EARLY CHILDHOOD

CARIES

SHAMEENA K
JR3
PEDIATRIC AND
PREVENTIVE DENTISTRY
 Definitio
ns
History

Terminol
ogies

Prevalence of
ECC Classification,
stages and pattern

Etiological risk factors for

development of
ECC
Consequences

Management and prevention

Caries risk
 DEFINITIONS

 In 1999, American Academy of Pediatric Dentistry (AAPD) defined ECC as “the presence of one or more
decayed (noncavitated or cavitated lesions), missing (due to caries), or filled tooth surfaces in any primary
tooth in a child aged 71 months or younger”.

 In children younger than 3 years of age, any sign of smooth-surface caries is indicative of severe early
childhood caries (S-ECC). From ages 3 through 5, 1 or more cavitated, missing (due to caries), or filled
smooth surfaces in primary maxillary anterior teeth or a decayed, missing, or filled score of ≥4 (age 3), ≥5
(age 4), or ≥6 (age 5) surfaces constitutes S-ECC.

Definition of early childhood caries (ECC).AAPD Reference Manual 2005-2006,2007,2008

Pitts et al,2018 at the Global ECC Summit proposed the clinical definition of ECC

 ECC is defined as “the presence of one or more decayed (noncavitated or cavitated lesions), missing (due
to caries), or filled tooth surfaces in any primary tooth” in a child under the age of six.

 The definition of severe early childhood caries (S-ECC) is 1) any sign of smooth- surface caries in a child
younger than three years of age, 2) from ages three through five, one or more cavitated, missing (due to
caries), or filled smooth surfaces in primary maxillary anterior teeth, or 3) a decayed, missing, or filled
score of greater than or equal to four (age three), greater than or equal to five (age four), or greater than or
equal to six (age five).

American Academy of Pediatric Dentistry. Policy on early childhood caries (ECC): Consequences and preventive strategies.The
Reference Manual of Pediatric Dentistry. Chicago, Ill.: American Academy of Pediatric Dentistry; 2022:
•
 HISTORY
 In 1862, an American physician, Abraham Jacobi, was the first to describe the clinical appearance of
early childhood caries, which he observed in one of his own children.

 In 1911, Eric Harries: - observed caries in preschool children: - comforter caries

 Beltrami in 1930s as “Les dents noire de tout- petits” which means “black teeth of the very young.”

 Dr. Ellias Fass, 1962 –termed as “Nursing bottle mouth”.

 In 1978, the American Academy of Pedodontics and the American Academy of Pediatrics released a
joint statement “Juice in Ready-to- Use Bottles and Nursing Bottle Caries” to address a severe form of
caries associated with bottle usage.

 In 1994, the Centres for Disease Control and Prevention coined the term Early childhood caries “in
order to better the multi-factorial pathogenesis of the disease”.

 Three years later, a further conference on early childhood caries, organised by the National Health
Institute (USA) , added two further definitions/descriptions, which were rampant infant caries and
early childhood dental decay (RIECDD).
TERMINOLOGIES FOR ECC
PREVALENCE OF ECC
• Dental caries of primary dentition is the 12th most prevalent disease affecting
about 530 million children globally.(Global Burden of Disease Study,2017).

• According to the United States HHS, early childhood caries (ECC) is five
times as frequent as asthma and seven times more common than hay fever.

Devan I, Ramanarayanan V, Janakiram C.Prevalence of early childhood caries in India: A systematic

review and meta- analysis. Indian J Public Health 2022;66:S3-11.
• Global Burden of Disease Study [Vos et al., 2016], 2.5 billion people affected and a
14.6% increase in dental caries over 10 years.
•

The global prevalence of dental caries in primary

teeth was 46.2%, and for permanent teeth, 53.8% [Kazeminia et al., 2020], with
lower estimates observed in European and higher estimates in African [Frencken et al.,
2017] countries.

• Worldwide, untreated dental caries in deciduous teeth was the tenth most
prevalent and the fourth most expensive chronic disease to treat condition among
Sonia Nathwith
children, et alprevalence
The Globalpeak
Prevalence andof
at 6 years Severity of Dental
age [Petersen, Caries
2008; among Racially
Kassebaum et
Minoritized Children: A Systematic Review and Meta-Analysis. Caries Res 2023;57:485–508.
al., 2015].
Suchithra MS, Sreedharan S, Thomas V, Bindhu R N . Dental caries experience in preschool children of
Thiruvananthapuram, Kerala: Is it related to the sociodemographicfactors? IOSR J Dent Med Sci 2018;17:
• Global Prevalence of Early Childhood Caries Among Children Younger Than
36 Months: 2007–2017

The prevalence ranged from 0.3% to 69.6%

 Among children younger than 36 months, the mean prevalence was highest in North America
(31.7%) and South Asia (30%) and lowest in sub-Saharan Africa (14.3%; P = .86).

