Early Childhood Caries
Short Description
Early Childhood Caries...
Description
Early Childhood Caries You can’t educate a child who isn’t healthy and you can’t keep a child healthy who isn’t educated. -- M. Joycelyn Elders,
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Rampant caries in infants and young children has long been recognized as a clinical syndrome. Jacobi – an American pediatrician is first credited with describing nursing caries in 1862
Beltrami in 1930 recognized this pattern of early caries as “les dents noire de tout-petit” - “black teeth of the very young”
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Dr. ELIAS FASS, 1962
Described caries pattern as “nursing bottle mouth” “Nothing is so shocking to a dentist as the examination of a child patient suffering from rampant caries” “All the primary upper anterior teeth , upper and lower primary first molars and the lower primary canine teeth, except the lower four anterior teeth are either unaffected or are very slightly carious.”
“all the children were put to bed, either for the night or for a nap, with a nursing bottle of milk from which they drank while lying down to help them all asleep.”
“the lower incisors were not affected.” he concludes as – “a great effort on part of the physicians to direct the parent to earlier routine dental examinations of the very young child would be rewarded by prevention ……… of such conditions as nursing bottle mouth. Later the term nursing bottle caries was succeeded by “nursing caries”
in 1985 the term “baby bottle tooth decay" was proposed by Healthy Mothers-Healthy Babies Coalition as an alternative which would be more appropriate for patient acceptance and would focus attention on potential damage of using a nursing bottle. IN 1994, CONFERENCE AT THE CENTRES FOR DISEASE CONTROL AND PREVENTION RECOMMENDED THE LESS SPECIFIC TERM “EARLY CHILDHOOD CARIES”
TERMINOLOGIES – J PUBLIC HEALTH DENT. 1999
LABIAL CARIES (L.C.) CARIES OF THE INCISORS RAMPANT CARIES (R.C.) NURSING BOTTLE CARIES (N.B.C.) NURSING CARIES (N.C.) BABY BOTLE TOOTH DECAY (BBTD) MAXILLARY ANTERIOR CARIES (M.A.C.) EARLY CHILDHOOD CARIES (ECC) EARLY CHILDHOOD DENTAL DECAY RAMPANT DENTAL CARIES SEVERE EARLY CHILDHOOD CARIES (S-EEC)
S-EEC NURSING CARIES BABY BOTTLE TOOTH DECAY RAMPANT CARIES
a major problem that may have hinderd efforts to combat this condition is lack of case definitions and diagnostic criteria for ecc & s-ecc
CLASIFICATION SYSTEMS FOR ECC -DEVELOPED BY JHONSEN & COLLEAGUES
1. LESIONS ASOCIATED WITH DEVELOPMENTAL DEFECTS: A. pit & fissure defects-one or more lesions in pits & fissures of primary molars. B. hypoplasia – altered enamel contour with detectable rough surface and darkened enamel or dentin, including caries adjacent to an area of hypoplasia and caries on medial aspect of facial surface of primary canine.
2.smooth surface lesions: a. facial-lingual lesions (only cavitated lesions, white spot lesions were excluded) – one or more lesions on a facial or lingual surface of any tooth or an aproximal surface of an incisor tooth.
b. aproximal molar lesions – one or more lesions on an aproximal surface of a primary molar or distal surface of a primary canine. c. facial-lingual plus aproximal lesions.
3.rampant caries: 14 out of 20 primary teeth having carious lesions including atleast one mandibular incisor. the tooth surfaces with the highest prevalence of caries were the smooth surfaces of primary molars and incisors. patient with the facial –lingual pattern were at the highest risk of developing caries in mixed dentition compared with patients with other pattern.
CARIES ANALYSIS SYSTEM (CAS) Douglass et al FOUR PATTERNS OF CARIES IN PRIMARY TEETH:
-FISSURE PATTERN
-MAXILLARY ANTERIOR PATTERN
-POSTERIOR PROXIMAL PATTERN
-POSTERIOR BUCCO-LINGUAL SMOOTH Pattern
Children with maxillary anterior pattern had 2.4 times higher two –year increments of pits & fissure caries compared with caries free children. they also had 8 times higher caries increments in the buccal/lingual and proximal areas than caries free children.
Children with the fissure pattern were also 3-4 times more likely to develop caries compared with disease free children. In high disease populations- smooth surfaces of maxillary incisors are involved first followed by pit & fissure surfaces.
Veerkamp and Weerheijm classification
It claims to account for the stage of development of the dentition and severity of dental caries (initial and cavitated). Dental caries occurs in successive stages starting late in the first year (10 months) and ending in the fourth year of life (48 months) Four stages: Initial, damaged, deep lesions and traumatic At each stage a different group of teeth are involved and dental caries can range from enamel demineralization to cavitation involving enamel and dentin. This system has not been validated.
Suggestions for Classification
Most classifications are based on the presence of decayed or filled maxillary incisors. The diagnostic criteria have relied mostly on the presence of cavitation or stickiness.
