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Correspondence and Reprint requests : Dr.

Hamid Reza
Poureslami, Associate Prof., Department of Pediatric Dentistry,
Member of Kerman Oral and Dental Disease Research Centre,
Dental School, Shafa Ave. Kerman, Iran. Tel : 00983412118074,
Fax : 00983412118073
[DOI10.1007/s1209800802161]
[Received June 30, 2007; Accepted November 5, 2007]
Special Article
Early Childhood Caries (ECC) An Infectious
Transmissible Oral Disease
Hamid Reza Poureslami and Willem Evert Van Amerongen
1
Department of Pediatric Dentistry, Faculty of Dentistry, University of Medical Sciences Kerman,
1
Department of Pediatric Dentistry, Academic Centre for Dentistry Amsterdam, Netherlands
ABSTRACT
Dental caries in babies and toddlers is called Early Childhood Caries (ECC). It is an infectious and transmissible die-to-
bacterial disease. Detailed knowledge regarding the acquisition and transmission of infectious agents facilitates a more
comprehensive approach toward prevention. Mutans streptococci are important organisms in the initiation and progression
of dental caries. Recent evidence demonstrates that these bacteria are found in the mouths of pre-dentate infants and are
acquired via vertical and/or horizontal transmission from human reservoirs. This information should facilitate the focusing of
clinical interventions that prevent or delay infant infection, thereby reducing the prevalence of dental caries (ECC) in babies
and toddlers. [Indian J Pediatr 2009; 76(2) : 191-194] E-mail: hamid42pour@yahoo.com
Key words : Early Childhood Caries; Mutans Streptococci; Dental caries; Fluoride; Chlorhexidine
Early Childhood Caries is defined as the presence of 1 or
more decayed (noncavitated or cavitated lesions), missing
(due to caries), or filled tooth surfaces in any primary
tooth in a 71- month or younger child. In children
younger than 3 years of age, any sign of tooth smooth
surface caries is indicative of severe early childhood caries
(S-ECC).
1
Background
Dental caries is a multi-factorial disease. These factors are
the presence of cariogenic microorganisms, fermentable
carbohydrates in the diet, susceptible tooth and host, and
time. Dental caries in young children (ECC) can be
characterized as a carbohydrate induced infectious
bacterial disease which can cause severe damage to a
childs primary dentition. (Fig. 1).
The clinical appearance of the teeth in ECC is typical
and follows a specific pattern. There is usually early and
progressive carious involvement of the primary upper
incisors in first years of age followed by the involvement
of the upper and lower first primary molars, and the
upper canines and sometimes lower canines (according to
the sequence of eruption). The lower incisors are usually
unaffected because of salivary flow from sub-lingual
glands, and the contact of tongue and lips at the time of
feeding that covers the lower incisors. Therefore, milk and
carbohydrates spread over all teeth except the lower
incisors and prevent pudding or gathering of milk around
these teeth.
2, 3
(Fig. 2)
Fig. 1. Brief overview of the caries process
2
Indian Journal of Pediatrics, Volume 76February, 2009 191
H.R. Poureslami and W.E. Van Amerongen
192 Indian Journal of Pediatrics, Volume 76February, 2009
ECC is a serious public health problem. The American
Academy of Pediatric Dentistry (AAPD) has recognized
the unique and virulent nature of ECC. It begins soon
after dental eruption, develops on smooth surfaces and
progresses rapidly. ECC not only affects teeth, but also
may lead to more widespread health issues such as:
chewing difficulty, malnutrition, gastrointestinal
disorders, delayed or insufficient growth (especially in
regard to the height and/or weight gain), poor speech
articulation, low self-esteem and social ostracism.
4
ECC manifestations may include pain, acute and
chronic abscesses, fever, swelling of the lip and/ or cheek,
no appetite and lethargy. The consequences include a
higher risk of new carious lesions, increasing dental
treatment cost and time, emergency visits, increasing days
with restricted activity, later caries in the permanent
dentition and malocclusion.
5
The objective is to review of
the current studies for etiology, prevention and treatment
of early childhood caries.
Prevalence
ECC continues to be a global public health problem.
Despite water fluoridation, it has been a significant
problem in many developing countries and some
minority communities in western industrialized nations.
EEC has been found in general population but is more
prevalent in low socioeconomic groups.