 Between 2007 and 2017, an estimated 64.6 million children younger than 36 months were
affected by ECC.

 In 1 country (Egypt), ECC prevalence ranged between 51% and 75%.

• Global Prevalence of Early Childhood Caries Among Children Aged 36 to 71
Months: 2007–2017

The prevalence from 6.3% to 98.1%.

 The number of affected children aged 36 to 71 months was estimated to be 173.5
million.

 In this age group, 55 countries had caries prevalence greater than 50% with
estimated 152.8 million children affected (88% of all affected children in this age
group globally).
PREVALENCE OF ECC IN INDIA

• The last National Oral Health Survey conducted in India by the Dental Council of India in 2002–
2003 shows that the prevalence of dental caries in children aged 5 years to be 50% with mean
decayed, missing, and filled teeth (DMFT) of 1.9. Among the 12‑year‑old children, the caries
prevalence was 52.5% with DMFT of 1.8, and in 15‑year‑old children, the prevalence was 61.4%
with DMFT of 2.3.

Bali RK, Mathur VB, Talwar PP, Chanana HB. National Oral Health Survey and Fluoride Mapping, 2002-2003,
India. Delhi: Dental Council of India; 2004
Suchithra MS, Sreedharan S, Thomas V, Bindhu R N . Dental caries experience in preschool children of Thiruvananthapuram,
Kerala: Is it related to the sociodemographicfactors? IOSR J Dent Med Sci 2018;17:
Ganesh A, Muthu MS, Mohan A, Kirubakaran R. Prevalence of Early Childhood Caries in India - A Systematic Review.
Indian J Pediatr. 2019 Mar;
 Northern India
43.8%
51.6% 47%

Western India Central India Eastern India

43.8% 62.3% 50.4%

Southern India
47% 44.6%

Devan I, Ramanarayanan V, Janakiram C.Prevalence of early childhood caries in India: A

systematic review and meta-analysis. Indian J Public Health 2022;66:S3-11.
PREVALENCE OF ECC IN KERALA
• In 2018, Suchithra et al. conducted a study about dental caries experience in
preschool children in Thiruvananthapuram, Kerala and its relation to the
sociodemographic factors and found that the prevalence of ECC to be 59.6% and
children belonging to lower socioeconomic data are prone to caries.
CLASSIFICATION
A) Based on the pattern of ECC presentation (Johnston & Meissner 1994).
B) Based on the severity of ECC and etiology (Wayne 1999).
C) HARRIS & GARCIA GODOY(1999)

• VERY MILD Clinically, light demineralization usually at the gingival crest & no cavitation.

• MILD Demineralization at the gingival 3rd of the tooth & moderate cavitation.
• MODERATE Frank cavitation on multiple tooth surfaces.

• SEVERE Widespread destruction of tooth; partial to complete loss of clinical crown.

D) Classification of ECC and Severe Early Childhood Caries (S-ECC) (Drury TF, Horowitz AM,1999,at a workshop
in Bethesda)

Age (months) Early childhood caries Severe early childhood caries

<12 1 or more dmfs surfaces 1 or more smooth dmf surfaces.

12–23 1 or more dmfs surfaces 1 or more smooth dmf surfaces.

24–35 1 or more dmfs surfaces 1 or more smooth dmf surfaces.

36–47 1 or more dmfs surfaces 1 or more cavitated, filled, or

missing (due to caries) smooth

surfaces in primary maxillary

anterior teeth or dmfs score >4.

48–59 1 or more dmfs surfaces 1 or more cavitated, filled, or

missing (due caries) smooth

surfaces in primary maxillary

• anterior teeth or dmfs score >5.

E) Kirthiga and Muthu`s OXIS Classification 2018 (The types of interproximal contact areas
of primary molars)

Greater risk for proximal caries:- I and S type

F)According to Marth Ann Keels,2021
• Early childhood caries (ECC):- Caries disease patterns in the primary dentition
that involve the presence of any caries lesion (non-cavitated or cavitated),
missing, or filled tooth surfaces in the primary dentition occurring in children
less than or equal to three years of age.

• Late Childhood Caries (LCC) :- Caries disease patterns in the primary

dentition involving any caries lesion occurring after age three until
exfoliation of the primary dentition.

