Early Childhood Caries from an Epidemiologic, Microbiologic, and Immunologic viewpoint

1. Early Childhood Caries from an Epidemiologic, Microbiologic, and Immunologic viewpoint Emily Mellion DDS Pediatric Dental Resident PGY1

2. What is ECC

3. ECC – Significant Public Health Problem • Consequences of ECC include • Higher risk of new carious lesions in primary and permanent teeth • hospitalizations • Emergency room visits • Increased treatment cost • Risk of delayed physical growthand development • Loss of school days • “Policy on Early Childhood Caries, ECC: Classifications, Consequences, and Preventive Strategies” JAAPD. V 35,No. 6. Pg 13-14. 2011.

4. Early Childhood caries • Not self-limiting • Most Common chronic infectious disease of childhood • Presence of disease is dependent upon virulence of bacterial agent, host resistance, and environment

5. Epidemiology of ECC • Low SES • Minority status • Maternal Smoking • Maternal levels of MS • Parental income/education level • Fluoridation • Infant feeding practice

6. Epidemiology of ECC • NHANES survey of children 2-5 from 1988-1994 the amount of children with dental caries was 24.2% and from 1999-2004 it increased to 27.9% • NHANES survey also found that 18% of caucasian children 2-5 experienced dental caries while 40% in Mexican community and 29% in the African American community • Dye BA, Tan S, Smith V, et al. Trends in oral health status: United States, 1988–1994 and 1999–2004. Vital and Health Statistics. Series 11. 2007;(248):1–92

7. Microbiologic aspect of ECC

8. Classifying bacteria as cariogenic • An organism must exhibit tropism for teeth • Must be acidogenic • Must be aciduric • Must use refined sugar • Ernest Newbrun

9. S.Mutans • Main culprit in Early Childhood Caries • Gram + cocci, facultative anaerobe • Early colonizer, forming dental plaque/biofilm • Metabolizes sucrose to lactic acid

10. Window of Infectivity • Earliest colonizers of infant mouth at first few days of life: s.oralis, s.mitis, s.salivarius • Defined period of time when S.mutans is acquired by infants • Time period is between 19-30, mean age of 26 months • 46 mother-child pairs monitored from birth-5 yr, acquisition of MS occurred in 38 children at median age 26mo. • S.Mutans colonization • Correlated to emergence of primary teeth and total surface area of teeth • Caufield, P et al. “Initial acquisition of mutans streptococci by infants; evidence for a discrete window of infectivity” J Dent Res. 1993. Jan,72(1): 37-45

11. Transmission of S.mutans from mother to child • Vertical transmission • Saliva, milk, etc. • The higher S.mutans level in mother correlates with higher S.mutans level in child • Higher S.mutans levels in mom lead to earlier s.mutans colonization In child

12. Microbial risk indicators of ECC • Plaque samples gathered from cohort of twins from Brazil • Low SES, 91% never been to Dentist • Plaque samples gathered from caries free sites and caries rich sites in oral cavity • Plaque was studied and simple univariate test was applied to determine over abundance/underabundance of bacterial species in diseased children relative to caries free children • Compared data by using Gene expression data analysis to determine over/underabundance of bacteria in caries active children

13. Results: • Caries active species: Actinomyces, S.mutans, Lactobacillus Corby, P.M et al. “Microbial Risk Indicators of Early Childhood Caires.” Journal of Clinical Microbiology, Nov. 2005 p 5753-5759. Vol 43, No.11

14. Molecular analysis of bacterial species associated with childhood caries • Purpose of study: to compare bacteria found in mouths of children with ECC to caries-free children by using molecular identification methods • Methods • Plaque was studied from children without ECC and in healthy sites, white spot lesions, and deep lesions in children with ECC • Goal to study known bacterial species and identify new bacteria associated with caries

15. Griffen, AL. Becker, Mitzi et al. “Molecular Analysis of Bacterial Species Associated with Childhood Carise.” Journal of Clinical Microbiology. Mar 2002. p. 1001-1009. Vol 40. No. 3

16. Results • s.sobrinus- in the past it has been closely related to s.mutans but it is very hard to differentiate it from s.mutans in cultures and in this test was not significantly associated with caries • Actinomycesgerencseria was found around white spot lesions • Veillonella found in progressing lesions • 10 novel species were identified by this study and technique

17. S.parasanguinis • Gram positive bacteria • Have pili and fimbriae that allow the bacteria to adhere to oral surfaces • Previously been linked to caries, but not thought to play major role • Significantly associated with early childhood caries in this study

18. Bifidobacterium • Gram positive, non-motile, often branched anaerobic bacteria found in mouth • Finding suggests role in progressing lesion • In past, has not been highly associated with caries • Possible role in deep caries in children • More studies need to be done

19. Immunologic aspect of ECC

20. Early Childhood Caries Immunology • Development of the oral immune system • Infant serum- serum antibodies reach oral environment • Infant saliva- Immunoglobulins • Maternal milk • Maternal serum- (crossing placental barrier)

21. Infant Saliva/Serum • Immunoglobulins- Y shaped protein produced by plasma cells used by immune system to identify and neutralize bacteria and viruses • 3 main functions of antibodies in immune system • Bind to pathogens preventing them from entering or damaging cells • Coating pathogens for removal by macrophages and other cells • Cause destruction of pathogen by triggering other immune responses such as fixation of complement

22. IgM • FIRST Ig to be made by fetus and FIRST Ig to be made by B cells when it is stimulated by an antigen • When baby is born immune system has not developed and mainly protected by IgM • Higher levels of IgM in infant are correlated with intra-uterine infection

23. IgG • IgG is the only class that crosses placentato the fetus during pregnancy • Major Ig in serum and vascular spaces • Fetus only protected by IgG from Mother • Levels of infant’s own IgG start to rise after birth (around 3 mo), but don’t reach adequate level until about 1 yr.

24. IgA • Antibody that plays critical role in mucosal immunity • Main Ig found in mucous secretions including tears, saliva, colostrum, and secretions in GU, GI, and respiratory tract. • sIgA immune mechanism in saliva • Makes adherence to teeth hard • Survives proteolytic enzymes

25. sIgA • It appears at time of s.mutans • Titer for sIgA approaches that of an adult by 10 yrs • Major Ig protecting us from cariogenic bacteria • sIgA deficiency • Undetectable IgA in blood and secretions, but no other Ig deficiencies • Patients exhibit increased risk of developing dental caries • Tar et al. “Oral and Dental conditions of children with selective IgA deficiency.” Pediatric Allergy Immunology. 2008 Feb; 19 (1) 33-6

26. Maternal IgG IgM Infant IgG Developed immune system

27. Maternal Milk • Contains all immunoglobulin types (passive immunity) • Contains large quantities of sIgA • Antibodies are formed as mother was exposed to infectious agents and can protect child’s cells against pathogens • Contains leukocytes, mostly macrophages and neutrophils that phagocytose microbial pathogens • Contains several non-specific factors that help with antimicrobial effects • Lysozyme, lactoferrin

28. Conclusion • ECC is most chronic infectious disease of childhood • Higher levels found in low SES, minorities, high levels of maternal s.mutans • Window of Infectivity • Microorganisms associated with ECC • S.mutans, lactobacillus, Bifidobacterium, Actinomyces, Veillonella, S.parasanguinis, s.sobrinus • Infant immune response • IgG(fetus)-> infant IgM -> infant IgG -> sIgA • Main antibody involved with cariogenic bacteria • sIgA