Early Childhood Caries (ECC):

what’s in a name?
A. DE GRAUWE, J.K.M. APS, L.C. MARTENS

ABSTRACT. Aim It is evident from the number of published scientific papers on Early Childhood Caries (ECC)
that interest in this problem has grown in recent years. Many authors have been trying to devise a clear
definition or classification for ECC. The aim of this review was to inventory the prevalence of ECC and to seek
a consensus regarding definition and diagnosis. Further attention was paid to the aetiological factors including
the role of microrganisms. Finally, education, parenting and treatment procedures were discussed. Methods
For this review, epidemiological studies on caries prevalence in children aged between 0 and 36 months were
compiled through a systematic approach using Medline. Review This clearly showed that ECC continues to be
a serious public health problem and that there is a great variety of definitions and diagnoses used worldwide,
reflected in the prevalence data. This review confirms the multicausal aetiology and the need for further
research. The authors strongly support the recommendations formulated at the workshop in Bethesda 1999, and
the policy statements by the AAPD. Conclusion More efforts should be made to reach the high risk groups
within populations, in order to reduce the prevalence of ECC and S-ECC (Severe Early Childhood Caries) and
consequently to ameliorate the quality of life of these children. Long-term intervention studies are required for
the evaluation of these efforts.

KEYWORDS: Early Childhood Caries, Case definition, Prevalence, Diagnosis, Aetiology.

Introduction diagnosis. Further attention was paid to the

For years, rampant caries in the primary dentition of
infants and young children has been described by
several terms including: nursing bottle caries, nursing
caries, rampant caries, baby bottle caries, baby bottle
tooth decay, milk bottle syndrome and prolonged
nursing habit caries. Supported by the report of the
Bethesda workshop [Drury et al., 1999] the term
Early Childhood Caries (ECC) is actually preferred.
ECC is a serious oral health problem, especially in
disadvantaged communities in both developing and
industrialized countries in which undernutrition is
common. In many cases, it is thought to be initiated
and exacerbated by inappropriate feeding with a
nursing bottle. Nowadays, however, more attention is
paid to environmental factors, which supports the
widely accepted multicausal aspect of dental caries.
The aim of this review was to inventory the
prevalence of ECC as reported in the literature and to
look for a consensus regarding definition and
Department of Paediatric Dentistry and Centre for Special Care
PaeCaMed research, Ghent University, Belgium
aetiological factors including the role of
microrganisms. Finally, education, parenting and
treatment procedures were discussed.
Clinical description
The term Early Childhood Caries (ECC) as the
specific virulent form of caries in the primary
dentition of infants and young children seems to
replace all other terms, as noted above, ever used to
indicate a severe form of caries at a very young age
(<3 years). These terms, however, are useful as they
describe the problem and ascribe a possible cause in
a form that could be understood by parents,
caretakers and the public. Although the ‘bottle’ has
been described as the most frequent cause, there are
others that could also lead to ECC. The term ‘nursing
caries’ is more inclusive, but it assumes that
breastfeeding or other nursing practices alone could
cause the condition. Therefore, the term ‘Early
Childhood Caries’ has become widely accepted in the
most recent literature as a more general term that
includes breast-feeding, as well as the use of
sweetened pacifiers, which may be significant

62 EUROPEAN JOURNAL OF PAEDIATRIC DENTISTRY • 2/2004

 EARLY CHILDHOOD CARIES

Typical characteristics of ECC

I. Rapid development. Progression from the enamel into the dentine occurs in 6 months or less.

II. Maxillary incisors are affected first. These teeth usually erupt around 8 months of age.

III. The next teeth to be affected are the primary maxillar and mandibular molars, which begin to erupt around 12 months of age.

IV. Finally, when the disease becomes very severe and remains untreated, the mandibular incisors are also affected.

TABLE 1 - Typical characteristics of Early Childhood Caries.