–A classic LCC pattern would consist of caries lesions involving not only the
occlusal, but also most importantly the proximal surfaces of posterior teeth.
 Veerkamp and Weerheijm (1995) defined the patterns as stages that occur in overlapping time periods

initial Ages 10-20 months

damaged Ages 16-24 months

deep lesions Ages 20-36 months

traumatic Ages 30-48 months

Veerkamp JS, Weerheijm KL. Nursing-bottle caries: The importance of a development perspective. ASDC J Dent Child (1995)
62(6):381–386.
ETIOLOGY
Dental caries is considered to be an infectious disease with chronic evolution, a chronic
destructive process of multicausal nature. Carious disease is considered a condition
acquired as a result of the simultaneous interaction of at least three factors, which
constitute Keyes' triad:

a) The host represented by the quality of dental hard structures and the quantity and quality
of saliva.

b) Food diet or fermentable nutrient substrate.

c) Microbial flora colonizing the tooth surface.

To these three factors is added a fourth represented by the exposure time of dental surfaces
to the action of fermentation acids to produce demineralisation.
Nikiforuk, Gordon. 1985. Understanding Dental Caries: Etiology and Mechanisms, Basic and Clinical Aspects. Vol. 1. S. Karger AG.
Fejerskov and Manji,
1990
 Etiology not a single factor.
A complex interplay of microbial,
genetic, biochemical, social and
physical environmental, and health-
influencing behavioral factors
(Fisher- Owens et al. 2007)

Fisher-Owens SA, Gansky SA, Platt LJ, et al. Influences on children's oral health: a conceptual
model. Pediatrics. 2007;120(3):e510-520.
• Objective: To conduct a systematic review of the literature on risk factors for
dental caries in deciduous teeth of children aged six years and under, to give a
scientific framework for the international collaborative studies on inequalities in
childhood caries.

• Results: 1029 papers were identified from the electronic search, 260 met the prima
facie inclusion criteria. 183 were excluded once full copies of these papers were
obtained. Of the 77 studies included, 43 were cross sectional, 19 cohort studies, 8
case control studies and 7 interventional studies. Few obtained the highest quality
scores. 106 risk factors were significantly related to the prevalence or incidence of
caries.
 RISK FACTORS NO OF FACTORS
Sociodemographic factors 19
Dietary factors 29
Oral hygiene 10
Factors related to breastfeeding/bottle feeding 25

Oral microbial flora 3

Other factors 38

Total 123

Kirthiga M, Muthu Murugan, Ankita Saikia, Richard Kirubakaran, Risk Factors for Early Childhood Caries: A Systematic Review and Meta-
Analysis of Case Control and Cohort Studies.Pediatr Dent 2019;41(2):95-106.
 • Of the 19 sociodemographic factors, gender (male),socioeconomic status and low household
income were found to be frequently implicated in most studies.

• Among all the dietary factors, the most commonly investigated risk factor was frequency of
eating foods high in sugar more than once per day.

• Increased maternal intake of cheese during pregnancy may significantly decrease the risk of
developing dental caries in children.

Kirthiga M, Muthu Murugan, Ankita Saikia, Richard Kirubakaran, Risk Factors for Early Childhood Caries: A Systematic
Review and Meta-Analysis of Case Control and Cohort Studies.Pediatr Dent 2019;41(2):95-106.
• There were 38 factors which belonged to other factors category. Among them,
enamel hypoplasia was the most commonly studied.

• All studies that included the presence of enamel hypoplasia as a potential risk
factor for ECC concluded that the risk of developing dental caries was
significantly increased.
• Oliveira AF et al in 2006 observed a total of 224 children, with enamel defects
from the age of 12 to 54 months, for the presence of ECC.

• At 12 months, none of the infants showed the presence of dental caries. At 42

months, 9.2 percent of children presented with carious teeth; at 54 months, 48.4
percent of the children with dental caries showed the presence of enamel defects.
The study also concluded that enamel hypoplasia was the most common category
of enamel defect associated with dental caries.
 Hypoplasia-associated Severe Early Childhood Caries
• Quantitative disturbance of mineralized tissue formation during tooth development.

• For the primary dentition, the disturbance occurs either pre-natally or in early childhood (Seow, 1991;
Li et al., 1995; Seow et al., 2005).

• The enamel of primary teeth develops from approximately the 13th week of gestation to three years of
age.

• Developmental stage and degree of insult as the primary teeth form

• Typically, EHP manifests on those teeth that are at critical stages of secretion of organic matrices and
mineralization around the time of insult (i.e., the central incisors, laterals, and canines, and less
frequently on first and second molars that are mineralized postnatally).

