Constant problems with your kid's teeth? They may have Developmental Defects of the Enamel...

Some children have their teeth brushed by their parents every day, eat a balanced diet, have never had soft drinks, and only have treats on very special occasions; yet, have sensitive teeth, or enamel chipping off, or teeth that keeps getting cavities. Why?

 One reason could be that some of their primary teeth are affected by developmental defects of the enamel (DDE)(1-3).

  What is DDE?

Developmental defects of the enamel (also known as “chalky teeth”, “weak enamel”,  “enamel defects”, “enamel hypoplasia”, “enamel hypomineralization”) occur in primary and permanent teeth during tooth development (3-6). The enamel (the outer layer of the tooth crown) that are affected, may be of poorer quality (hypomineralization, weaker and more porous enamel) and/or lower quantity (hypoplasia, thinner or missing enamel) (4, 5, 7, 8). 

When teeth with DDE erupt into the mouth, the affected enamel appear different from “normal”, ranging from subtle demarcated white opacities to diffused yellow-brown patches (7-8). In some cases, there may be a mixture of demarcated opacities, diffused discolouration and areas of thinner or missing enamel (7, 8). 

DDE-affected teeth are more susceptible to sensitivity, acid challenges, dental decay, tooth wear and breakdown. The most commonly affected primary teeth are upper central incisors and second molars.

What causes DDE?

The exact cause of DDE is not yet known. Research evidence suggests that enamel formation may be disrupted during tooth development by stresses such as maternal illness during pregnancy, maternal smoking / alcohol consumption during pregnancy, difficult birth, preterm birth, neonatal oral intubation, infantile fevers, and inflammation, infections, hospitalization and medication during the first year of life (3-5, 9-13). For example, Schuler et al. (2018), reported a 7x risk of enamel defects and dental caries in preterm infants (13). Children born with cleft lip and palate and medically compromised children are more at risk of enamel defects in their primary and permanent teeth (14-17). Recently, infantile eczema has also been associated with higher risk of DDE (13).

Localized DDE that affect one or more teeth but not the entire dentition, are generally chronological (4). The presence of DDE in the primary teeth does not always mean that the permanent teeth will be affected. This is different from genetic conditions such as amelogenesis imperfecta, in which every primary and permanent teeth are affected (8, 18).

 For example, stresses that occur during 7wks in utero to 3mths after birth may affect the enamel quality and quantity of primary incisors. Primary incisors start to form at approximately 7wks in utero (18). At birth approximately 5/6 of the maxillary incisor crown and 3/5 of the mandibular incisor crown have been formed. After birth, the primary Incisor crowns continue to form (18). The primary incisor crowns are completed at 3mths of age and erupt into the mouth at approximately 7mths of age (18). 

 The neonatal line is often visible on primary incisors and is a common location for DDE. This line demarcates enamel formation before and after birth. Microscopically, enamel at the neonatal line is less mineralized and less organized structurally (4).

How prevalent is DDE?

DDE in the primary teeth are relatively common. The prevalence in the literature varies from 2.7% to over 40%, depending on the definition of DDE, assessment method, study design etc. (2, 4, 19-21).

 Why is DDE bad?

In addition to being less aesthetic, teeth with DDE are much more prone to sensitivity, breakdown, acid attacks, and tooth wear, dental decay (4, 6, 22-25). 

In a paper by Milgrom et al. (2000) that investigated the risk of dental decay and enamel defects in children aged 6-36mths in the USA, it was reported that, “The odds of having any white spot lesions or enamel cavitation were 9.6 times greater for children with any hypoplasia’ (22). In 2012, Caufield and co-authors (2012) recommended “hypoplasia-associated severe early childhood caries” as a separate type of dental decay in young children, because the presence of enamel defects appear to be significantly associated with rampant decay in at-risk children (6).

Generally, the more severe the DDE, the higher the risk of dental caries (24-26). Caries in primary teeth increase the risk of caries in permanent teeth.