[Johnston and Messer, 1994; Wyne, 1999].
Furthermore there is a strong belief that
environmental factors such as social deprivation are
most important [Ramos-Gomez et al., 2002;
Quinonez et al., 2001].
ECC is a form of early, moderate and late dental
decay that affects the primary teeth of infants and
toddlers. It develops in tooth surfaces that are usually
at low risk for caries, such as the labial surfaces of
maxillary incisors and lingual and buccal surfaces of
maxillary and mandibular molars. ECC usually
begins with the maxillary primary incisors, initially
developing a dull white demineralized band, the so-
called ‘white spot’, along the gingival margin. As the
condition progresses, caries develops and may evolve
to a complete destruction of the crown, leading to
root stumps. ECC always begins with an early stage;
starting with white or brown spots, appearing at the
gum line. In the moderate stage, cavitation starts and
caries begins to spread to the maxillary molars. In the
severe stage, the caries process destroys the maxillary
teeth, and spreads to the mandibular molars. Finally,
in very severe cases the mandibular incisors are
affected (Table 1). The pattern of caries development
is characteristic for the disease and is affected by the
sequence of eruption of the primary teeth, the
duration of the causative behaviour and the patterns
of tongue movement and oral muscular action
[Horowitz, 1998].
Classification
During the last 20 years, different research groups
have attempted to develop classification systems for
ECC. In a first approach [Wyne, 1999], the
severeness of ECC can be defined in three types and
associated with different aetiology. In Type I (mild to
moderate) ECC was defined as the existence of
‘isolated carious lesion(s)’ involving incisors and/or
molars. The most common causes are usually a
combination of semi-solid or solid food and lack of
oral hygiene. In Type II (moderate to severe) ECC
was described as ‘labiolingual lesions’ affecting
maxillary incisors, with or without molar caries,
depending on the age of the child and stage of the
disease. Typically are the unaffected mandibular
incisors. The cause is usually inappropriate use of a
feeding bottle or at-will breast-feeding or a
combination of both, with or without poor oral
hygiene. Finally, a Type III (severe) ECC was
described as carious lesions affecting almost all teeth
including the mandibular incisors. A combination of
cariogenic food substances and poor oral hygiene is
the cause of this type of ECC.
A system developed by Johnston and Messer
[1994] classifies ECC into 3 main patterns:
- lesions associated with developmental defects (pit
and fissure defects and hypoplasia);
- smooth surface lesions (labial-lingual lesions,
approximal molar lesions);
- rampant caries.
The latter was defined as having caries in 14 out of
20 primary teeth, including at least one mandibular
incisor.
Another, but not specifically ECC, classification
system is the Caries Analysis System (CAS) of Ismail
and Sohn [1999]. The CAS defines 4 patterns of
caries in the primary teeth, according to the site of
occurrence. This classification system excludes the
buccal and lingual surfaces of the maxillary canines,
the buccal, lingual and mesial surfaces of the
mandibular canines, and all tooth surfaces of the
mandibular incisors. The fissure pattern was 3 to 4
times more likely to develop caries compared with
disease-free children. Children with the maxillary
anterior pattern had 2.4 times greater two-year
increments of pit and fissure caries compared with
caries-free children and they also had 8 times more
caries increments in the buccal/lingual and proximal
areas than caries-free children.