• Both pre- and post-natal stresses adversely affect ameloblasts and odontoblasts during tooth formation
and can result in both hypoplastic and hypomineralized enamel. (Suckling, 1989; Sabel et al., 2008)
P.W. CaufieldJ Dent Res 2012;91(6):544-550
Association of Mutans Streptococci and Enamel hypoplasia

• Surface irregularities on the smooth surfaces of the teeth favors colonization of mutans streptococci(Li et al., 1994).
• Low-birthweight children with EHP were 4.4 times more likely to be infected by MS than non-EHP children.(Wan et
al. (2003)

P.W. CaufieldJ Dent Res 2012;91(6):544-550

Accepted for publication December 14, 2009.
• The class 3 and 4 frenum attachment in a nursing infant has the potential to create
dental caries if the upper lip is abnormally restricted and forms a pocket to trap
retained milk on completion of nursing.

• The possibility of caries development increases when a thick fibrous attachment

limits the normal function and mobility of the upper lip.
• Infants who breastfeed and are born with an abnormal maxillary frenum
attachment often present with a different pattern of dental caries: facial caries on
the upper incisors that often include incisal notching.
In addition, abnormal maxillary attachments appear to be a contributing factor for
the following:
• Large diastema development between the maxillary central incisors.

• Decalcification and caries development in the mesial areas of the maxillary

central incisors.

• Difficulty cleaning the interproximal areas between the upper incisors, an area
that normally prevents plaque buildup through self-cleaning.

• Poor latching on the mother’s nipple, difficult or painful nursing, and impaired
labial movements for a full and engaging smile.
 RISK FACTORS FOR THE DEVELOPMENT OF ECC
PRIMARY SECONDARY

• Dental plaque • Immunological

• Mutans Streptococci • Tooth maturation & defects

• Infant feeding patterns
• Race and ethnicity
• Tooth brushing
• Salivary factors • Acid fruit drink

• Sugars • Socioeconomic status

• Oral Clearance of Carbohydrates
• Dental knowledge
• Bovine milk , Human milk
• Fluorides • Stress

• Other factors
A) PLAQUE

• More important in the carious process is the plaque tooth interface.

• The mechanism of carbohydrate degradation to form acids in the oral cavity by

bacterial action occurs through enzymatic breakdown of sugar.

• The mere presence of acid in the oral cavity is of far less significance than the
localization of acid upon the tooth surface.

• Dental plaque acts as a reservoir for holding acids at a given point for relatively
long periods.
• Factors in plaque that may be responsible for the initiation of caries are:

a. The ability of the plaque to buffer the pH changes caused by a carbohydrate

exposure. This is also related to the rate of and diffusion or concentration of the
lactic acid produced in the plaque.

b. The quantitative and qualitative changes in the plaque microflora. Thus the
presence of streptococcus mutans, in higher levels [ cari- ogenic] as compared
to more benign microorganisms [Actinomyces, Veilonella] will determine the
predisposition to caries.
• Carious lesions have a higher percentage and incidence of certain bacterial
species: Streptococcus mutans, Streptococcus sobrinus, and Lactobacilli, isolated from
advanced caries. The specific plaque hypothesis was based on this finding, believing
only specific bacteria caused the disease.

• Indeed, Streptococcus mutans, in particular, are strongly linked to caries, but caries can
develop in sites where Streptococcus mutans are absent.

• This observation gave rise to the nonspecific plaque hypothesis, where caries is believed
to result from the net metabolic activity of the microbiota of the biofilm.

Rathee M, Sapra A. Dental Caries. [Updated 2023 Jun 21]. In: StatPearls . Treasure Island (FL): StatPearls
Publishing; 2025 Jan-
 • Although the etiology of dental caries is not completely specific, a limited type of bacteria
is consistently found in higher numbers from the affected areas. The currently accepted
concept is the ecological plaque hypothesis.

• The ecological plaque hypothesis believes that dental caries is not caused by a specific
type of microorganism acting alone but is the result of a shift in the microbiota of the
dental biofilm towards more cariogenic species.

• Oral acidic conditions from regular sugar consumption select the bacteria that empathize
more with this environment and eliminate the benign species that do not tolerate such
conditions.

Rathee M, Sapra A. Dental Caries. [Updated 2023 Jun 21]. In: StatPearls [Internet]. Treasure Island (FL):
StatPearls Publishing; 2025 Jan-
B) ORAL MICROBIOME

 Colonization of oral mucosal surfaces begins at birth with the introduction of

bacteria and fungi through multiple paths, including maternal transmission
during childbirth, parental exposures, diet and horizontal transmission from
caregivers and peers.

 The oral microbial community continues to develop with the eruption of primary
teeth in early infancy and establishment of permanent dentition in children,
evolves into a complex and diverse microbiome
 Oral microbial colonization is traditionally considered to take place after birth;
however, according to studies there commence of the human microbiome before
birth.

