304 May 2003, Vol. 69, No.

5 Journal of the Canadian Dental Association

C LINICALP RACTICE

E arly childhood caries (ECC) is a particularly virulent

form of dental caries that is characterized by an overwhelming
infectious challenge and is associated with
unusual dietary practices. ECC initially presents with
smooth-surface carious lesions affecting the primary maxillary
incisors (PMIs). As the disease progresses, decay appears
on the occlusal surfaces of the primary maxillary first molars,
with subsequent spread to other primary teeth, resulting in
the eventual destruction of the primary dentition.
ECC is a public health problem that continues to affect
babies and preschool children worldwide. A comprehensive
review of the epidemiology of ECC showed that its prevalence
varies from population to population; however,
disadvantaged children, regardless of race, ethnicity or
culture, are most vulnerable.1 High-risk North American
populations include many different groups. Almost 30% of
125 Mexican-American children (847 months of age)
living in the Yakima Valley (Washington State) were
reported to have ECC.2 Serwint and others3 reported that
20% of 110 Mexican-American children (1836 months of
age) who were patients of a hospital-based pediatric practice
in Los Angeles had ECC. Results from epidemiology studies
show that Native American children are at high risk for
ECC. The prevalence of ECC among Navajo (n = 1,463)
and Cherokee (n =144) children enrolled in Head Start, a
federally funded program for preschool children living in
poverty, was 72% and 55% respectively.4 Similar observations
were reported by Kelly and Bruerd,5 who observed a
high prevalence of ECC among 515 American Indian
(41.8%) and Alaskan Native (66.8%) children enrolled
in Head Start programs in Oklahoma and Alaska respectively.
Albert and others6 found that the prevalence of ECC
in a population of 260 preschool Inuit children was 65%.
Non-Native American children enrolled in Head Start
programs also display high levels of ECC. In an examination
of 1,230 children (35 years of age) in 37 Head Start

Causes, Treatment and Prevention of Early

Childhood Caries: A Microbiologic
Perspective
Robert J. Berkowitz, DDS
Abstract
Early childhood caries (ECC) is a virulent form of dental caries that can destroy the primary dentition of
toddlers
and preschool children. It occurs worldwide, afflicting predominantly disadvantaged children. High-risk North
American populations include Hispanic and Native American children, as well as children enrolled in Head
Start,
a federally funded program for preschool children living in poverty. The prevalence of EEC among these
children
ranges from 11% to 72%. ECC is an infectious disease, and Streptococcus mutans is the most likely
causative agent;
diet also plays a critical role in the acquisition and clinical expression of this infection. Early acquisition of
S. mutans is a key event in the natural history of the disease. Acquisition may occur via vertical or horizontal
transmission. Primary oral colonization by S. mutans coupled with caries-promoting feeding behaviours results
in
accumulation of these organisms to levels exceeding 30% of the total cultivable plaque flora which in turn
leads to
rapid demineralization of tooth structure. Treatment of ECC is costly because the cooperative capacity of
babies and
preschool children usually necessitates the use of general anesthesia. Treatment usually consists of
restoration or
surgical removal of carious teeth along with recommendations regarding feeding habits. However, this
approach
has resulted in unacceptable clinical outcomes, and relapse rates of approximately 40% have been reported
within
the first year after dental surgery. Primary prevention of ECC has largely been restricted to counselling
parents about
caries-promoting feeding behaviours. This approach has also had minimal success. Newer strategies
addressing the
infectious component through use of topical antimicrobial therapy appear promising.
MeSH Key Words: child, preschool; dental caries/microbiology; streptococcal infections/epidemiology
J Can Dent Assoc 2003; 69(5):3047
This article has been peer reviewed.
Journal of the Canadian Dental Association May 2003, Vol. 69, No. 5 305
Causes, Treatment and Prevention of Early Childhood Caries: A Microbiologic Perspective
programs in Arkansas, Louisiana, New Mexico, Oklahoma
and Texas, the prevalence of ECC was 18.5% for 3-yearolds,
22.4% for 4-year-olds and 27.9% for 5-year-olds.7
The prevalence of ECC in Head Start programs in 2 Ohio
communities (total of 200 children 3.55 years of age)8 and
St. Thomas, U.S. Virgin Islands (375 children 35 years of
age)9 was 11% and 12% respectively. Overall, then, the
prevalence of ECC for these high-risk North American
populations ranged from 11% to 72%.