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A. DE GRAUWE, J.K.M. APS, L.C. MARTENS
Age (months) Early Childhood Caries
<12 1 or more dmfs surfaces
12-23 1 or more dmfs surfaces
24-35 1 or more dmfs surfaces
36-47 1 or more dmfs surfaces
48-59 1 or more dmfs surfaces
60-71 1 or more dmfs surfaces
TABLE 2 - Proposed case definitions of Early Childhood Caries (ECC) and Severe Early Childhood Caries (S-ECC) by the
participants at the workshop in Bethesda 1999 [Drury et al., 1999]
A fourth classification system, proposed by Veerkamp
and Weerheijm [1995], claims to account for the stage
of development of the dentition and severity of dental
caries (initial and cavitated). This classification system
assumes that dental caries occurs in successive stages
starting late in the first year (10 months) and ending in
the fourth year of life (48 months). The four stages were
referred to as: initial, damaged, deep lesions and
traumatic. At each stage, a different group of teeth are
involved and dental caries can range from enamel
demineralization (opaque white demineralization) to
cavitation involving enamel and dentine.
Despite all valuable efforts to classify ECC lesions
clinically, there is also a great need for diagnosing and
reporting the condition for research purposes. In this
respect, a workshop was held in April, 1999, in
Bethesda, USA. In a report from this meeting Drury et
al. [1999] (Table 2) defined ECC as “the presence of 1
or more decayed (non-cavitated or cavitated lesions),
missing (due to caries), or filled tooth surfaces” in any
primary tooth in a child 71 months of age 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 >4 (age 3), >5 (age
4), or >6 (age 5) surfaces constitute S-ECC (Table 2).
The participants of the workshop, noted above,
recommended that the term ‘Severe Early Childhood
Caries’ refers to children with ‘atypical’, ‘progressive’,
‘acute’ or ‘rampant’ pattern of dental caries.
64
Severe Early Childhood Caries
1 or more smooth dmf surfaces
1 or more smooth dmf surfaces
1 or more smooth dmf surfaces
1 or more cavitated, filled, or missing (due to caries) smooth
surfaces in primary maxillary anterior teeth or dmfs score >4
1 or more cavitated, filled, or missing (due to caries) smooth
surfaces in primary maxillary anterior teeth or dmfs score >5
1 or more cavitated, filled, or missing (due to caries) smooth
surfaces in primary maxillary anterior teeth or dmfs score >6
Prevalence of ECC
Epidemiological studies on caries prevalence in
children aged between 0 and 36 months were
compiled through a systematic search of published
literature and was carried out in a series of stages:
- a literature search was performed via the Medline
database using a keyword filter including: Early
Childhood Caries, nursing caries, nursing bottle
caries, baby bottle tooth decay, baby bottle
syndrome, baby bottle caries and rampant caries.
- non-English abstracts were not considered.
Existing review articles or papers dealing with
nomenclature, definition or diagnosis were especially
taken into consideration.
From a systematic review of clinical diagnostic
criteria of ECC [Ismail and Sohn, 1999], it became
obvious that the prevalence of ECC varied from 2.1%
in some welfare centers in Sweden to 85.5% in rural
Chinese children. This wide variation was due to the
differences in case definition and diagnostic criteria of
ECC and to the wide range of areas worldwide, both
industrialized as deprived.
The accurate prevalence of ECC in a population is,
however, very difficult to determine, as toddlers and
preschool age children in general are difficult to
examine. Moreover, they are not readily accessible
for examination [Horowitz, 1998]. Significant
cultural and ethnic differences in feeding practices,
the location of dental decay and the number of teeth
involved in the process, also explain the difficulty of
standardizing and optimizing diagnostic and
epidemiological criteria for ECC. According to the
EUROPEAN JOURNAL OF PAEDIATRIC DENTISTRY • 2/2004

Country/City/State Authors
The Netherlands Weerheijm et al., 1998
USA Horowitz, 1998
Puerto Rico Lopez del Valle et al., 1998
Brazil Dini et al., 2000
Rome (Italy) Petti et al., 2000
Zagreb (Croatia) Lulic-Dukic et al., 2001
Brazil Rosenblatt et al., 2002
Sao Paolo (Brazil) Santos and Soviero, 2002
Ghent (Belgium) Martens et al., 2004a
TABLE 3 - An overview of prevalence data on ECC reported in the literature since 1998.
American Association of Pediatric Dentistry
(AAPD), the decay level in 3 to 5 year old children
may be as high as 90% in some populations
[Horowitz, 1998]. It is assured, however, that the
national prevalence of ECC in the USA can be
estimated between 3 and 6% [Horowitz, 1998],
which is consistent with the reported ECC prevalence
in western countries (≤5%) [Johnston and Messer,
1994].
Nevertheless, reported prevalences of ECC seem to
vary from country to country and from area to area. As
the above mentioned review by Ismail and Sohn
[1999] summarized all studies until 1998, Table 3
gives an overview of prevalence data found worldwide
since that time. As there are also national and local
data and as well data from industrialized and
developing countries, it is obvious that all these data
should be interpreted with caution and should not be
used to calculate a mean prevalence of ECC for the
world. The only common finding from these studies, is
that in all cases the most affected teeth were the
maxillary incisors. Non-cavitated carious lesions on
smooth surfaces were more prevalent than cavitated
lesions in primary teeth in children aged 6 to 18
months.
Once over the age of 18 months, cavitated carious
lesions become more apparent [Grindefjord et al.,
1993]. One study reported that the highest prevalence
of ECC is found in the 3 to 4 year old age group and
that boys are significantly more affected compared to
girls, aged between 8 months and 7 years [Ramos-
Gomez et al., 2002].
EUROPEAN JOURNAL OF PAEDIATRIC DENTISTRY • 2/2004
EARLY CHILDHOOD CARIES
Age group Prevalence (%)
28 months 9.3%
1-3 years 3-6%
6-47 months 62.6%
3-4 years 46%
3-5 years 7.6%
2-5 years 30%
12-36 months 28.5%
0-36 months 41.6%
24-36 months 18.3%
Bacterial relationships of ECC
Streptococcus mutans. This organism is known to
colonize the oral cavity as soon as hard dental tissue
is present. These bacteria are vertically transmitted
from mother or caregiver in general to the child.
Their virulence expression is strongly associated
with consumption of carbohydrates, especially
sucrose. The latter explains their abundance in active
carious lesions. It should be stressed that controversy
exists about the fact that individual carious teeth in
the same mouth can harbour a different population of
S. mutans strains, or at least the same genotype in
considerably different proportions. Consequently, S.
mutans is by far the most important microrganism in
the caries process. The role of non-mutans
streptococci is still unclear, despite their extreme
abundance in the oral cavity.
Other bacteria. On the other hand, Lactobacilli
comprise less than 1% of the total cultivable oral
microflora and still their numbers appear to reflect
the carbohydrate consumption of the host. They can
be found in carious dentine, saliva and on mucosal
surfaces. Because Enterococci have only been
recovered in very low numbers from several oral
sites (in immuno and medically compromised
patients), little is known about their role in the caries
process. Several Actinomyces species have been
cultured from the mouth, but from the literature it is
clear that they should be associated with health,
rather than with the initiation of carious lesions.
Veillonella species are lactate dependent and as a
consequence they are abundantly present in
65
A. DE GRAUWE, J.K.M. APS, L.C. MARTENS