 Studies reported the presence of microorganisms in amniotic fluid in up to 70%

of the pregnant women, and particularly the presence of several oral
microorganisms, such as Streptococcus, Fusobacterium, Neisseria, Prevotella,
and Porphyromonas, in the human placenta.
• Approximately 20% of the preterm and extreme LBW infants by week 1 and over 50% of the
preterm/extreme LBW infants by week 6 were colonized with pathogens, e.g., methicillin-
resistant Staphylococcus aureus (MRSA). (Underwood, M. A. & Sohn, K. 2017)

• Bacterial communities colonized on infants born vaginally resemble mothers’ vaginal bacterial
communities, predominantly Lactobacillus, Prevotella, Bacteroids, TM7, and Sneathia spp.,
whereas the bacterial profile of infants born by cesarean section resemble those present in
mothers’ skin, predominantly Staphylococcus, Corynebacterium, Slackia, Veillonella,
and Propionibacterium spp
WINDOW OF INFECTIVITY
• Caufield (1993) monitored oral cavity levels from birth upto 5 years.

• He noted the initial acquisition of mutans streptococcus and designated the time
period as ‘window of infectivity’.

• As the teeth erupt in into the oral cavity they provide a virgin habitat, which
enables MS to colonize the oral cavity avoiding competition with other indigenous
bacteria.

• Thus the window period in deciduous teeth the MS is established by 19-31 months
of age and may have difficulty in establishing later because it would need to
compete with other indigenous bacteria.
• Krass etal (1967) Edrman et al (1975) reported that at 2-6 yrs of age the child is
less susceptible to acquiring MS.

• The ‘Second Window Infectivity’ is present in permanent dentition between 6-12

years of age (Klock and Kroske (1977). 90% of teenager have MS colonization
while others found only 3% of adults (mothers).

• Davey and Rogers (1984) reported that children acquire additional strain of MS as
they get older and new teeth emerge but remain undetected since they are present
in low numbers.
MUTANS STREPTOCOCCUS

 The most frequently detected early colonizers in the oral cavity are Streptococcus
(Streptococcus epidermidis and Streptococcus salivarius), Staphylococcus spp., and
Fusobacterium.
 The reasons for the high abundance of Streptococcus in the early oral cavity lie in:

(a) Streptococcus spp. are capable of adhering to epithelial cells

(b) Streptococcus spp. are one of the dominant bacterial groups found in human
breastmilk; the oral settlement of Streptococcus spp is initiated by direct transmission via
physical contact through breast feeding, facilitated by an appropriate nutrient supply in
breast milk that favors the growth of Streptococcus spp and further reinforced by
repeated breast milk feeding.
 Among Streptococcus species, Streptococcus salivarius is the most often found species
in the oral cavity of the new born, its abundance reaches the highest at 3 months of age,
accounting for 10%–15% of the total Streptococcal species.

 The abundance of S. salivarius decreases steadily its peak at 3 months, likely opposing to
teeth eruption.
Virulence of mutans streptococci;

 Mutans streptococci synthesize α-1,3-rich water insoluble glucans from sucrose (Tanzer et al.
1984). Glucans increase the thickness of plaque, and result in enhanced rates of sugar diffusion
and acid production at the deeper plaque layers (Van Houte J et al., 1985).

 Synthesize intracellular polysaccharides (IPS), which support continual acid production during
periods of low concentration of exogenous substrate and fosters tooth demineralization during
periods of low salivary secretion (Spatafora G et al. 1995).

 Mutans streptococci produce large amounts of acid, particularly lactic acid, which are potent in
driving tooth demineralization (Johnson ED et al., 1980).

 Production of dextranase allows the invasion of mutans streptococci to replace earlier colonizing
dextran-producing bacteria such as S. sanguis (Tanzer JM, 1989).
Colonization of mutans streptococci in dental plaque;

• Initial attachment of the mutans streptococci is now thought to be independent of

sucrose, and mediated by adhesions on the bacterial surface interacting directly
with the salivary proteins.

• In the absence of sucrose, other bacteria such as S. sanguis have a higher affinity
for pellicle-coated teeth than mutans streptococci.

• But in the presence of fermentable carbohydrates, especially sucrose, mutans

streptococci irreversibly adhere to the pellicle through the synthesis of glucans
mediated by glucosyltransferases produced by the bacteria (Bowen WH et al.,
1991; Loesche WJ,11 1986).
ESTABLISHMENT OF MUTANS STREPTOCOCCI IN INFANTS

• Most studies including predentate children show that mutans streptococci are usually not cultured
from the oral cavity prior to the eruption of teeth. The reason for the low prevalence in predentate.