Because ECC is an infectious disease, this paper reviews
current information regarding the causes, treatment and
prevention of ECC from a microbiologic perspective.
Causes
Microbiological Risk Factors
Microbial Characteristics of ECC: Bacteriologic studies10
12 have demonstrated that in children with ECC,
Streptococcus mutans regularly exceeded 30% of the
cultivable plaque flora. This dense level
of dental infection was associated with
carious lesions, white spot lesions and
sound tooth surfaces near the lesions.
Conversely, S. mutans typically constitutes
less than 0.1% of the plaque flora
in children with negligible to no caries
activity.13 These observations, together
with other published results,1416 clearly
illustrate the concept that ECC is an
infectious disease and that S. mutans is
the most likely infectious agent; clearly
diet also plays a critical role in the clinical expression of this
infection.
Early Acquisition of S. mutans: The mouth of a normal
predentate infant contains only mucosal surfaces exposed
to salivary fluid flow. S. mutans could persist in such an
environment by forming adherent colonies on mucosal
surfaces or by living free in the saliva and duplicating at a
rate exceeding the washout rate of salivary flow. Because the
oral flora averages only 2 to 4 divisions per day17 and swallowing
occurs every few minutes, it is reasonable to assume
that bacteria cannot maintain themselves in saliva by proliferation,
but instead must become attached to an oral
surface. Previous studies (reviewed by Gibbons and Van
Houte18) demonstrated that S. mutans has a feeble capacity
to become attached to epithelial surfaces. Therefore, it
seemed unlikely that these organisms could colonize the
mouth of a normal infant before the eruption of teeth.
Earlier clinical studies1924 reported that S. mutans could
not be detected in the mouths of normal predentate
infants; instead, the organisms were found only after the
insertion of acrylic cleft palate obturators or eruption of
primary teeth. Accordingly, the concept that S. mutans
required a nonshedding oral surface for persistent oral colonization
became a basic tenet of oral microbial ecology.
However, more recent clinical studies2527 have demonstrated
that S. mutans can colonize the mouths of predentate
infants; the furrows of the tongue appear to be an
important ecological niche. Tanner and others,28 using
DNA probe technology, reported that S. mutans was
present in 55% of plaque samples and 70% of tongue
scraping samples of 57 children 618 months of age living
in Saipan, Commonwealth of the Northern Mariana
Islands, western Pacific. These recent studies on acquisition
of S. mutans raise doubt that a nonshedding oral surface is
required for colonization.
Early Acquisition of S. mutans and Dental Caries: Early
colonization by S. mutans is a major risk factor for ECC as
well as future dental caries. Alaluusua and Renkonen29
performed longitudinal assessment for S. mutans colonization
and dental caries in children 24 years of age; children
who harboured S. mutans in their plaque at the age of 2 had
the most caries activity by the age of 4.
The mean DMFS score in these children
was 10.6, whereas in children in
whom colonization occurred later, the
mean DMFS score was 3.4 at age 4
(p < 0.005). Similar observations were
made by Kohler and others,30 who
reported that 89% of children with
S. mutans colonization by 2 years of age
had carious lesions by 4 years of age
and a mean DMFS score at that time of
5.0; in contrast, only 25% of children
not infected with S. mutans before 2 years of age had experienced
dental caries by 4 years of age, and they had a mean
DMFS score of 0.3. In another longitudinal evaluation,
Gindefjord and others31 evaluated 786 children at 1 year of
age for caries risk factors (S. mutans infection, exposure to
fluoride, dietary habits, oral hygiene) and re-examined
them at 3.5 years of age for the presence of dental caries.
The presence of S. mutans at 1 year of age was the most
effective predictor of caries at 3.5 years of age. These observations,
together with other published results,32,33 illustrate
that early infection with S. mutans is a significant risk factor
for future development of dental caries.
Transmission of S. mutans: The major reservoir from
which infants acquire S. mutans is their mothers. The
evidence for this concept comes from several clinical
studies in which S. mutans strains isolated from mothers
and their babies exhibited similar or identical bacteriocin
profiles3436 and identical plasmid or chromosomal DNA
patterns.3741 Successful colonization of infants by
maternally transmitted S. mutans cells may be related to
several factors, including magnitude of the inoculum,42
frequency of small-dose inoculations13 and minimum
infective dose.43 Berkowitz and others42 reported that the
Early colonization
by Streptococcus mutans
is a major risk factor
for ECC and
future dental caries.