Bacterial species References Typical characteristics Additional information

Mutans streptococci Aluluusua et al., 1996 - fermentation of simple carbohydrates - associated with caries activity
S. mutans Marchant et al., 2001 - tolerance to low environmental pH levels in young children
S. sobrinus Tanzer et al., 2001 - vertically transmitted
- only within the presence of hard
oral tissues (teeth, prosthodontics)

Non-mutans Marchant et al., 2001 - uncertain role in the caries process

streptococci - extremely abundant in the oral cavity
S. salivarius

Lactobacilli Marsh and Martin, 1999 - number in saliva reflects simple - dorsum of the tongue
L. fermentum Marchant et al., 2001 carbohydrate consumption by the host - usually cultured from carious dentine
L. casei Tanzer et al., 2001 - comprise less than 1% of the total
cultivable microflora

Enterococci Tanzer et al., 2001 - not frequently found in the human - immuno and medically compromisedt
oral cavity patients have been associated with
their presence in the oral cavity

Actinomyces Marchant et al., 2001 - carbohydrate users - isolated from both carious
A. naeslundii Tanzer et al., 2001 - not associated with initiation of ECC and sound surfaces
A. odontolyticus - more associated with health
A. israelii - the most predominant Actinomyces
species in plaque of ECC
individuals is A. israelii

Veilonella Bradshaw and Marsh, 1998 - lactate users, thus abundant

Marchant et al., 2001 in carious dentine

TABLE 4 - Oral bacterial associations with caries reported in the literature.

established carious lesions. Table 4 summarizes all
microrganisms associated with the caries process.
Aetiology
Dietary factors. Many studies suggest that children
with ECC have a high frequency of sugar intake, not
only from fluids given in a nursing bottle, but also
from sweetened solid foods. This dietary
characteristic is likely to be one of the most
significant caries risk factors in ECC.
Although improper nursing bottle-feeding habits
are the most frequently cited causes of ECC, the
disease may occur in children who are breastfed at
will [Weerheijm et al., 1998], and beyond one year
of age, and in those who are given sweetened
pacifiers or frequent sugar-containing snacks
[Horowitz, 1998]. The cariogenic contents of the
nursing bottle include bovine and human milk,
nursing formulas, sweetened milk, fruit juices,
carbonated and non-carbonated soft drinks. The
frequency and the duration of the habit, along with
the ingestion of cariogenic solids (e.g. biscuits), are
a very important aspect of this condition [Johnston
and Messer, 1994; Peressini, 2003]. Ad libitum
exposure to cariogenic substances during the night
intensifies the risk of caries, as oral clearance and
salivary flow rate are decreased during sleep
[Milnes, 1996; Berkowitz, 2003].
Milk. Milk (human and bovine) and infant milk
formulas present a complex role in the aetiology of
ECC as they contain protective components against
caries such as calcium, phosphorous, casein and
other proteins, which provide a protective organic
coating on enamel. Bovine milk has a higher
concentration of calcium and phosphorous than
human milk, bound in organic and inorganic
molecules and also in free ionic form. In vitro