• The organisms are usually first detected when the first primary teeth emerge into the oral cavity, or
when obturators for palatal clefts are inserted.

• The infection rate of mutans streptococci increases with age, as well as the number of teeth present
in the infant’s mouth.

• This probably reflects the increasing number of retentive sites for bacterial colonization.

• The age at which mutans streptococci are first acquired in infants is thought to influence their
susceptibility to caries, i.e. the earlier colonization, the higher is caries risk (Berkowitz RJ et al.,
1980; Caufield PW, 1993).
TRANSMISSION OF MUTANS STREPTOCOCCI:

 Strong correlation between salivary mutans streptococci counts in mothers and their children
have been reported.

• Definition of transmission of microorganisms, as stated by Berkowitz (2006), which defines

vertical transmission as: “transmission of microbes from caregiver to the child and horizontal
transmission as the transmission of microorganisms among children of similar age groups
(siblings or in school/ nursery).”
 Vertical transmission refers to the interfamilial transfers of S. mutans. Comparing the species
obtained from infant with the father, it has been accepted that the vertical transfer of these
bacteria are mostly from the mother because they show more similarities (71%–90%) with the
species in the mother.

 The probability of observing matching S. mutans genotypes between mother and child varies
according to the traditional baby care habits, cultures, and situation of having close contact
between mother and child.

 Li et al. showed that intimate contact by breastfeeding influenced the transmission of S. mutans.
It was also observed that S. mutans transmission was significantly higher in baby girls than in
baby boys, which is most likely because girls have earlier tooth eruption.

Li Y, and Caufield PW. The fidelity of initial acquisition of mutans streptococci by infants from their mothers. J
Dent Res 1995; 74(2): 681–685.
 Mothers with salivary levels of MS >105 CFU/ml of saliva have >50
per cent rate of transmission of the bacteria to their 10-16 months old
children compared with a rate of only 30 per cent in the case of
mothers with only 103 CFU/ml of saliva.

Berkowitz RJ, Turner J, Green P. Maternal salivary levels of Streptococcus mutans and primary oral infection of
infants. Arch Oral Biol. 1981;26:147–9
  The horizontal transmission refers to the S. mutans transmission from the environment (from people
living in a certain group to each other) to the child.

 It was stated that the environments where children are together such as kindergartens create suitable
environments for the spread of infective bacteria.

 In the literature, the horizontal transmission in the kindergarten environment was investigated and it was
found that there were bacteria of similar genetics among the children.

 It is stated that horizontal transmission is not only a transmission between children but also a transmission
from other individuals (siblings,sitters, teachers, etc.) children are with for a long time.
Manchanda S, Sardana D, Liu P, Lee GHM, Lo ECM, Yiu CKY. Horizontal Transmission of Streptococcus mutans in
Children and its Association with Dental Caries: A Systematic Review and Meta-Analysis. Pediatr Dent 2021
• The major species associated with severe ECC included Streptococcus
mutans, Scardovia wiggsiae, Veillonella parvula, Streptococcus
cristatus, and Actinomyces gerensceriae.
• S. wiggsiae was significantly associated with severe ECC children in the
presence and absence of S mutans detection.
• Study concluded that anaerobic culture detected as wide a diversity of
species in ECC as that observed using cloning approaches. The major
caries-associated species were S. mutans and S. wiggsiae, the latter of
which is a candidate as a newly recognized caries pathogen.
In this systematic review and meta-analysis, statistically significant difference
between C. albicans prevalence in the oral cavity of children with ECC compared to
those without ECC were noted. Moreover, individuals with oral Candida presence were
associated with >5 times odds of experiencing ECC.
• Xiao et al in 2016 examined the maternal relatedness of C.albicans isolated from S-
ECC children and found that the mothers of S-ECC children were also highly
infected with oral C. albicans (>80% detection in both saliva and plaque samples)
and more than 60% of the S-ECC children were carrying the same C.
albicans strains as their mothers.