2
Some studies
have shown a prevalence rate as high as 80% for EEC in
different countries.
6
In the United States of America ECC
is the single most common chronic childhood disease. It is
5 times more common than asthma, 7 times more
common than hay fever, and 14 times more common than
chronic bronchitis.
5
According to statistics from 1988 to
1994, ECC has affected 18% of the children aged 2 to 4
years, and its prevalence in high-risk North American
populations has ranged from 11% to 72%.
5,11
The
prevalence of ECC is 19.5% to 44% in Iranian children
7
and 9.3% in Dutch child population.
8
Causes
Knowledge about the natural history of EEC like any
other infectious disease (e.g. HIV) facilitates a more
comprehensive approach toward its prevention and can
utilize this concept to inhibit and/or reduce dental caries
in very young children.
9
ECC is an infectious disease, and Mutans streptococci
(MS) including the species streptococcus mutans and
streptococcus sobrinus are the most likely causative
agents. Lactobacilli also participates in the development
of caries lesions and has an important role in lesion
progression not its initiation.
10
Diet also plays a crucial
role in the acquisition and clinical expression of this
infection. Early acquisition of MS is a key event in the
natural history of the disease.
11
Acquisition may occur via
vertical or horizontal transmission.
Vertical transmission is the transmission of microbes
from caregiver to child. The major reservoir from whom
the infant acquires MS is mother. Successful infant
Fig. 2. Child's Teeth with ECC.
Fig. 3. Strategies for the Prevention of ECC
24
Community Professional Home care
Education Early detection Dietary habits
Water fluoridation diet counseling fluoride dentifrices
Community and fluoride, chlorhexidine tooth-brushing
Personal development
Control of transmission
of cariogenic bacteria
Early Childhood Caries (EEC) An Infectious Transmissible Oral Disease
Indian Journal of Pediatrics, Volume 76February, 2009 193
colonization of maternally transmitted MS cells may be
related to several factors which, in part, include
magnitude of the innoculum, frequency of small dose
inoculations, and a minimum infective dose. Mothers
with dense salivary reservoirs of MS are at high risk for
infecting their infants very early in life.
9
According to a recent study, neonatal factors may also
increase the risk for early acquisition of MS via vertical
transmission. Infants delivered by cesarean section
acquire MS earlier than the vaginally delivered infants.
The investigators hypothesized that vaginal delivery may
expose newborns to early protection against S. mutans
colonization. That is, by being exposed to numerous
bacteria earlier and with great intensity, the pattern of
microbial acquisition is affected. Cesarean infants are
delivered in a more aseptic manner, resulting in an
atypical microbial environment that may increase
susceptibility to subsequent early S. mutans colonization.
12
Horizontal transmission is the transmission of
microbes between members of a group. More recent
reports indicate that vertical transmission is not the only
vector by which MS are perpetuated in human
populations and horizontal transmission also occurs. This
is important given the socioeconomic changes in
communities over the past 2 to 3 decades. For example,
the introduction of day-care centers (nurseries) may
provide another vector for acquisition of these organisms.
9
In the earliest period of childhood, when the child is
physically dependent on mother, the quantity of maternal
(or nannys) MS is one of the most important factors
influencing initial colonization in the childs mouth.
13
MS
can colonize the mouth of pre dentate infants via vertical
(mother, nanny) and/ or horizontal( brothers, sisters or
other babies at the nursery) transmission.
9
Poor maternal
oral hygiene and higher daily frequencies of snacking and
sugar exposures increase the likelihood of transmission of
infection from mother to babies.
14
Time span between MS colonization and caries lesion
development is approximately 13 to 16 months. In more
high-risk babies (pre-term and/or low weight infants,
with hypo-mineralized teeth) this duration is likely to be
much shorter.
13
There is also considerable presumptive
evidence that malnutrition/ under-nutrition during the
prenatal and perinatal periods causes hypoplasia. A
consistent association exists between enamel
hypomaturation/ hypoplasia and ECC.
14, 15
In S-ECC caries may become clinically evident as early
as 12 to 16 months of age, usually appearing first on the
labial-gingival and lingual surfaces of the upper incisors.