66 EUROPEAN JOURNAL OF PAEDIATRIC DENTISTRY • 2/2004


studies reported enamel to be 20% less soluble in an
acidic buffer if initially exposed to bovine milk.
Infant milk formulas, bovine and human breast milk
contain relatively high concentrations of lactose,
which is potentially cariogenic [Yiu and Wei, 1992].
Under conditions conductive to ECC, human milk
can be more cariogenic than bovine milk due to its
lactose content, 7 versus 4.8% respectively, while
the concentrations in infant formulas vary
considerably
Soya-based formulas could be considered as a
good substitute for natural milks, but the added
carbohydrates used in these formulas are mostly
sucrose derivates [Horowitz, 1998]. Under normal
dietary conditions, milk is minimally cariogenic and
may even be cariostatic [Ripa, 1988]. However, it is
important to emphasize that adding sucrose to milk
renders milk cariogenic. This does not contradict the
clinical evidence attributing ECC to milk, as affected
children may have aberrant, rather than normal
dietary habits, in association with inadequate oral
hygiene and a minimal fluoride exposure.
Fruit juices and soft drinks. These contain a lot of
sucrose and have a low pH (pH 3-4), which presents
a potentially erosive and cariogenic effect. Loss of
enamel from excessive consumption of fruit drinks in
children has been documented in several studies. The
abusive use of fruit juices and soft drinks in
combination with inappropriate remineralization
activity by saliva eventually result in a predominant
enamel demineralization process [Seow, 1998] and
are a common finding in ECC, since they are usually
given at will to the child and preferentially in a bottle.
Syrup additives (e.g. vitamin preparations). These
may be added by parents to the nursing fluid. Sucrose
sweetened medication, such as paediatric antibiotic
preparations have also been implicated in the
development of ECC [Horowitz, 1998].
Salivary factors. It is known that the salivary flow
rate is at the lowest during the night, due to the
circadian rhythm. With regard to ECC, the continuous
feeding of sugar-containing substances at night time,
when the flow rate is the lowest, increases the caries
risk of the child significantly. If cariogenic liquids are
consumed frequently, teeth may be exposed to
cariogenic conditions for lengthy periods with only
short intervals allowing salivary remineralization of
demineralized enamel [Ripa, 1988].
As the hard dental tissues are immunologically
inactive, specific salivary (host) defense mechanisms
against bacterial colonization and pathogenic activity
of cariogenic organisms are essential. These host
immune mechanisms include specific immune
EUROPEAN JOURNAL OF PAEDIATRIC DENTISTRY • 2/2004
EARLY CHILDHOOD CARIES
factors, derived from saliva (serum immunoglobulin
A, sIgA) or serum and gingival crevicular fluid
(immunoglobulin G, IgG) and non-specific
antimicrobial systems derived mainly from saliva,
and phagocytic cells which transudate through the
gingival crevice [Lehner et al., 1976; Twetman et al.,
1981; Tenovuo et al., 1987].
Oral clearance. In children with ECC, the sleep-
time consumption of sugar is a common
characteristic. The cariogenicity of the substrate
increases significantly, as the length of contact time
between the plaque and substrate increases. The
clearance of glucose is the slowest on the labial
surfaces of the maxillary incisors and the buccal
surfaces of the 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 [Ripa, 1988; Milnes, 1996].
Oral hygiene. Primary infection with streptococcus
mutans by vertical transmission is unavoidable, but
measures should be taken to reduce the bacterial
numbers that are transferred, for example by
avoiding transfer by sharing spoons or cleaning a
pacifier in the mothers mouth. Tooth brushing with
fluoridated toothpaste by the parents or caretakers
should start as soon as the first primary teeth erupt
and this at least two times a day. This
recommendation however is not appropriate for
areas where adequate fluoridation is present (e.g.
Ireland), which implies that the use of fluoridated
toothpastes in children could be prohibited. The use
of a pea size of paste, however, can probably avoid
any risk. A gentle sideways scrub using a multi-
tufted toothbrush and an adapted toothpaste, low in
fluoride concentration (≤500 ppm), are
recommended by the European Academy of
Paediatric Dentistry [Oulis et al., 2000].
Furthermore, brushing more than once a day and
having less than two in-between meals a day is
strongly recommended [Martens et al., 2004b].
Environmental and living condition factors. ECC
is one of the most prevalent diseases of infants and
toddlers from families with a low income and from
families with an immigrant and ethnic minority
background [Hallett, 2000]. Currently, although
ECC is recognized as an infectious disease, its
extent and severity vary with cultural, genetic and
socioeconomic influences. Significant negative
correlations have been shown between the
socioeconomic level of a family and the prevalence
of ECC in that same family, and between poor oral
hygiene and the prevalence of ECC [Santos and
67
A. DE GRAUWE, J.K.M. APS, L.C. MARTENS