• Xiao J, Moon Y, Li L, Rustchenko E, Wakabayashi H, Zhao X, Feng C, Gill SR, McLaren S, Malmstrom H, Ren Y, Quivey R, Koo
H, Kopycka-Kedzierawski DT. Candida albicans carriage in children with severe early childhood caries (s-ecc) and
maternal relatedness. PLOS ONE. 2016;11:e0164242. doi: 10.1371/joural.pone.0164242. [
Health condition in Oral microorganisms Oral microorganisms Study type from which
children with increased relative with decreased relative association is identified
abundance abundance
Earlychildhood caries Streptococcus mutans Actinomyces Case
Streptococcus salivarius control(Bowen,2011;Joha
Streptococcus sobrinus nsson,2016)
Streptococcus
parasanguinis Prospective cohort(Gross,
Streptococcus wiggsiae E. L. et al; Richards, V. P.
Streptococcus exigua et al.2017)
Lactobacillus salivarius
Parascardovai denticolens
Porphyromonas
Veillonella
Candida albicans
C) INFANT FEEDING PATTERNS

 Research shows that human breastfeeding in infants has many advantages and has not
been epidemiologically associated with caries in the absence of other factors such as
poor oral hygiene or a carbohydrate diet.
 Breastfeeding in combination with other carbohydrates has been found in vitro to be
highly cariogenic.
 Frequent night time bottle feeding with milk is associated with, but not consistently
implicated in, S-ECC.
 Breastfeeding more than seven times daily after 12 months of age is associated with
increased risk for ECC.
 Night time bottle feeding with juice, prolonged use of a sippy or no-spill cup, and
frequent between-meal consumption of sugar-containing snacks or drinks (e.g., juice,
formula, soda) will increase the risk of caries.

McDonald RE, Avery DR. Dentistry for the Child and Adolescent. 11th ed. St. Louis (MO): Elsevier; 2016
 AAPD endorses the policy statement of the American Academy of Pediatrics (AAP) on
breastfeeding and the use of human milk. The AAP statement includes the acknowledgment that
“breast-feeding ensures the best possible health as well as the best development and psychosocial
outcomes for the infant.”

 However, both organizations discourage extended or excessive frequency of feeding times (from
the breast or bottle) and encourage appropriate oral hygiene measures for infants and toddlers.

 The AAPD suggests that “ad libitum nocturnal breast-feeding should be avoided after the first
primary tooth begins to erupt”

American Academy of Pediatric Dentistry. Policy on dietary recommendations for infants, children, and adolescents. The
Reference Manual of Pediatric Dentistry. Chicago, Ill.: American Academy of Pediatric Dentistry; 2022:96-100.
• S. mutans in the oral cavity of 1-year old infants was more prevalent in formula-
fed than in breastfed infants.(Parisotto, T. M.,2010)

• In addition to breastfeeding and bottle feeding, introducing comforting oral device,

such as pacifier, has been found to serve as a potential risk factor for the
colonization of S. mutans in infant’s mouth in early infancy.(Plonka, K. A. et
al,2012)
D) SALIVARY FACTORS

• A broad and complex relationship between saliva and caries has been recognized.

• Under normal physiological conditions, the saliva is supersaturated in terms of calcium and phosphorous with respect
to the enamel surface.

• This prevents the hydroxyapatite from dissolving in the oral environment as long as the pH of the environment is
maintained.

• The primary factor affecting the composition of saliva is the flow rate, which may change with the type, intensity, and
duration of the stimulus. Saliva’s pH and buffering ability are influenced by the amount of bicarbonate present.

• Tooth demineralization happens when saliva’s actual pH stays below the critical pH for an extended period of time.
Below the critical pH, which is about 5.5 for enamel, saliva loses its phosphate and calcium saturation, allowing the
hydroxyapatite in the dental enamel to disintegrate.

• A pH drop, initially is countered by the buffering action of the saliva due to the bicarbonates and the phosphates.
Stimulated saliva, with a higher bicarbonate content is said to be more effective in its buffering action than
unstimulated saliva.
 Salivary biomarkers
 Saliva contains many innate defense molecules that participate in the protection of oral tissues by
either direct antimicrobial effect or interference with microbial colonization.

 These molecules include AMPs (cathelicidin peptide LL-37, alpha-defensins, beta-defensins,

histatins and Statherian), major salivary glycoproteins (mucins, proline-rich proteins (PRPs) and
immunoglobulins) and minor salivary glycoproteins (agglutinin, LF, cystatins and lysozyme).

 These proteins play specific functional roles in the first line of defense of the oral cavity.

 There is a highly significant correlation between higher caries prevalence in preschool children
with higher levels of microbials, such as mutans streptococci, C. albicans and Prevotella spp.,
and salivary proteins, including IgA, IgG immunoglobulins, PRP and histatin peptides, in saliva
compared with caries-free individuals.
Hemadi AS, Huang R, Zhou Y, Zou J. Salivary proteins and microbiota as biomarkers for early childhood caries risk
assessment. Int J Oral Sci. 2017 Nov;9(11):e1.
E) SUGARS

• Sucrose, glucose, and fructose found in fruit juices and vitamin C drinks as well as in
solids are probably the main sugars associated with infant caries

• Sucrose, the most widely used sugar, is considered the most important in dental caries, as
it is the only substrate used for bacterial generation of plaque dextrans (Newbrun 1982).

