|Year : 2015 | Volume
| Issue : 3 | Page : 229-233
Apgar index as a probable risk indicator for enamel defects in primary dentition: A cross sectional study
S. V. S. G. Nirmala, Mohammed Akhil Quadar, Sindhuri Veluru, Namratha Tharay, Naveen Kumar Kolli, MS Minor Babu
Department of Pedodontics and Preventive Dentistry, Narayana Dental College and Hospital, Chinthareddypalem, Nellore, Andhra Pradesh, India
|Date of Web Publication||9-Jul-2015|
Dr. S. V. S. G. Nirmala
Department of Pedodontics and Preventive Dentistry, Narayana Dental College and Hospital, Chinthareddypalem, Nellore - 524 003, Andhra Pradesh
Source of Support: None, Conflict of Interest: None
| Abstract|| |
Aim: The aim of the present study was to investigate the association of Apgar index with that of enamel defects and to explore gender predilection as a co-variable in the formation of enamel defects. Materials and methods: A random sample of 108 individuals (46 boys and 62 girls) aged 4-5 years (mean - 4.4 years) were included in the study. A questionnaire containing subject's demographic information, Apgar Index (AI), enamel hypoplasia and hypocalcification was collected. Intraoral examination of the subjects was performed by using the type III diagnostic criteria recommended by WHO for oral health surveys. According to the modified index for developmental enamel defects, visual and tactile examinations of the entire primary dentition were performed.The data obtained was analysed using chi-square test. Results: Of all the examined individuals 18 (16.7%) showed enamel defects, of which 10 (9.3%) were having enamel hypoplasia, 4 (3.7%) were having enamel hypocalcification and 4 (3.7%) were having both. Correlation of the enamel defects such as hypoplasia, hypocalcification and both had no significant relationship with the gender (P = 0.36). Conclusion: Subjects with lower Apgar Index exhibited more hypoplastic and hypocalcified teeth both qualitatively and quantitatively. If the Apgar value is less than 6, the vulnerability for the development of enamel defects has considerably increased. Gender of the individuals did not influence the final outcome.
Keywords: Apgar index, enamel defects, primary dentition
|How to cite this article:|
Nirmala S, Quadar MA, Veluru S, Tharay N, Kolli NK, Minor Babu M S. Apgar index as a probable risk indicator for enamel defects in primary dentition: A cross sectional study. J Indian Soc Pedod Prev Dent 2015;33:229-33
|How to cite this URL:|
Nirmala S, Quadar MA, Veluru S, Tharay N, Kolli NK, Minor Babu M S. Apgar index as a probable risk indicator for enamel defects in primary dentition: A cross sectional study. J Indian Soc Pedod Prev Dent [serial online] 2015 [cited 2021 Jan 18];33:229-33. Available from: https://www.jisppd.com/text.asp?2015/33/3/229/160396
| Introduction|| |
Tooth development begins in utero and extends into adult life. Enamel matrix formation begins at 4 months of intrauterine life. Process of remodeling, which is generally seen in hard tissues such as bone, does not occur in the enamel because of the loss of ameloblasts, this is the reason why the enamel defects cannot be repaired.  Pindborg in 1982 listed the most common causes for enamel defects are hypoxia, hypocalcaemia, renal disorders, nutritional deficiencies and viral infections.  Enamel defects are classified as hypoplasia and hypocalcification by Weinmann et al. in 1945. 
Enamel hypoplasia, is a quantitative disorder and manifested as a lack of enamel in pits, fissures or other surfaces of the tooth whereas hypocalcification is the defective mineralization of enamel, and it is mainly a qualitative disorder.  Genetic and environmental factors play an important role in the formation of enamel hypoplasia, which disturb the enamel synthesis and secretion of the organic matrix of enamel leading to enamel hypoplasia. Both can occur in the opposition stage of tooth development as a result of an insult to the cells. 
Neonatal line or ring present on primary teeth and first permanent molar is also a type of hypoplasia. Any insult during enamel and dentin formation, as well as disturbance indicative of the trauma or change of environment at the time of birth may result in neonatal ring/line. In traumatic births the formation of enamel may even cease at this time.  Enamel hypoplasia is far more common in prematurely born children than in normal term infants. They not only drew attention to the widely recognized staining of teeth in children who suffered from Rh hemolytic disease at birth but also reported enamel hypoplasia in these cases.  Grahnen and Larsson have also shown an increased incidence of enamel hypoplasia in premature children but interestingly no difference was observed in caries incidence. 