Soviero, 2002]. Prevention and parental education

Ethnic minority background, low socioeconomic
environments, single parents, and minimal
educational background are consistent predictors of
dental disease in childhood. However, not all
minority children living under these circumstances
do consistently experience ECC and the opposite has
not been shown to be true either [Quinonez et al.,
2001]. Social class may influence caries risk in
several ways. Individuals from lower socioeconomic
status experience financial, social and material
disadvantages that compromise their ability to care
for themselves, obtain professional health care
services, and live in a healthy environment, all of
which can lead to reduced resistance to oral and
other diseases. Socioeconomic status is generally
measured by indicators of human capital, such as
income, education or occupational prestige that offer
advantages to individuals and families.
Another approach is to assign a social status
position based on ecological measures derived from
place of residence [Reisine and Psoter, 2001]. There
are, however, relatively few case-control or
longitudinal studies that assess the relationship
between the socioeconomic status and the incidence
of caries among young children. Moreover, it should
be considered that an interpretation of
socioeconomic status indicators can vary by cultural
context and that caution should be exercised in
generalizing the findings for other countries.
Therefore, cultural factors must be considered in any
intervention to reduce or prevent ECC.
As a result of improper parenting ECC appears to
be a problem of over-indulgence and lack of parental
restraint rather than of abusive neglect or lack of
education [Ripa, 1988; Eronat et al., 1992].
Information on ECC can be distributed to new
parents from birthing centers, paediatricians’ offices,
maternal clinics and dental offices. Families with
infants who are at high risk of developing ECC
should be especially targeted. Through prevention-
oriented educational programs, prospective parents
and new parents can be alerted about the condition
and the causes of ECC [Ripa, 1988].
The American Academy of Pediatric Dentistry
(AAPD) revised its policy on ECC in 2003. The AAPD
discourages inappropriate feeding practices of infants
and toddlers and encourages appropriate preventive
measures (Table 5). Children should be weaned from
the bottle or breast by 12 months and they should not
be put to bed with a bottle containing liquids other than
water. Weaning methods include progressively diluting
the liquid in the nursing bottle until it is completely
replaced with water or offering a pacifier that has not
been dipped in sweet substances [Johnston and Messer,
1994; Reisine and Psoter, 2001].
Treatment
Usually, ECC is diagnosed when the prevention
and treatment should already have been started. The
treatment of ECC is multifactorial and depends on
the patient’s and parents’ motivation toward a dental

AAPD policy statement on Early Childhood Caries

1. Infants should not be put to sleep with a bottle. Ad libitum nocturnal breast-feeding should be avoided after the first primary tooth
begins to erupt.

2. Parents should be encouraged to have infants drink from a cup as they approach their first birthday. Infants should be weaned from the
bottle at 12 to 14 months of age.

3. Repetitive consumption of any liquid containing fermentable carbohydrates from a bottle or no-spill training cup should be avoided.

4. Oral hygiene measures should be implemented by the time of eruption of the first primary tooth.

5. An oral health consultation visit within 6 months from eruption of the first tooth and no later than 12 months of age is recommended
to educate parents and provide anticipating guidance for prevention of dental disease.

6. An attempt should be made to assess and decrease the mother’s/primary caregiver’s mutans streptococci levels to decrease the
transmisson of cariogenic bacteria and lessen the infant’s or child’s risk of developing ECC.

TABLE 5 - Summary of policy statement of the American Academy of Pediatric Dentistry concerning early childhood caries
[revised 2003].