• The frequency of consumption of sugar-containing food is directly proportional to the

caries experience. The frequency of in between meal snacks of candies, cookies, chewing
gum or carbonated beverages play an important role in increasing the caries rate.

• Frequent ingestion of sucrose even with a relatively low concentration of 1.25 % will cause
a drop in pH to between 4 and 5.
 The American Heart Association and International Association of Paediatric Dentistry
(IAPD) recommend reducing sugar consumption in early childhood and not offering any
free sugars to children under 2 years of age [Vos et al., 2017; Pitts et al., 2019].

 Besides, the WHO advises intake of free sugars to be less than 10% of total energy
intake for children and adults [WHO, 2015].

 Even with these recommendations, the prevalence of early sugar consumption is high
worldwide, with sugar consumption in the first year of life ranging from 44% to 98%
[Wang et al., 2018; Feldens et al., 2020].
 Additionally, the American Academy of Pediatrics recommends that 100 percent
fruit a day for children between the ages of one and three.

• Early introduction of sugar in the child’s diet resulted in a higher prevalence of

caries in early childhood – the earlier the introduction of sugar, the greater the risk
of caries development.
F) ORAL CLEARANCE OF CARBOHYDRATES

 In infants with ECC, the sleep time consumption of sugar is another common
characteristic.
 The low salivary flow during sleep decreases oral clearance of the sugars and increases
the length of contact time between plaque and substrates, thus increasing the
cariogenicity of the substrate significantly.
 In this regard, Hanaki M,et al.18 (1993) reported that clearance of glucose is slowest
on the labial surfaces of the maxillary incisors and buccal surface of mandibular
molars.
 These site differences in oral clearance may explain, in part, the distribution of the
carious lesions in ECC, which are characteristically localized to the maxillary primary
incisors and first molars.
G) BOVINE MILK

 The cariogenicity of milk is often questioned because plain bovine milk is the common fluid
placed in the feeding bottle in many cases of ECC.

 Most of the studies prove that milk is not cariogenic and in fact, it may exhibit some cariostatic
effect.

• The mechanisms of protection by milk appear to work are decreasing demineralization and
increasing remineralization of enamel, increasing the calcium and phosphate concentrations in
plaque and increasing the acid buffering capacity of plaque.
H) HUMAN MILK

 Compared to bovine milk, human breast milk has a lower mineral content, higher
concentration of lactose (7% vs 3%), and less protein (1.2 g vs 3.3 g per 100 ml), but these
differences are probably insignificant in terms of cariogenicity.
 Breastfeeding for six to seven months or more might increase dental caries risk due to
simultaneous events that occur during the same period, such as the eruption of primary teeth.
(Kato et al. in 2015)
 Breastfeeding up to 12 months of age is not associated with an increased risk of dental caries.
(R Tham1 et al 2015)
 A systematic review revealed that breast feeding for more than a year and at night might be
associated with an increased prevalence of dental caries .(Valaitis Ret al 2000)
 Tanaka K, 2012 concluded in their study that the increased maternal intake of cheese during
pregnancy may significantly decrease the risk of developing dental caries in children.
(I) Tooth Brushing

• As ECC starts on surface that can be easily accessed by routine tooth brushing,
oral hygiene levels may be associated with caries risk.

• Increased frequency and better oral hygiene levels are associated with lower
caries levels in preschool children.

• A major problem confronting the investigation of the relationship between tooth

brushing and ECC is the methodological issue of assessing the frequency of
brushing, quality of plaque removal, and actual levels of oral hygiene.
(J)FLUORIDES

 Although the benefits of water fluoridation and postnatal fluoride

supplementation in the primary dentition are well known, there is minimal
information on the cariostatic effects of topical fluoride in the early primary
dentition, particularly in the prevention of ECC.

 The topical effects of fluoride are complex, and include changes on the mineral
phases, as well the modulation of metabolic effects on mutans streptococci and
other bacteria in dental plaque.
 Even at very low concentration, fluoride can affect the demineralizing process in a
carious lesion by decreasing the rate of subsurface dissolution and enhancing the
deposition of fluoridated apatite in the surface zone.

 In dental plaque, fluoride can act as a direct inhibitor of enzymes, which affects the
metabolic activity of mutans streptococci.

 This reduces the acid tolerance of mutans streptococci by affecting the functioning of
proton extruding ATPases, which results in cytoplasmic acidification and inhibition of
glycolytic enzymes.
SECONDARY RISK FACTORS