The literature also states that neurological disorders supplement enamel defects in 70% of the subjects, which has also been observed by Murray et al., in the primary dentition. , Furthermore, there was an analogous association between enamel and neurological defects, and suggested a diagnostic value for enamel defects and also some association between enamel hypoplasia, rickets and respiratory distress in low-birth-weight infants. ,
Apgar scoring system was introduced by Dr. Apgar V. in 1953, which is used to assess the clinical status of a newborn infant at 1 min after birth and need for prompt intervention to establish breathing.  Apgar index (AI) is used for the evaluation of general, neural and behavioral status of newborns.  Apgar score is a measure of the vitality of the newborn infant on the basis of heart rate, respiration, color, muscle tone, and reflex irritability. AI is one of the first indices used for early diagnosis of infant anomalies. The technique involves 1 st to 5 th min assessment of skin color, heartbeats, muscular tonicity, primary motor reflex and rate of respiration. AI value of 7-10 is considered normal, whereas a value of <6 indicates special medical measures  [Table 1].
A strong association was found between low Apgar score and cerebral palsy in children born to term or with normal birth weight, whereas studies in children with a low birth weight or born preterm have shown conflicting results. Low birth weight and immaturity are closely related to the risk of cerebral palsy and are also associated with a low Apgar score. 
A case-control study in Denmark found that a low 5-min Apgar score was associated with increased risk for autism, elevated risk of hospitalization for epilepsy and for pneumococcal disease by the age of 12 years. ,, A low 1-min Apgar score was associated with increased odds of asthma by the age of 3 years,  and the extent and severity of dental enamel defects in the primary dentition was negatively associated with Apgar scores.  To our knowledge, there were no studies related to the AI with enamel defects in the Indian population. Hence, the present study aimed to investigate the association of AI with that of enamel formation defects and to explore gender predilection as a co-variable in the formation of enamel defects.
| Materials and Methods|| |
This descriptive, retrospective study was carried out in the department of pediatrics, Narayana Medical Hospital, Nellore, Andhra Pradesh, India. A random sample of 108 individuals (46 boys and 62 girls) aged 4-5 years (mean-4.4 years) were included in the study. Subjects having teeth with noticeable cracks, caries lesions and restorations, subjects with precise caries patterns such as baby bottle caries lesion, subjects with a history of systemic or debilitating diseases or local confounding factors such as traumatic habits leading to enamel abrasion, were excluded from the study. The study procedure was explained to the parents of the children and signed written consent form was obtained from them. This study was approved by the Institutional Ethical and Research Committee.
A questionnaire containing subject's demographic information, AI, enamel hypoplasia and hypocalcification were collected. The data regarding the AIs of the subjects was noted by referring to the past medical history of the patients from their parents at the time of their birth.
Intraoral examination of the subjects was performed by using the type III diagnostic criteria recommended by WHO for oral health surveys according to the modified index for developmental enamel defects. After drying the teeth, visual inspection and tactile examination were performed for entire primary dentition (buccal, lingual/palatal and incisal/occlusal) using a sharp, sterile dental explorer. Enamel defects were classified as hypoplasia or hypocalcification.
To measure the intra-examiner agreement of data subjects were examined twice on a random basis and also after completion of the examination of all subjects. The intra-examiner reliability was found to be established at 95%.
The data analysis was performed using Chi-square test. All the quantitative data were presented in mean values. P < 0.05 was considered to be statistically significant.
| Results|| |
A total of 108 individuals (46 boys and 62 girls) aged 4-5 years (mean-4.4 years) were included in the study. Correlation of individual variables of AI with gender is given in [Table 2]. Among all the examined individual variables of the Apgar scoring system, reflex irritability (P = 0.001) and heart rate (P = 0.024) showed statistically significant correlation when compared with gender whereas remaining parameters were not statistically significant [Table 2].