16
To summarize the first event in the natural history of
the infectious disease ECC is primary infection by MS The
second event is accumulation of MS to pathogenic level,
resulted from frequent and prolonged dietary exposure
of caries promoting sugars. The third event is rapid
demineralization of enamel resulting in cavitations of
tooth structure. In other words, primary oral colonization
by MS is coupled with caries promoting feeding
behaviors.
11
TREATMENT AND PREVENTION
Treatment of ECC is often problematic and costly because
the cooperative capacity of babies is low. Treatment
usually consists of restoration or surgical removal of
carious teeth. However, this approach does little to bring
the disease under control and relapse rates of
approximately 40% have been reported within the first
year after dental surgery, because recurrence of caries
around restored teeth and occurrence of new decays are
common.
11, 17
Prevention of cariogenic feeding behavior is one of the
approaches for preventing ECC. Children with ECC
usually have nocturnal feeding on demand, breast feeding
or bottle feeding, and sweet liquids consumption
frequently. These types of feeding behaviors increase the
risk of dental caries, so must be reduced or stopped.
11
Also the knowledge that the most important risk factor
related to caries in babies is acquisition of MS helps for
determination of an optimal preventive approach and
interceptive treatment. Earlier studies demonstrated that
infants acquire MS only after the eruption of primary
teeth. Caufield et al suggested that the acquisition of MS
most likely takes place during a window of infectivity
from 19 to 31 months of age.
18,19
But more recent studies
indicate that MS can also colonize the mouths of
predentate infants.
9,11-13,16,20,21
Therefore, a promising
approach towards primary prevention of ECC is the
development of strategies that target the infectious
component of this disease, such as preventing or delaying
primary acquisition of MS at an early age through
suppression of maternal reservoirs of the organism.
11
For this, it is better that primary prevention of ECC
begins in the prenatal and perinatal periods (include
pregnancy and first month of birth) and addresses the
health of both mother and infant. Mothers or nannys
teeth must be examined. Infants whose mothers have
high levels of MS due to untreated dental decays are at
greater risk of acquiring the organisms. Mothers dental
rehabilitation can delay infant inoculation.
22, 23
There are 3 general approaches that have been used to
prevent ECC (Fig. 3). All 3 approaches include training of
mothers or caregivers to follow healthy dietary and
feeding habits in order to prevent the development of
ECC. Early screening for signs of caries development,
starting from about 7 to 8 month of age, could identify
infants who are at risk of developing ECC and assist in
providing information for parents about promoting oral
H.R. Poureslami and W.E. Van Amerongen
194 Indian Journal of Pediatrics, Volume 76February, 2009
health and preventing the development of tooth decay.
High risk infants include those with early signs of ECC,
poor oral hygiene (of both infant and mother), limited
exposure to fluorides, and frequent exposure to sweet
liquids. These babies should be targeted with a
professional preventive program that includes oral
hygiene instructions for mother and baby, using fluoride
and antibacterial topical agents, and diet counseling.
24
Pediatricians can give the following recommendations for
prevention of ECC to mothers and nannies.
4,24
Elimination of active dental caries lesions, gingival
disease and using agents such as fluoride and
chlorhexidine (tooth-paste, mouth-wash, gel, varnish).
Twice daily tooth-brushing of the dentate infant (from
about 7
th
month of age).
Oral health evaluation of the infant by a pediatric
dentist before the first birthday.
Infants should not be put to sleep with a bottle and
nocturnal breastfeeding should be avoided after the
first primary tooth begins to erupt.
Mothers 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.
An attempt should be made to assess and decrease the
mothers/ primary caregivers MS level to decrease the
transmission of cariogenic bacteria and lessen the
infants or childs risk of developing ECC.
Alter saliva-sharing activities, such as tasting food
before feeding and sharing tooth brushes.
REFERENCES
1. American Academy of pediatric Dentistry, Originating
Council: Definition of Early Childhood Caries (ECC): Pediatr
Dent 2003; 25: 9.
2. Seow WK. Biological mechanisms of early childhood caries.
Community Dent Oral Epidemiol 1998; 26: 8-27.
3. Tinanoff N. Introduction to the early childhood caries
conference: initial description and current understanding.
Community Dent Oral Epidemiol 1998; 26: 5-7.
4. American Academy of pediatric Dentistry, Originating Group
and Review Council: Policy on ECC: Classification,
Consequences, and Preventive Strategies. Pediatr Dent 2003;
25: 24-28.