…………….The classification of ECC should be expanded to include age and other predictors of dental caries.
The nomenclature – ECC is not descriptive in terms of risk factors, characteristic of the condition and prevention. CDOE – 1999;27 :318
Type –I (mild to moderate ECC) :
a carious lesion or two involving incisors or molars.
The existence of isolated carious lesion(s) involving molars and/or incisors Cause – a combination of cariogenic semi-solid or solid food and lack of oral hygiene. The number of affected teeth usually increases as the cariogenic challenge persists
Type – II (moderate to severe ECC)
Labio-lingual carious lesions affecting maxillary incisors, with or without molars depending on the age of the child and stage of the disease and unaffected mandibular incisors. Cause – inappropriate use of feeding bottle or at will breast feeding or a combination of both, with or without poor oral hygiene.
Poor oral hygiene most probably compounds the cariogenic challenge. This type of ECC could be found soon after the first teeth erupts. Unless controlled it may proceed to become type III ECC.
Type III : (severe ECC)
Carious lesions affecting almost all the teeth including the lower incisors. Cause : a combination of cariogenic food and poor oral hygiene. This condition is usually found between 3-5 years
The condition is rampant and involves tooth surfaces which are usually unaffected by caries.
Definition
ECC is defined as “the presence of one 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 .
Severe – ECC refers to children with atypical, progressive, acute or rampant patterns of dental caries.
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Proposed case definitions of ECC and S-ECC Drury et al age in months
ECC
S-ECC
4
48-59
1 or more dmf surfaces
1 or more cavitated, filled or missing (due to caries) smooth surfaces in dec. max. ant. Teeth or dmfs score > 5
60-71
1 or more dmf surfaces
1 or more cavitated, filled or missing (due to caries) smooth surfaces in dec. max. ant. Teeth or dmfs score > 6
IN 1994, CONFERENCE AT THE CENTRES FOR DISEASE CONTROL AND PREVENTION “EARLY CHILDHOOD CARIES”
the link between bottle habits and caries was not absolute. but this term did not negate the basic reasons for tooth demineralization in a very young children – extensive exposure to a cariogenic diet and early infection with cariogenic bacteria.
SUPPORT FOR THE TERM ECC
the finding that sleeping with a bottle of milk or other sweetened beverages does not always cause caries. only small proportions of these children actually get caries. surveys from China, Thailand and Tanzania where feeding with baby bottles is rare, show high caries rate in primary maxillary incisors, a pattern that is generally assumed to be due to bottle feeding practices. children who are 4-5 years old (bottle use discontinued) develop caries in the maxillary anterior teeth. the potential cariogenicity of the most common bottle contents - milk & milk formulas – remain unclear.
Caries pattern of ECC in the primary dentition
Dental caries in young children develops on all teeth and tooth surfaces.
A hierarchy of caries attack on different teeth and tooth surfaces have been described.
Caries pattern
% of children by caries pattern White
Black
Hispanic Chinese
Pits & 22.4 fissures
38.9
52.2
62
Max.ant 13.8 .
17.5
13
43.2
Post.pr oximal
5.2
3.2
7.2
14.7
Postr. Faciallingual
3.4
3.2
2.9
8.4
Caries pattern
3-4 year old children with life-time exposure to fluoride water showed ECC pattern – E D Max. Inc C Mand.Inc
In a Japanese study Mand E – max centrals – mand. D – max lat – max canine – mand lat – mand canine
Aboriginal Australian children Mand molars – max molars – max inc – max can – mand inc – mand can
ECC when associated with nursing bottle: max inc, molars
Stages of early childhood caries DCNA 2000
A. Normal B. Very mild: clinical appearance show very mild demineraisation usually at gingival crest and no cavitation C. Mild: clinical appearace shows demineralization in gingival third of tooth and moderate cavitation
D. Moderate: clinical appearance shows frank cavitation on multiple tooth surface. E. Severe: clinical appearance consists of wide spread destruction of tooth and partial to complete loss of clinical crown
• 1960 – Keyes demonstrated that dental caries is an infectious,transmissible disease • 1975 – Mutans Streptococci (MS) implicated as the principle bacterial component responsible for dental caries in Humans
Biological mechanisms of early childhood caries
The bacterial flora and host defense systems in the young infant are in the process of being established.
The tooth surfaces of newly erupted are immature and may show hypoplastic defects. The source of carbohydrate may be sugars in drinks and solid food consumed by the infant. Children with ECC have high levels of MS which generally are acquired from their mothers. Such high numbers of acidogenic micro-organisms combine with frequent cho intake to produce abundant acid that lowers plaque pH for extended periods and demineralizes the child’s teeth.
Tooth maturation & defects
Newly exposed enamel surfaces undergo final stages of post-eruptive maturation and hardening, when ions such as fluoride are incorporated. The period immediately after eruption and prior to final maturation is when the tooth is most susceptible to caries. Thus a combination of recently erupted immature enamel in an environment of cariogenic flora with frequent ingestion of fermentable carbohydrates may render teeth susceptible to caries
Developmental defects of enamel
Partial or total (enamel hypoplasia)
Change in translucency (opacity)
Generalized enamel defects in primary dentition Hereditary diseases, acquired prenatal and post natal conditions such as - Birth prematurity, low birth weight, infections, malnutrition, metabolic disorders and chemical toxicity.
