|How to cite this article:
Naveen Kumar PG, Bhate PM, Rai R, Mohammadi SN. Enamel hypoplasia and dental caries. Ann Trop Med Public Health 2016;9:90-1
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Naveen Kumar PG, Bhate PM, Rai R, Mohammadi SN. Enamel hypoplasia and dental caries. Ann Trop Med Public Health [serial online] 2016 [cited 2016 Mar 28];9:90-1. Available from: https://www.atmph.org/text.asp?2016/9/2/90/177374
Enamel is a unique mineralized tissue in its method of development, structure, and chemical nature. Mature enamel containing meager organic matrix is the most mineralized and hardest tissue in the body. Enamel has an ability to resist heavy occlusal forces and various noxious chemicals. However, enamel is also prone to defects. 
Developmental defects of enamel (DDE) can be defined as alteration of enamel that results from disturbances during amelogenesis. Since enamel does not undergo remodeling, the defects that occur during its formation will be permanently present.  According to their clinical appearance, DDE can be classified into demarcated opacity, diffuse opacity, and hypoplasia. Opacity is a qualitative defect involving an alteration in translucency of enamel, and it may present a white, yellow, or brown color that maybe demarcated or diffused. Enamel hypoplasia (EHP) is a quantitative defect associated with a reduced thickness of enamel during the secretory stage of amelogenesis. 
The prevalence of DDE was reported to be 40.2% in primary and 52% in permanent dentition  while EHP was observed to be only 0.6% in primary and 0.8% in permanent teeth,  which was less than the prevalence of other classes of DDE.
EHP is one of the several forms of DDE identified by the Fédération Dentaire Internationale, Commission on Oral Health (1992), and it is defined as a quantitative disturbance of mineralized tissue formation during tooth development. 
Defective enamel sites (hypoplasia or hypocalcification) may provide favorable local environment for adhesion and colonization of cariogenic bacteria, and they may remain at the base of the defect in contact with exposed dentin; thus dental caries on these defective sites may develop more rapidly (Li et al., 1996). Defective enamel has higher acid solubility than normal enamel and is more susceptible to caries attack (Zheng et al., 1998). 
The association between EHP and dental caries has been reported in several cross-sectional studies by Matee et al. (1994), Pascoe and Seow (1994), Li et al. (1996), Ellwood and O’Mullane (1996), Kanchanakamol et al. (1996), Milgrom et al. (2000), Montero et al. (2003), and Daneshkazemi and Davari (2005), and two longitudinal studies by Lai et al. (1997) and Oliveira et al. (2006) [Table 1].
|Table 1: Pre- and post-natal antecedents linked to developmental enamel defects and enamel hypoplasia
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The pivotal study linking EHP and elevated levels of Mutans Streptococci (MS) was first reported by Li et al. (1994). Wan et al. (2003) confirmed that low birth weight children with EHP were 4.4 times more likely to be infected by MS than non-EHP children. 
Enamel defects such as EHP appear to be a significant and reliable risk marker or predictor for dental caries; however, most of these studies were cross-sectional and did not account for other important factors such as fluoride exposure. 
Based on the above observation nursing bottle caries can coexist with or exacerbate preexisting EHP or be a separate and distinct form of early childhood caries. 
The Iowa Fluoride Study (IFS) is a longitudinal study of a cohort (from birth) concerning the relationships among fluoride exposures, biological and environmental factors, and oral health. Using data collected in the IFS on dental caries and EHP for primary teeth and information on important covariates, Hong et al. reports on the association between EHP and dental caries among primary second molars in children aged 5 years: 36.8% children with hypoplasia had caries, whereas only 16.9% children without EHP had caries (relative risk = 2.17). In children aged 9 years, the prevalence of caries was 52.9% with hypoplasia and only 34.5% without EHP (relative risk = 1.52). 
It is to be realized that the clinical course of caries is different when associated with EHP since the accumulation of plaque in these areas accelerates the caries process. Improving oral hygiene should be the major consideration. Parents need to be educated about additional agents like probiotics, and toothpaste with a pronounced remineralizing and antimicrobial properties should be used to alter/ slow down the caries process. 
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