Let’s talk about early childhood caries and the microbiome associated with this prevalent disease in children. I will be referring to early childhood caries as ECC. ECC is defined as the presence of one or more decayed, missing, or filled tooth surfaces in any primary tooth in a child under the age of six.

According to dentists, Dental Caries can be referred to as both the process and the resultant carious lesion. The process involves interactions over time between bacteria that produce acid, a substrate that the bacteria can metabolise, and many host factors that include teeth and saliva.

“A continuum of disease states of increasing severity and tooth destruction ranging from sub-clinical enamel demineralisation to lesions with dentinal or pulpal involvement, with or without surface breakdown”

Featherstone 2004

Early childhood caries means the presence of one or more decayed, missing or filled tooth surface in any primary tooth in a child under the age of six

Featherstone 2004

This image shows the definition of severe early childhood caries. However, In the international association of paediatric dentistry global summit on early childhood caries in Bangkok in 2015,  it was agreed not to use this definition as it causes many confusions.

any sign of smooth-surface caries in children younger than 3 years of age

from 3 to 5 years:

• dmft in primary maxillary anterior teeth ⩾ 1

or

• dmft ⩾4 (age 3)
• dmft ⩾5 (age 4)
• dmft ⩾6 (age 5)

Drury et al. 1999

These are some of the alternative terminology used to describe early childhood caries. You may have heard some of these terms such as rampant caries, nursing caries or nursing bottle caries.

• • • • feeding bottle syndrome
      • nursing bottle mouth
      • labial caries
      • baby bottle tooth decay
      • caries of incisors
      • comforter caries
      • rampant caries

• maxillary anterior caries
• rampant early childhood dental decay
• bottle-mouth decay
• early childhood caries
• early childhood tooth decay
• severe early childhood caries
• feeding bottle tooth decay

These images show the clinical  presentation of ECC

You can see

• rampant caries
• Caries affecting surfaces that are generally low risk
• Caries pattern corresponds to order of tooth eruption of the primary teeth, they are seen in maxillary incisors followed by posterior teeth
• Mandibular anterior teeth are usually unaffected – this is thought to be because of salivary flow and the position of the tongue. If they are affected, this would indicate an extremely high risk

Prevalence of ECC Worldwide

The mean prevalence for  ECC is 23.8% and 57.3% in children younger than 36 months and children aged 36 to 71 months, respectively.

• children younger than 36 months: 23.8%
• children 36 to 71 months: 57.3%

El Tantawi et al. 2018

Prevalence of ECC In Australia

In Australia:

• In 2012-14, roughly 2 in 5 children had experienced decay in their primary teeth, and 1 in 4 children had experienced decay in their permanent teeth.
• Children in low-income households were twice as likely to have untreated decay in their primary teeth as children in high-income households.
• This table from the Australian Institute of health and welfare shows mean dfmt in children 5 yrs of age to be  2.32.

• primary teeth → 42%
• low – income households →twice as likely to have untreated decay in the primary teeth

 Australian Institute of health and welfare 2016

In a recent systematic review, 123 risk factors have been associated with ECC . the most important ones being dentinal caries, high levels of S.Mutans and enamel defects.

There are different risk factors for ECC caries including microbial factors, feeding habits, socioeconomic factors and many more. I will briefly discuss some of these risk factors and spend a little more time on the microbiome associated with ECC.

• 123 risk factors
• the strongest risk factor in the high – income countries

○dentinal caries

○high levels of S. mutans

• in upper-middle-income countries

○enamel defects

Kirthiga et al. 2020

Other risk factors include:

• Feeding habits and sugar exposure
• Frequent and prolonged consumption of sugars
• Use of nursing bottles, sippy cups and feeding cups filled with sugary fluids
• Bottle feeding behaviour during sleep
• On-demand breastfeeding and nocturnal breastfeeding
• And Habits such as grazing

Socioeconomic factors also have an important role in Early childhood caries :

• Children from families with:
• Low income
• Low educational level
• Low dental health literacy
• And Single parents are more at risk

In the next image you can see caries occur when the balance between the pathological factors and protective factors are are disturbed.

In children with ECC, S. Mutans makes up 30-50% of the plaque flora and 10% of the salivary flow.

