...dental caries?
According to Pure Dentistry Dentists in Brisbane, untreated caries adversely affects children's quality of life and can result in severe consequences including risk of dental sepsis.
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.
According to Featherstone 2004, “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”
What is early childhood caries?
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 Drury et al. 1999, the presence of one or more decayed, missing or filled tooth surface in any primary tooth in a child under the age of six (6)
What is severe early childhood caries?
Below is 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.
According to Drury et al. 1999, 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)
Early childhood caries (ECC), formerly known as:
These are some of the alternative terminology used to describe early childhood caries. You may have heard some these terms such as rampant caries, nursing caries. Nursing bottle caries/nursing 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
How do early childhood caries look like?
These photos show the clinical appearance of ECC. You can see
- rampant caries
- Caries affecting surfaces that are generally low risk
- Lesions appear as teeth erupt –caries pattern corresponds to order of tooth eruption of the primary teeth, they are seen in maxillary incisors followed by posterior teeth (both the maxillary and mandibular first primary molars)
- 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 extremely high risk
How can I protect my baby’s teeth from cavities?
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.
early detection
- visual
- tactile
- radiographs
- fluorescence
- transillumination
- electrical conductance
How Common is Early Childhood Caries?
The mean prevalence for Early Childhood caries is 23.8% and 57.3% in children younger than 36 months and children aged 36 to 71 months, respectively.
According to El Tantawi et al. 2018,
- children younger than 36 months: 23.8%
- children 36 to 71 months: 57.3%
Prevalence of ECC 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 the mean dfmt in children 5 yrs of age to be 2.32.
There are different risk factors for early childhood 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.
According to the Australian Institute of health and welfare 2016,
- primary teeth → 42%
- low - income households →are twice as likely to have untreated decay in the primary teeth
ECC Risk Factors
In a recent systematic review there 123 risk factors have been associated with Early Childhood caries the most important ones being dentinal caries, high levels of S.Mutans and enamel defects. According to Kirthiga et al. 2020,
- 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
Other risk factors are:
Feeding habits and sugar exposure
Frequent and prolonged consumption of sugars from liquids
The use of nursing bottles, sippy cups and feeding cups filled with sugary fluids enhances the frequency of exposure
Bottle feeding behaviour during sleep intensifies the risk of caries-
On-demand breastfeeding and nocturnal breastfeeding
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
- Single parents
According to Anil & Anand 2017,
ECC microbial risk factors
In children with ECC, S. Mutans makes up 30-50% of the plaque flora and 10% of the salivary flow.
Berkowitz et al. 1984: In children with ECC, S. Mutans constitutes:
- 30 to 50% of plaque flora
- 10% salivary flow
Ramos-Gomes et al. 2010: early establishment of S. Mutans is a significant risk factor for future development of dental caries
Let's discuss 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
Leeuwenhoek 1677:
first studies on the composition of oral bacteria occurred following Leeuwenhoek's observation of his own plaque
Sampaio- Maia & Monteiro-Silva 2014:
The number of microorganisms that colonize the oral cavity:
- 700 species
- 19000 phylotypes
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.
Dzidic et al. 2018
microbial exposure can start in- utero as they can cross the placenta
Hegde et al. 2001
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)
What are the pathogenic bacteria?
Studies evaluating the microbiota associated with early childhood caries found various genera, suggesting that there was not a single pathogen, but a pathogenic population that correlated with the development of early childhood caries. Clonal analysis of 80 children identified that the microbiome diversity was less in children with ECC compared to clinically caries-free children.
- 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
Vertical transmission is the transmission of S. Mutans from 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
Alves et al. 2009
- from primary caregiver to child
- 30-60% of mutans streptococci strains isolated from mothers and their babies are similar or identical
Berkowitz 2006
- early colonization of mutans streptococci in infants → vertical transmission pattern
- maternal contact is usually strong during the early months of life
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.
Caufield et al. 1993
window of infectivity
- 19 to 31 months
- limited ability to adhere to epithelial surface
Wan et al. 2001; Tanner et al. 2002; Cephas et al. 2011
- S. Mutans and lactobacilli are found in edentulous infants saliva samples
Horizontal transmission of mutans streptococci 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 mutans streptococci strains, which indicates that horizontal transmission may be another vector for organism acquisition. Bacteriocin typing demonstrated that when a child acquires mutans streptococci after age 5, there is a similarity between the mutans strains between family members, including fathers and siblings.
Domejean et al. 2012
- between siblings and other members of the family
Mattos- Graner et al. 2001
- acquiring S. Mutans after the age of 5
- The similarity between family members, including fathers and siblings
Are there any protective bacteria in the mouth?
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.
Becker et al. 2002
- protective bacteria
- Streptococcus Sanguinis
- pyruvate oxidase →toxic quantities of hydrogen peroxide →inhibit other species such as S. Mutans
- ↑S. Sanguinis in healthy controls on teeth with sound enamel compared to children with severe early childhood caries
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
I started my research on a different topic looking at a new fissure sealant material last year. During the past year working at PCH and OHCWA, I have seen so many children with ECC that made me change my research topic to look more closely at the 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.
- a systematic review to identify the gaps
compare the oral microbiome of children with ECC with children without ECC - compare the oral microbiome of the primary caregiver with their children
- Investigate if there is the ratio of S. Mutans / S. Sanguinis, above which children are more at risk of ECC
This is a preliminary outline of how the study will be carried out.
After ethics approval, we 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
- comparing
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
- 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
And these consequences can continue to be problematic in permanent dentition.
Consequences of untreated dental caries
According to Li and Wang 2002, Children having caries in their primary teeth are three times more likely to develop caries in their permanent teeth.
Early childhood caries 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.
Casamassimo et al. 2009
The management of ECC
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
Different caries risk assessment tools can be used and most of them look at biological, protective and clinical factors.
Management options include:
- cessation of dietary habit
- fluoride and/or CPP-ACP application
- use of biofilm moderating/antimicrobial products
- fissure sealants
- restoration of teeth
- small lesion - intracoronal tooth-coloured restorations
- extensive lesions
- anterior teeth: composite resin-strip crowns
- posterior teeth: stainless steel crowns
- Baby tooth extraction
Risk assessment tools
- Cariogram
AAPD
CAMBRA
Conclusion
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.
- ECC is a prevalent infectious disease
- many contributing factors
- role of bacteria not fully understood
- preventable
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