 Teeth with DDE are difficult to restore, as these teeth are often hypersensitive and difficult to anaesthetize (4, 5). Moreover, the enamel changes that happen at the microscopic level may adversely affect the adherence of restorative materials and the durability of fillings in teeth with DDE (4)

If the primary teeth are affected by DDE, are the permanent teeth at higher risk?

While DDE in primary teeth do not always lead to DDE in permanent teeth. DDE in the second primary molars are associated with higher risks of DDE in the permanent teeth by approximately 20-25% (19, 23). The authors suggested a shared cause for their occurrence and concluded that DDE in primary molars can be used as a predictor for DDE in permanent incisors and first molars (19, 23). In the permanent teeth, molar incisor hypomineralization (MIH) is the most common form of DDE.

Early detection is key to minimizing problems 

Teeth with DDE may breakdown quickly once in the mouth (5). Therefore, early assessment / detection soon after teeth eruption is really important (4, 23). Time is of the essence. Leave a DDE-affected tooth unprotected in a challenging oral environment for a few months, could result in pain, breakdown or infection.

Treatment options

DDE teeth with white or yellow opacities may not require intervention, except for stringent oral hygiene habits and minimizing sweet, sour and sticky foods and beverages. In at-risk children, fissure and surface sealants and remineralization therapy may help to protect the affected enamel. In severe cases, where enamel has been lost or the tooth is sensitive, restorations with glass ionomer cement and/or composite resins; or stainless steel crowns ; and sometimes extractions, may be indicated.

REFERENCES

1. Hong L, Levy SM, Warren JJ, Broffitt B. Association between enamel hypoplasia and dental caries in primary second molars: a cohort study. Caries Res 2009; 43(5): 345-353. DOI: 10.1159/000231571.

2. Costa FS, Silveira ER, Pinto GS, Nascimento GG, Thomson WM, Dermarco FF. Developmental defects of enamel and dental caries in the primary dentition: A systematic review and meta-analysis. J Dent 2017; 60: 1-7. DOI: 10.1016/j.dent.2017.03.006.

3. Vargas-Ferreira F, Salas MM, Nascimento GG, Targuinio SB, Faggion CM Jr, Peres MA, Thomson WM, Demarco FF. Association between developmental defects of enamel and dental caries: A systematic review and meta-analysis. J Dent 2015; 43(6): 619-628. DOI: 10.1016/j.dent.2015.03.011.

4. Salanitri S, Seow WK. Developmental enamel defects in the primary dentition: aetiology and clinical management. Aust Dent J 2013; 58(2): 133-140. DOI: 10.1111/adj.12039.

5. Seow WK. Developmental defects of enamel and dentine: challenges for basic science research and clinical management. Aust Dent J 2014; 59(Suppl.1): 143-154. DOI: 10.1111/adj.12104.

6. Caufield PW, Li Y, Bromage TG. Hypoplasia-associated severe early childhood caries – a proposed definition. J Dent Res 2012; 91(6): 544-550.

7. Dabiri D, Eckert GJ, Li Y, Seow K, Schroth RJ, Warren J, Wright JT, Zhao S, Fontana M. Diagnosing developmental defect of enamel: pilot study of online training and accuracy. Pediatr Dent 2018; 40(2): 105-109.

8. Ghanim A, Elfrink M, Weerheijm K, Marino R, Manton D. A practical method for use in epidemiological studies on enamel hypomineralisation. Eur Arch Paediatr Dent 2015; 16(3): 235-246. DOI: 10.1007/s40368-015-0178-8.

9. Wagner Y. Developmental defects of enamel in primary teeth -findings of a regional German birth cohort study. BMC Oral Health 2016; 17(1): 10. DOI: 10.1186/s12903-016-0235-7.

10. Tsang AK. The special needs of preterm children – an oral health perspective. Dent Clin North Am 2016; 60(3): 737-756. DOI: 10. 1016/j.cden.2016.02.005.

11. Takaoka A, Goulart AL, Kopelman BI, Weller RM. Enamel defects in the complete primary dentition of children born at term and preterm. Pediatr Dent 2001; 33(2): 171-176.