Of all the examined individuals 18 (16.7%) of them showed enamel defects among which 10 (9.3%) were having enamel hypoplasia, 4 (3.7%) having enamel hypocalcification and 4 (3.7%) having both enamel hypoplasia and hypocalcification. No significant correlation was observed between the enamel defects with the gender (P = 0.36). When the overall score of the individual parameters of AI was assessed it showed that 18 (6 males and 12 females) were moderately depressed and 90 (40 males and 50 females) were normal, which was not statistical significant with a P = 0.384 [Table 3].
|Table 3: Correlation of enamel defects and overall scores of Apgar index with gender|
Click here to view
| Discussion|| |
This study was focused to investigate whether or not AI is of any significance in the prediction of enamel formation defects with that of the gender. Our findings indicated a negative correlation (P = 0.36) between the Apgar value and the existence of enamel hypoplasia, hypocalcification and both with respect to the gender.
Etiological factors for the development of enamel defects can be broadly divided into two types: Systemic and local. The systemic factors may be categorized as genetically determined, chromosomal anomalies, congenital defects, inborn errors of metabolism, neonatal disturbances, infectious diseases, neurological disturbances, endocrinopathies, nutritional deficiencies, nephropathies, enteropathies, liver diseases and intoxications. 
Apgar index was genetically determined, which may occur as an isolated phenomenon or as a part of other disorders such as epidermolysisbullosa, pseudo-hypoparathyroidism and taurodontism. Congenital defects include heart disorders and unilateral facial hypoplasia and hypertrophy.
Inborn errors of metabolism responsible for enamel defects are galactosemia, phenylketonuria, alkaptonuria, erythropoietic porphyria and primary hyperoxaluria. Neonatal disturbances which are significant in the development of enamel hypoplasia are premature birth and hypocalcaemia.
Based on Apgar scoring system, infants are observed systematically at birth for their need of immediate care. Forecasting of long-term outcomes was never a goal of the Apgar scoring system research.  However; it provides initial evidence for considering long-term outcomes of any type such as developmental and neurological.
Low Apgar scores certify developmental scrutiny during the early years of life but, if unaccompanied by neonatal seizures, they do not appear to predict more doubtful developmental dysfunction evident at the age of school entry.  However, Behnke et al. suggested that after controlling birth weight and gestational age, the Apgar scores did not predict morbidity in low-birth-weight infants and, therefore, should not be used to provide a developmental prognosis. 
The outcomes may moderately explain the principal cause of this relative disagreement. They found that among the components of the Apgar score, respiratory effort, muscle tone and reflex activity interrelated well with one another; heart rate correlated less comparatively and colors the least, leading to different responses of AI components. 
Studies were conducted to correlate Apgar scores with various outcomes including development, later delinquency, intelligence and neurological development for the purpose of research and AI scores were inversely correlated with enamel defects. ,,, Our study demonstrated that decreased AI scores had strongly correlated with the development of enamel defects. Though the subjects with lower Apgar values exhibited more hypoplastic and hypocalcified teeth when compared with that of the individuals of higher Apgar values, the results were not statistically significant. There was a sudden rise in the number of individuals who are affected with enamel defects having the Apgar value of ≤6. Thus, it is suggested to carry out more intense and stringent oral screening for the subjects with Apgar values of ≤6.
Gender of the individuals did not influence the final outcome. Future research may be focused towards the investigation of the association of Apgar scoring system components with developmental enamel defects in a larger number of individuals. Furthermore, the study of the association of developmental, craniofacial and musculoskeletal anomalies with AI also seems to be exciting.
Managing enamel defects is challenging to the pediatric dentist because of their unaesthetic appearance, dentinal sensitivity and subsequent susceptibility to dental caries. Furthermore, if it is not treated in time it affects the quality of life.
| Conclusion|| |
From this study it may be concluded that the Apgar scoring system can be used as an indicator for risk assessment of enamel defects among the individuals with primary dentition. If the Apgar value is found to be below the critical value of 6 then the vulnerability for the development of enamel defects has considerably increased. Enactment of specific preventive measures at an early age may ascertain to be extremely beneficial.
| References|| |
Aminabadi NA, Farahani RM, Gajan EB. Apgar index as a correlate of enamel defects of primary dentition. Oral Health Prev Dent 2008;6:331-5.
Pindborg JJ. Aetiology of developmental enamel defects not related to fluorosis. Int Dent J 1982;32:123-34.