306 May 2003, Vol. 69, No. 5 Journal of the Canadian Dental Association
Berkowitz
frequency of infant infection was approximately 9 times
greater when maternal salivary levels of the organism
exceeded 105 colony-forming units (CFU)/mL than when
maternal salivary reservoirs were less than or equal to
103 CFU/mL (58% vs. 6%). Suppression of maternal
reservoirs of S. mutans prevented or delayed infant infection,
44 and only 3 (11%) of 28 babies whose mothers
underwent suppression of the S. mutans reservoir (by dental
treatment and topical antimicrobial therapy) were infected
by 23 months of age; in contrast, 17 (45%) of 38 babies
in the control group (whose mothers did not undergo
S. mutans suppression) were infected. In both groups the
percentage of infected babies increased with age; nevertheless,
at 4 years of age fewer babies in the test group were
infected.
Two recent reports indicate that vertical transmission is
not the only vector by which S. mutans is perpetuated in
human populations. Mattos-Graner and others45 isolated
S. mutans from groups of nursery school children (1230
months of age) and genotyped the isolates with primed
polymerase chain reaction and restriction fragment-length
polymorphism analysis. They reported that many children
had identical genotypes of S. mutans, which indicated that
horizontal transmission may be another vector for acquisition
of these organisms. In addition, van Loveren and
others,46 using bacteriocin typing, demonstrated that when
a child acquires S. mutans after the age of 5 years, there may
be similarity in S. mutans strains in mother, father and
child, which indicates that horizontal transmission can also
occur among family members. These findings are of importance
given the socio-economic changes in Western culture
over the past 2 decades (for example, the use of daycare
facilities for babies and preschool children when both
parents are employed).
Dietary Risk Factors
Although ECC is an infectious disease, the role of diet in
acquisition of the infection47 and development of the
disease48 is critical. Children with ECC have frequent and
prolonged consumption of sugars from liquids.2,4952
Caries-promoting sugars such as sucrose, glucose and
fructose, contained in fruit juices and many infant formula
preparations,5355 are readily metabolized by S. mutans and
lactobacilli to organic acids that demineralize enamel and
dentin. The use of nursing bottles and sippy cups
enhances the frequency of exposure. This type of feeding
behaviour during sleep intensifies the risk of caries, as oral
clearance and salivary flow rate are decreased during sleep.
In addition, caries-promoting feeding behaviours result
in an increase in the magnitude of dental reservoirs of
S. mutans.48
Clinical Significance
The preceding narrative strongly suggests that the first
event in the natural history of the infectious disease ECC is
primary infection by S. mutans. The second event is accumulation
of S. mutans to pathogenic levels, secondary to
frequent and prolonged dietary exposure to cariespromoting
sugars. The third event is rapid demineralization
of enamel, which results in cavitation of tooth structure.
Treatment
The current standard of care for treatment of ECC
usually necessitates general anesthesia, with all of its potential
complications, because the level of cooperative behaviour
of babies and preschool children is less than ideal. In a
1993 study, Milnes and others56 found that the costs associated
with the treatment of ECC for a Canadian aboriginal
population (for travel, lodging, medical care and facilities,
and general anesthesia) were a significant drain on
government resources. A 1994 report indicated that the cost
of treating a child with ECC exceeded US$2,000.57 More
recent data have shown that costs have escalated. For example,
the average cost for facilities and general anesthesia,
excluding dental services, at Strong Memorial Hospital,
University of Rochester Medical Center, is US$3,500.
Thus, this disease places a huge burden on third-party
payers (insurance companies and government medical
welfare agencies), as well as on parents least likely to be able
to afford it.