68 EUROPEAN JOURNAL OF PAEDIATRIC DENTISTRY • 2/2004


care, the extent of the decay and the age and
cooperation of the child, as treatment should be
performed under optimal circumstances. Many
preventive measures, which demand cooperation of
the parents, seem to fail [Yiu and Wei, 1992; Benitez
et al., 1994] but have been successful when
consistently and repeatedly carried out [Kowash et
al., 2000]. The approaches to restorative treatment of
ECC are covered more fully in a paper within this
issue of the journal [Attari and Roberts, 2004].
Conclusion and recommendations
From the above review it becomes clear that ECC is
not only an infectious dental disease, but there are
also socioeconomic factors involved. ECC is still a
serious public health problem, but with a great
variety of definitions and diagnoses used worldwide.
For this reason the authors strongly support the
recommendations formulated at the workshop in
Bethesda, 1999, and support the policy documents by
the AAPD.
Unfortunately, most children with ECC are seen by a
dental practitioner when the disease has already
reached extensive proportions and the children already
complain of toothaches and difficulties during eating.
Therefore it would be advisable to reach these children
in time and to inform the parents about the possible
causes of ECC. Parental guidance is the main corner
stone of a campaign to prevent ECC. Parents should get
the information before the child is born and the first
dental visit of the infant and mother should be before
the primary teeth erupt at about 8 months of age.
Parents should be instructed about the cariogenic
potential of certain foods and drinks and the
cariogenic potential of various ‘family-bound habits’.
These should include cleaning the child’s pacifier in
their own (mother’s) mouth, sharing spoons, no tooth
brushing, prolonged breast feeding, nursing bottles
with sucrose containing drinks during the night etc.
Finally, more efforts should be made to reach the
high risk groups within populations, in order to
reduce the prevalence of ECC and S-ECC and
consequently to ameliorate the quality of life of these
children. Long-term intervention studies are required
for evaluation of these efforts.
References
Attari N, Roberts JF. Prevention and treatment approaches to
EEC. Eur J Paediatr Dent 2004;5:???-???.
Alaluusua S, Matto J, Gronroos L, Innila S, Torkko H, Asikainen
S, Jousimies-Somer H, Saarela M. Oral colonization by more
EUROPEAN JOURNAL OF PAEDIATRIC DENTISTRY • 2/2004
EARLY CHILDHOOD CARIES
than one clonal type of mutans streptococcus in children with
nursing-bottle dental caries. Arch Oral Biol 1996
Feb;41(2):167-73.
American Academy of Pediatric Dentistry, Policy on Early
Childhood Caries (ECC). In: Classifications, Consequencies
and Preventive Strategies. Pediatr Dent vol 25:7; reference
manual 2003/2004. pp. 24-8.
Benitez C, O'Sullivan D, Tinanoff N. Effect of a preventive
approach for the treatment of nursing bottle caries. ASDC J
Dent Child 1994 Jan-Feb;61(1):46-9.
Berkowitz RJ. Causes, treatment and prevention of Early
Childhood Caries: a microbiologic perspective. J Can Dent
Assoc 2003 May;69(5):304-7.
Bradshaw DJ, Marsh PD. Analysis of pH-driven disruption of
oral microbial communities in vitro. Caries Res
1998;32(6):456-62.
Dini EL, Holt RD, Bedi R. Caries and its association with infant
feeding and oral health-related behaviours in 3-4-year-old
Brazilian children. Community Dent Oral Epidemiol 2000
Aug;28(4):241-8.
Drury TF, Horowitz AM, Ismail AI, Maertens MP, Rozier RG,
Selwitz RH. Diagnosing and reporting Early Childhood
Caries for research purposes. J Public Health Dent 1999
Summer;59(3):192-7.
Eronat N, Eden E. A comparative study of some influencing
factors of rampant or nursing caries in preschool children. J
Clin Pediatr Dent 1992 Summer;16(4):275-9.
Grindefjord M, Dahllof G, Ekstrom G, Hojer B, Modeer T.
Caries prevalence in 2.5-year-old children. Caries Res
1993;27(6):505-10.
Hallett KB. Early Childhood Caries: a new name for an old
problem. Ann R Australas Coll Dent Surg 2000 Oct;15:268-75.
Horowitz HS. Research issues in Early Childhood Caries.
Community Dent Oral Epidemiol 1998;26(1 Suppl):67-81.