In children with ECC,  S. Mutans constitutes:

• 30 to 50% of plaque flora
• 10% salivary flow

Berkowitz et al. 1984

early establishment of S. Mutans is a significant risk factor for the future development of dental caries

                                                                                         Ramos-Gomes et al. 2010

Will talk a little bit more about the role of bacteria in ECC. As seen in the previous images bacteria plays a major role in producing acids and initiating the caries process. It was thought that the number of microorganisms that colonize the oral cavity was around 700 species. Now it is thought to include 19 000 phylotypes.

first studies on the composition of oral bacteria occurred  following Leeuwenhoek’s observation of his own plaque

Leeuwenhoek 1677

the number of microorganisms that colonize the oral cavity:

• 700 species
• 19000 phylotypes

                        Sampaio- Maia & Monteiro-Silva 2014

It was thought that newborns had their initial microbial exposure at birth, but some authors argue that microbial exposure starts in-utero as they can cross the placenta. Maternal oral microbiota has been proposed to colonize the placenta, where it could influence foetal immune tolerance towards the mother’s microbiome. Only a pioneer subgroup of the initial microbial exposures will lead to permanent colonisation, which begins within the first 24 hours of life. At this stage, the most frequent colonizers of the oral cavity are Gram-positive cocci, including Streptococcus and Staphylococcus.

• microbial exposure can start in- utero as they can cross the placenta

Dzidic et al. 2018

• pioneer subgroups of the initial microbial exposure will lead to permanent colonization, beginning in the first 24 hours of life
• frequent colonizers of the oral cavity

○gram-positive cocci (streptococcus and staphylococcus)

Hegde et al. 2001

Studies have reported Streptococcus Sanguinis can prevent obvious damage to the host as a consequence of its growth. It has been reported that S. Sanguinis is able to produce pyruvate oxidase which is the main enzyme to produce toxic quantities of hydrogen peroxide, which can inhibit other species such as S.mutans.  A study by Becker et al compared 30 children with severe early childhood caries with healthy controls. S. Sanguinis was detected in healthy subjects and on teeth with sound enamel.

• protective bacteria
• Streptococcus Sanguinis

○pyruvate oxidase →toxic quantities of hydrogen peroxide  → inhibits other species such as S. Mutans

• ↑S. Sanguinis in healthy controls on teeth with sound enamel compared to children with severe early childhood caries

Becker et al. 2002

Horizontal transmission of S. Mutans can occur between siblings and peers. Genotyping of S. Mutans isolated from groups of nursery school children aged 12 to 30 months using PCR and restriction fragment-length polymorphism analysis found that many children contained identical genotypes of S. Mutans. which indicates that horizontal transmission may be another vector for organism acquisition. Bacteriocin typing demonstrated that when a child acquires S. Mutans after age 5, there is a similarity between the mutans strains between family members, including fathers and siblings.

• between siblings and other members of the family

Domejean et al. 2012

• acquiring S. Mutans after the age of 5

○ Similarity between family members, including fathers and siblings

Mattos- Graner et al. 2001

Vertical transmission is the transmission of S. Mutans from the primary caregiver to child.

Between 30 to 60% of mutans streptococci strains isolated from mothers and their babies exhibit similar or identical bacteriocin profiles and identical plasmid or chromosomal DNA patterns.

The early colonisation of mutans streptococci in infants is indicative of a vertical transmission pattern, as maternal contact is usually strong during the early months of life.

• from the primary caregiver to child
• 30-60% of mutans streptococci strains isolated from mothers and their babies are similar or identical

Alves et al. 2009

• early colonization of mutans streptococci in infants → vertical transmission pattern
• maternal contact is usually strong during the early months of life

Berkowitz 2006

It was thought that Streptococcus mutans and Lactobacilli began to colonise the infant oral cavity during a “window of infectivity” of 19-31 months. This concept was based on mutans streptococci’s limited ability to adhere to epithelial surfaces and therefore requiring a non-shedding oral surface for persistent oral colonization.

More recent studies have shown strep mutans and lactobacillus can be found in edentulous infants saliva and a non-shedding oral surface as persistent oral colonization is not required.