12. Silva MJ, Kilpatrick NM, Craig JM, Manton DJ, Leong P, Durgner D, Scurrah KJ. Etiology of hypomineralized second primary molars: a prospective twin study. J Dent Res 2018 Aug 3:22034518792870. DOI: 10.1177/0022034518792870. 

13. Schuler IM, Haberstroh S, Dawcyznski K, Lehmann T, Heinrich-Weltzien R. Dental caries and developmental defects of enamel in the primary dentition of preterm infants: case-control observational study. Caries Res 2018; 52(1-2) 22-31. DOI: 10.1159/000480124.

14. Nelson S, Albert JM, Lombardi G, Wishnek S, Asaad G, Kirchner HL, Singer LT. Dental caries and enamel defects in very low birth weight adolescents. Caries Res 2010; 44(6): 509-518. DOI: 10.1159/000320160.

15. Gravina DB, Cruvinel VR, Azevedo TD, Toledo OA, Bezerra AC. Enamel defects in the primary dentition of preterm and full-term children. J Clin Pediatr Dent 2013; 23(4): 391-395.

16. Sundell AL, Nisson AK, Ullbro C, Twetman S, Marcusson A. Caries prevalence and enamel defects in 5- and 10-year-old children with cleft lip and/or palate: A case-control study. Acta Odontol Scand 2016; 74(2): 90-95. DOI: 10.3109/00016357.2015.1044562.

17. Bossu M, Bartoli A, Orsini G, Luppino E, Polimeni A. Enamel hypoplasia in coeliac children: a potential clinical marker of early diagnosis. Eur J Paediatr Dent 2007; 8(1): 31-37.

18. Cameron AC, Widmer RP. (Eds). Handbook of Pediatric Dentistry. 4thEdition. Australia: Mosby Elsevier, 2013.

19. Elfrink ME, ten Cate JM, Jaddoe VW, Hofman A, Moll HA, Veerkamp JS. Deciduous molar hypomineralization and molar incisor hypomineralization. J Dent Res 2012; 91(6): 551-555. DOI: 10.1177/0022034512440450.

20. Elfrink ME, Ghanim A, Manton DJ, Weerheijm KL. Standardised studies on molar incisor hypomineralisation (MIH) and hypomineralised second primary molars (HSPM): a need. Eur Arch Paediatr Dent 2015; 16(3): 247-255. DOI: 10.1007/s40368-015-0179-7.

21. Correa-Faria P, Martins-Junior PA, Vieira-Andrade RG, Oliveira-Ferreira F, Marques LS, Ramos-Jorge ML. Developmental defects of enamel in primary teeth: prevalence and associated factors. Int J Paediatr Dent 2013; 23(3): 173-179. DOI: 10.1111/j.1365-263X.2012.01241.

22. Milgrom, P, Riedy CA, Weinstein P, Tanner AC, Manibusan L, Bruss J. Dental caries and its relationship to bacterial infection, hypoplasia, diet and oral hygiene in 6- to 36-month-old children. Community Dent Oral Epidemiol 2000; 28(4): 295-306.

23. Garot E, Denis A, Delbos Y, Manton D, Silva M, Rouas P. Are hypomineralised lesions on second primary molars (HSPM) a predictive sign of molar incisor hypomineralisation (MIH)? A systematic review and a meta-analysis. J Dent 2018; 72: 8-13. DOI: 10.1016/j.jdent.2018.03.005.

24. Vargas-Ferreira F, Zeng J, Thompson WM, Peres MA, Demarco FF. Association between developmental defects of enamel and dental caries in schoolchildren. J Dent 2014; 42(5): 540-546.

25. Massignan C, Ximenes M, da Silva Pereira C, Dias L, Bolan M, Cardoso M. Prevalence of enamel defects and association with dental caries in preschool children. Eur Arch Paediatr Dent 2016; 17(6): 461-466.

26. Foulds H. Developmental defect of enamel and caries in primary teeth. Evid Based Dent 2017; 18(3): 72-73. DOI: 10.1038/sj.ebd.6401252.