5. Filstrup SL, Briskie D, Fonseca M, Lawrence L, Wandera A,
Inglehart MR. ECC and quality of life: child and parent
perspectives. Pediatr Dent 2003; 25: 431-440.
6. Habibian M, Beighton D, Stevenson R, Lawson M, Roberts G.
Relationships between dietary behaviours, oral hygiene and
mutans streptococci in dental plaque of a group of infants in
southern England. Archives of Oral Biology 2002; 47: 491-498.
7. Poureslami HR. Study of Early Childhood Caries in children
of the Kerman (Iran). Europ Archives Pediatr Dent 2006; 2:
Abstract no.PD6-13.
8. Weerheijm KL, Uyttendaele-Speybrouck BF, Euwe HC, Groen
HJ. Prolonged demand breast-feeding and nursing caries.
Caries Res 1998; 32 : 46-50.
9. Berkowitz RJ. Mutans Streptococci: Acquisition and
transmission. Pediatr Dent 2006; 28 : 106-109.
10. Van Houte J. Role of microorganisms in caries etiology. J Dent
Res 1994; 73 : 672-681.
11. Berkowitz RJ. Causes, treatment and prevention of ECC: A
microbiologic perspective. J Can Dent Assoc 2003; 69: 304-307.
12. Li Y, Caufield PW, Dasanayake AP, Wiener HW, Vermund
SH. Mode of delivery and other maternal factors influence the
acquisition of streptococcus mutans in infants. J Dent Res 2005;
84: 806-811.
13. Law V, Seow WK. A longitudinal controlled study of factors
associated with mutans streptococci infection and caries
lesion initiation in children 21 to 72 months old. Pediatr Dent
2006; 28 : 58-65.
14. Wan AL, Seow WK, Purdie DM, Bird PS, Walsh LJ, Tudehope
DI. A longitudinal study of streptococcus mutans colonization
in infants after tooth eruption. J Dent Res 2003; 82: 504-508.
15. Milgrom P, Riedy CA, Weinstein P, Tanner AC, Manibusan L,
Bruss J. Dental caries and its relationship to bacterial infection,
hypo-plasia, diet and oral hygiene in 6 to 36-month-old
children. Community Dent Oral Epidemiol 2000; 28: 295-306.
16. Ramos-Gomez FJ, Weintraup JA, Gansky SA, Hoover CI,
Featherstone JD. Bacterial, behavioral and environmental
factors associated with ECC. J Clin Pediatr Dent 2002; 26: 165-
173.
17. Graves CE, Berkowitz RJ, Proskin HM, Chase I, Weinstein P,
Billings R. Clinical outcomes for ECC: influence of aggressive
dental surgery. J Dent Child 2004; 71: 114-117.
18. Ji Y, Rodis OM, Hori M, Nakai Y, Kariya N, Matsumura S,
Shimono T. Risk behaviors and their association with
presence of S. mutans or S. sobrinus and caries activity in 18-
month-old Japanese children. Pediatr Dental J 2005; 15: 195-
202.
19. Rodis OM, Okazaki Y, Kariya N, Ji Y, Kanao A, Hayashi M et
al. Presence of S. mutans or S. sobrinus in cariostatinoculated
plaque samples from Japanese mother-child pairs. Pediatr
Dental J 2005; 15 : 98-102.
20. Wan AL, Seow WK, Walsh LJ, Bird P, Tudehope DI, Purdie
DM. Association of S. mutans infection and oral
developmental nodules in pre-dentate infants. J Dent Res 2001;
80: 1945-1948.
21. Wan AL, Seow WK, Walsh LJ, Bird P, Tudehope DI, Purdie
DM. Oral colonization of S. mutans in six-month-old pre-
dentate infants. J Dent Res 2001; 80: 2060-2065.
22. Milgrom P. Response to Reisine and Douglass: psychosocial
and behavioral issues in early childhood caries. Community
Dent Oral Epidemiol 1998; 26: 45-48.
23. Schroth RJ, Moffatt ME. Determinations of ECC in a rural
Manitoba community: A pilot study. Pediatr Dent 2005; 27:
114-120.
24. Ismail AI. Prevention of Early Childhood Caries. Community
Dent Oral Epidemiol 1998; 26: 49-61.

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