• Mutans streptococci → initial colonization
• Streptococcus Sobrinus → caries initiation progression and development
• Lactobacilli → progression
• Actinomyces→ white spot lesion
• Bifidobacterium → deep carious lesions
• Less diverse microbiome in children with ECC

Kanasi et al. 2010

A preliminary outline of how a study can be carried out:

After ethics approval, they will collect saliva samples of 30 caries-free children and their caregivers and 30 children with ECC and their caregivers.

• ethics approval
• saliva collection
• culturing

○comparing

• group A & C
• group B & D
• group A & B
• group C & D

Saliva Sample of Children with ECC, N=30, Group A

Saliva Sample Caregivers of Children with ECC, N=30, Group B

Saliva Sample of caries-free children, N=30, Group C

Saliva Sample of Caregivers of caries-free children, N=30, Group D

potential implications of the study results are:

• a better understanding of the oral microbiome of children with and without ECC
• identity the protective ratio, if one exists, preventing ECC
• preventive strategies could be tailored to reduce the risk of ECC
• develop therapies to target the specific microflora

ECC is not just about holes in the baby teeth. It is usually associated with serious comorbidity affecting children, their families, the community and the health care system.

Although rare death can also occur due to untreated dental caries. In 2007 a 12-year-old boy, died from a brain abscess originating from an abscessed tooth that was left untreated for a long period of time.

Started a research on a different topic looking at a new fissure sealant material last year. During the past year working at Children’s hospital and Oral Health centre, I have seen so many children with ECC that made me change my research topic to look more closely at microbiome associated with this prevalent disease.

The plan is to:

• Conduct a systematic review to identify the gaps
• Compare the oral microbiome of children with ECC with caries-free children.
• Compare the oral microbiome of the primary caregivers with their children
• Investigate If there is a ratio of S.Mutans / S.Sanguinis above which children are more at risk of ECC

When talking about the microbiome of the oral cavity, we can look at the plaque, saliva or dentine microbiome. Culturing methods or molecular techniques can be used to identify the different species and phyla.

Many of the bacterial species can not be cultured and molecular techniques can be more specific.

The 16S ribosomal RNA gene codes for the RNA component of the 30S subunit of the bacterial ribosome. Because of the complexity of DNA–DNA hybridization, 16S rRNA gene sequencing is used as a tool to identify bacteria at the species level and assist with differentiating between closely related bacterial species.

○samples

• plaque
• saliva
• carious dentine

○technique

• culturing methods
• molecular techniques – 16S rRNA

This is important as consequences of ECC  can continue to be problematic in the permanent dentition.

Children having caries in their primary teeth are three times more likely to develop caries in their permanent teeth.

Li and Wang 2002

Prevention is always better than cure. Oral health education is a  critical step in the prevention of ECC.

• oral health education

○counselling

○reduce the S. Mutans reservoir → e.g elimination of  active dental caries lesions in mothers, siblings

○alter saliva sharting activities

○x2 daily brushing using fluoridated toothpaste

○dietary advice

○dental home no later than 1 year of age

Early detection using any of the mentioned methods in this slide is very important. White spot lesions are demineralised areas and a  sign of early decay and a risk factor for ECC.

• early detection

○visual

○tactile

○radiographs (Dental Xrays)

○fluorescence

○transillumination

○electrical conductance

Risk assessment tools

• Cariogram
• AAPD
• CAMBRA

Different caries risk assessment tools can be used and most of them look at biological, protective and clinical factors.

Management  of ECC

• cessation of dietary habit
• fluoride and/or CPP-ACP application
• use of biofilm moderating/antimicrobial products
• fissure sealants
• restoration of teeth e.g stainless-steel crown
  • small lesion – intracoronal tooth-coloured restorations
  • extensive lesions
    • anterior teeth: composite resin-strip crowns
    • posterior teeth: stainless steel crowns
• extractions

ECC is a prevalent infectious disease

• many contributing factors
• role of bacteria not fully understood
• preventable

To conclude,

• ECC is a prevalent infectious disease that can have a significant effect on children’s quality of life.
• The oral microbiome is only one factor contributing to this condition. This will be a limitation in the planned study as controlling other factors will be difficult.
• By better understanding of ECC hopefully, we can prevent its occurrence.