Weinmann JP, Svoboda JF, Woods RW. Hereditary disturbances of enamel formation and calcification. J Am Dent Assoc 1945;32:397-418.
Schour I. The neonatal line in the enamel and dentin of the human deciduous teeth and first permanent molar. J Am Dent Assoc 1936;23:1946-55.
Miller J, Forrester RM. Neonatal enamel hypoplasia associated with hemolytic disease and with prematurity. Br Dent J 1959;106:93-104.
Grahnen H, Larsson PG. Enamel defects in deciduous dentition of prematurely born children. Odontol Revy 1958;9:143.
McDonald RE, Avery DR, Lynch TR. Management of trauma to the teeth and supporting tissues. In: Dentistry for the Child and Adolescent. 5 th
ed. St. Louis: Mosby; 1987.
Murray GS, Johnsen DC, Weissman BM. Hearing and neurologic impairment: Insult timing indicated by primary tooth enamel defects. Ear Hear 1987;8:68-73.
Cohen HJ, Diner H. The significance of developmental dental enamel defects in neurological diagnosis. Pediatrics 1970;46:737-47.
Johnsen D, Krejci C, Hack M, Fanaroff A. Distribution of enamel defects and the association with respiratory distress in very low birthweight infants. J Dent Res 1984;63:59-64.
Apgar V. Proposal for a new method of evaluation of the new born infant. Curr Res Anesth Analg 1953;32:260-7.
American Academy of Pediatrics, Committee on Fetus and Newborn; American College of Obstetricians and Gynecologists and Committee on Obstetric Practice. The Apgar score. Pediatrics 2006;117:1444-7.
Lie KK, Grøholt EK, Eskild A. Association of cerebral palsy with Apgar score in low and normal birthweight infants: Population based cohort study. BMJ 2010;341:c4990.
Larsson HJ, Eaton WW, Madsen KM, Vestergaard M, Olesen AV, Agerbo E, et al.
Risk factors for autism: Perinatal factors, parental psychiatric history, and socioeconomic status. Am J Epidemiol 2005;161:916-25.
Ehrenstein V, Sørensen HT, Pedersen L, Larsen H, Holsteen V, Rothman KJ. Apgar score and hospitalization for epilepsy in childhood: A registry-based cohort study. BMC Public Health 2006;6:23.
Mahon BE, Ehrenstein V, Nørgaard M, Pedersen L, Rothman KJ, Sørensen HT. Perinatal risk factors for hospitalization for pneumococcal disease in childhood: A population-based cohort study. Pediatrics 2007;119:e804-12.
Metsälä J, Kilkkinen A, Kaila M, Tapanainen H, Klaukka T, Gissler M, et al.
Perinatal factors and the risk of asthma in childhood - a population-based register study in Finland. Am J Epidemiol 2008;168:170-8.
Apgar V. The newborn (Apgar) scoring system. Reflections and advice. Pediatr Clin North Am 1966;13:645-50.
Blackman JA. The value of Apgar scores in predicting developmental outcome at age five. J Perinatol 1988;8:206-10.
Behnke M, Eyler FD, Carter RL, Hardt NS, Cruz AC, Resnick MB. Predictive value of Apgar scores for developmental outcome in premature infants. Am J Perinatol 1989;6:18-21.
Hegyi T, Carbone T, Anwar M, Ostfeld B, Hiatt M, Koons A, et al.
The Apgar score and its components in the preterm infant. Pediatrics 1998;101 (1 Pt 1):77-81.
Riehn A, Petzold C, Kuhlisch E, Distler W. Fetal academia and neonatal encephalopathy. Z Geburtshilfe Neonatol 1998;202:187-91.
Gibson CL, Tibbetts SG. Interaction between maternal cigarette smoking and Apgar scores in predicting offending behavior. Psychol Rep 1998;83:579-86.
Nelson KB, Ellenberg JH. Apgar scores as predictors of chronic neurologic disability. Pediatrics 1981;68:36-44.
Wolf MJ, Wolf B, Bijleveld C, Beunen G, Casaer P. Neurodevelopmental outcome in babies with a low Apgar score from Zimbabwe. Dev Med Child Neurol 1997;39: 821-6.
[Table 1], [Table 2], [Table 3]