Treatment of ECC is usually restricted to surgical
removal or restoration of carious teeth coupled with recommendations
regarding feeding habits. Restorative dentistry
has little to no long-term impact on oral S. mutans populations58
and, as discussed below in the Prevention section,
recommendations regarding feeding behaviours have had
minimal impact. Not surprisingly, the clinical outcomes for
treatment of ECC are poor. Sheehy and others,59 using a
telephone survey, found that 23% of children treated for
ECC under general anesthesia required restorations or
extractions after the initial dental surgery. In another
study,60 52% of the cohort treated under general anesthesia
presented with new smooth-surface enamel lesions within
46 months after dental surgery. Eidelman and others,61
using a retrospective chart review, reported that 57% of
the study cohort who had been treated under general anesthesia
required treatment for new carious lesions within
624 months after the initial dental surgery. In another
retrospective study62 of 42 children with ECC treated
under general anesthesia at the Franciscan Childrens
Hospital and Rehabilitation Center in Boston, 45% had
experienced relapse by the end of 12 months after dental
surgery. Given the morbidity and cost associated with treatment
of relapse (e.g., general anesthesia, sedation, physical
restraint), the current standard of care for ECC, involving
Journal of the Canadian Dental Association May 2003, Vol. 69, No. 5 307
Causes, Treatment and Prevention of Early Childhood Caries: A Microbiologic Perspective
treatment under general anesthesia, results in unacceptable
clinical outcomes. New treatment strategies (e.g.,
chemotherapeutic, behavioural) must be developed to
address the causative factors associated with relapse if
improvements in clinical outcomes are to be realized.
Prevention
Prevention of cariogenic feeding behaviours is one
approach to preventing ECC. Regrettably, educating
parents about this risk factor has had minimal success.
Johnsen63 reported that 78% of parents of children with
ECC had attempted to substitute water for a cariogenic
liquid (e.g., apple juice, formula) in the bedtime nursing
bottle; this observation strongly suggests that these parents
were aware of the feeding practices associated with ECC. In
a survey of parents of 169 Inuit children with ECC, 54%
of the parents knew that naptime and bedtime bottle feedings
may be associated with ECC.6 Likewise, 25 of 38
Mexican-American parents whose children had ECC were
aware of the feeding behaviours associated with ECC.2
However, given the high prevalence of ECC in certain
groups, it appears that information and knowledge do not
always translate into appropriate parenting practices. Thus,
the parents of children with ECC are frequently aware of
the dietary practices associated with the development of the
disease, but they may not implement changes in feeding
behaviours.
A promising approach toward primary prevention of
ECC is to develop strategies that target the infectious
component of this disease, for example by preventing
or delaying primary acquisition of S. mutans at an early
age through suppression of maternal reservoirs of the
organism.44
Another approach is to prevent S. mutans from accumulating
to pathologic levels through topical application of
antimicrobial agents. This approach was recently applied in
a group of Puerto Rican babies at high risk for ECC.64 The
study population consisted of 83 subjects who were 12 to
19 months of age at the time of their entry into the study.
Inclusion criteria for the study included unremarkable
medical history, presence of 4 PMIs with no visible defects,
caries-free status (accordingly to clinical criteria), use of a
nursing bottle containing a cariogenic substance at naptime
or bedtime, and 2 consecutive S. mutans-positive cultures
from pooled PMI plaque. The subjects were randomly
assigned to 2 groups. In the experimental group (n = 39),
a 10% povidoneiodine solution was applied to the dentition
bimonthly for 1 year; in the control group (n = 44)
a placebo solution was applied in the same manner.
Treatment failure was defined as the appearance of one or
more white spot lesions on any of the PMIs during the
study period. Using the KaplanMeier procedure, the
authors estimated that 91% 5% of experimental subjects
and 54% 9% of control subjects experienced 12 months
of disease-free survival (log-rank test, 2-sided p = 0.001).
Therefore, bimonthly topical application of a 10%
povidoneiodine solution to the dentition of babies at high
risk for ECC increased disease-free survival. It is important
to determine, through larger and more in-depth clinical
trials, if this effect remains after the antimicrobial agent is
withdrawn before introducing 10% povidoneiodine therapy
into clinical practice as a primary prevention modality
for ECC. C
Acknowledgment: This paper is based on a presentation given at the
October 2001 CAPD annual meeting. The manuscript was supported
in part by NIDCR grant DE12595.
Dr. Berkowitz is professor and chief, division of pediatric dentistry,
Eastman department of dentistry, School of Medicine and Dentistry,
University of Rochester, Rochester, NY.
Correspondence to: Dr. Robert J. Berkowitz, Eastman Dental
Center, University of Rochester, 625 Elmwood Ave., Rochester, NY
14620. E-mail: [email protected].
The author has no declared financial interests.
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