenatal developmental period). Those with health events experienced only after the first month of child's birth up to 4 years of childhood (i.e. post-natal developmental period). Those with health events experienced during the peri--and post-natal developmental periods. HSPM: Hypomineralised Second Primary Molar.
|Printer friendly Cite/link Email Feedback|
|Author:||Ghanim, A.M.; Morgan, M.V.; Marino, R.J.; Bailey, D.L.; Manton, D.J.|
|Publication:||European Archives of Paediatric Dentistry|
|Date:||Jun 1, 2012|
|Previous Article:||The conduct of dental research: the protocol, a guide.|
|Next Article:||Post-operative pain and pain management in children after dental extractions under general anaesthesia.|