Ismail AI, Sohn W. A systematic review of clinical diagnostic
criteria of Early Childhood Caries. J Public Health Dent 1999
Summer;59(3):171-91.
Johnston T, Messer LB. Nursing caries: literature review and
report of a case managed under local anaesthesia. Aust Dent J
1994 Dec;39(6):373-81.
Kowash MB, Pinfield A, Smith J, Curzon ME. Effectiveness on oral
health of a long-term health education programme for mothers
with young children. Br Dent J 2000 Feb 26;188(4):201-5.
Lehner T, Challacombe SJ, Wilton JM, Caldwell J. Cellular and
humoral immune responses in vaccination against dental
caries in monkeys. Nature 1976 Nov 4;264(5581):69-72.
Lopez Del Valle L, Velazquez-Quintana Y, Weinstein P, Domoto P,
Leroux B. Early Childhood Caries and risk factors in rural Puerto
Rican children. ASDC J Dent Child 1998 Mar-Apr;65(2):132-5.
Lulic-Dukic O, Juric H, Dukic W, Glavina D. Factors
predisposing to Early Childhood Caries (ECC) in children of
pre-school age in the city of Zagreb, Croatia. Coll Antropol
2001 Jun;25(1):297-302.
69
A. DE GRAUWE, J.K.M. APS, L.C. MARTENS
Marchant S, Brailsford SR, Twomey AC, Roberts GJ, Beighton
D. The predominant microflora of nursing caries lesions.
Caries Res 2001 Nov-Dec;35(6):397-406.
Marsh P, Martin MV. Dental Caries. In: Oral Microbiology (4th
edition). Oxford: Wright; 1999. ch. 6, pp.82-103.
Martens L, Vanobbergen J, Willems S, De Maeseneer J.
Determinants of oral health in inner city children. 2004a
[Unpublished data].
Martens L, Vanobbergen J, Leroy R, Lesaffre E, Declerck D.
Variables associated with oral hygiene levels in 7-year-olds in
Belgium. Community Dent Health 2004b Mar;21(1):4-10.
Milnes AR. Description and epidemiology of nursing caries. J
Public Health Dent 1996 Winter;56(1):38-50.
Oulis CJ, Raadal M, Martens L. Guidelines on the use of
fluoride in children: an EAPD policy document. European
Journal of Paediatric Dentistry 2000;1(1):7-12.
Peressini S. Pacifier use and Early Childhood Caries: an
evidence-based study of the literature. J Can Dent Assoc 2003
Jan;69(1):16-9.
Petti S, Cairella G, Tarsitani G. Rampant early childhood dental
decay: an example from Italy. J Public Health Dent 2000
Summer;60(3):159-66.
Quinonez RB, Keels MA, Vann WF Jr, McIver FT, Heller K,
Whitt JK. Early Childhood Caries: analysis of psychosocial
and biological factors in a high-risk population. Caries Res
2001 Sep-Oct;35(5):376-83.
Ramos-Gomez FJ, Weintraub JA, Gansky SA, Hoover CI,
Featherstone JD. Bacterial, behavioral and environmental
factors associated with Early Childhood Caries. J Clin Pediatr
Dent 2002 Winter;26(2):165-73.
Reisine ST, Psoter W. Socioeconomic status and selected
70
behavioral determinants as risk factors for dental caries. J
Dent Educ 2001 Oct;65(10):1009-16.
Ripa LW. Nursing caries: a comprehensive review. Pediatr Dent
1988 Dec;10(4):268-82.
Rosenblatt A, Zarzar P. The prevalence of early childhood caries
in 12- to 36-month-old children in Recife, Brazil. ASDC J
Dent Child 2002 Sep-Dec;69(3):319-24, 236.
Santos AP, Soviero VM. Caries prevalence and risk factors
among children aged 0 to 36 months. Pesqui Odontol Bras
2002 Jul-Sep;16(3):203-8.
Seow WK. Biological mechanisms of Early Childhood Caries.
Community Dent Oral Epidemiol 1998;26(1 Suppl):8-27.
Tanzer JM, Livingston J, Thompson AM. The microbiology of
primary dental caries in humans. J Dent Educ 2001
Oct;65(10):1028-37.
Tenovuo J, Grahn E, Lehtonen OP, Hyyppa T, Karhuvaara L,
Vilja P. Antimicrobial factors in saliva: ontogeny and relation
to oral health. J Dent Res 1987 Feb;66(2):475-9.
Twetman S, Lindner A, Modeer T. Lysozyme and salivary
immunoglobulin A in caries-free and caries-susceptible pre-
school children. Swed Dent J 1981;5(1):9-14.
Veerkamp JS, Weerheijm KL. Nursing-bottle caries: the
importance of a development perspective. ASDC J Dent Child
1995 Nov-Dec;62(6):381-6.
Weerheijm KL, Uyttendaele-Speybrouck BF, Euwe HC, Groen
HJ. Prolonged demand breast-feeding and nursing caries.
Caries Res 1998;32(1):46-50.
Wyne AH. Early Childhood Caries: nomenclature and case definition.
Community Dent Oral Epidemiol 1999 Oct;27(5):313-5.
Yiu CK, Wei SH. Management of rampant caries in children.
Quintessence Int 1992 Mar;23(3):159-68.
EUROPEAN JOURNAL OF PAEDIATRIC DENTISTRY • 2/2004