Localized trauma & infections
cariogenic bacteria • Mutans Streptococci (MS) • S. mutans, S. sobrinus, S. sanguinis, S. salivarius, S. milleri • Lactobacilli • L. acidophilus, L. casei • Actinomyces • While not the first to colonize the tooth, studies have shown S. mutans to be the main culprit in dental caries
Mutans Streptococci
The main bacteria implicated in ECC are a group of bacteria termed Mutans Streptococci Most commonly isolated in human dental caries – S.mutans and S.sobrinus M.S. are the principal bacterias isolated from children with ECC
The dental plaque concentrations of S.mutans in children with ECC ranged from an average of 30%40% to over 50% of the total cultivable plaque and 10% of the salivary flora. In breast fed children with rampant decay S.mutans levels were 100 times higher than in children without decay. Heavy infection by MS of more than one clonal type reflects high frequency of sugar consumption
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Virulence of mutans streptococci
Synthesize α-1-3-rich, water-insoluble glucan uniquely from sucrose.
ms produce 3 different glucosyltranferases(GTF) each with a distinct affinity for particular surfaces. GTF-B adheres to bacterial surfaces & micro-organisms that become glucan producers GTF-C binds to saliva-coated tooth surface & forms glucans thereby providing binding sites for microorganisms ….Irreversible adhesion and colonization to the tooth surface. Synthesize intracellular polysaccharide (IPS) (not by S.sobrinus)
Produce large amounts of acids particularly lactic acid Production of dextranase – replaces S.sanguis & S.mitis Acidurity is extremely high – the molecular basis for high acid tolerance resides in their ability to pump out proteins from their cytoplasm by ATPase within 3 months virulent bacteria can account for 75% of the oral flora. In a study, SM isolates were taken from caries free, caries active, root caries & lab strains were incubated with neutrophils. The caries free strain displayed the highest level of neutrophil activation. - MS most successful in evading recognition by the human immune system
Like many gram positive organisms SM produces its own antibiotic – mutacins which inhibit growth of other streptococci and gram positive organisms by stopping enzyme functions & generation of ATP. The production of mutacins varies among isolates of S.mutans.
In a study of 20 sets of mothers and their children, transmission of S.mutans was found in 9 cases. Bacterial strains shared between mother and child produced mutacins that were active against a broader spectrum of oral flora than did non-transmitted strains.
Establishment of mutans streptococci in infants
Studies including predentate children show that mutans streptococci are not cultured from the oral cavity prior to the eruption of teeth – ms require non-shedding surface to colonize Oral flora averages only 2-4 divisions per day & swallowing occurs every few minutes
Infection rate of ms increases with age as well as the number of teeth present in the infants mouth. - it reflects the increasing number of retentive sites for bacterial colonization Majority of the studies have shown that some infants are infected in the age group under 1 year old i.e., coinciding with time of emergence of the incisors
In contrast Caufield and co-workers found that the initial acquisition of ms in 38 out of 46 children occurred at a median age age of 26 months (9-44 months), coinciding with the emergence of primary molars
The age at which ms are first acquired in infants is thought to influence their susceptibility to caries, in that the earlier the colonization, higher the caries risk.
Determining the age of infection
Understanding the disease process The efficacy of microbial screening tests at different ages optimal period to intervene with preventive strategies
Transmission of mutans streptococci
Transmission is mediated via saliva .
The most common routes of infection are close contacts, everyday nursing items such as pacifiers, baby bottles and spoons. Minimum infective dose is necessary for implantation, which is enhanced by repeated inoculation. Primary carer of the infant, usually mother provide the reservoir to ms that infect the child Salivary concentrations of 105 CFU MS/ml of saliva were associated with 52% infection rate in their children compared to only 6% infection rate when the maternal saliva concentration was 103 or below
The Window of Infectivity • In 1993, Page Caufield and Colleagues presented a paper with evidence to support a discrete “window of infectivity” for MS Colonization
• Oral bacterial levels of 46 mother-child pairs from infant birth to age 5 were studied to determine the age of acquisition of Mutans Streptococci
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• “Window of Infectivity” is used to describe the time period when children are at greatest risk for acquiring MS • MS colonization occurs between 19 – 31 months of age, but has been seen as early as 10months is some populations/studies • A second “window” is speculated to occur when 1st molars are erupting
Window of infectivity Combination of
frequent and close maternal contacts.
cessation of lactation with its protective antibodies.
an immature immune response.
Individual susceptibility.
When does the “Window” end?
• Window appears to close after all primary teeth erupt
• Once a stable plaque or biofilm covers the tooth surface, MS is less likely to be established • Children ages 2-6 years have been shown to be less susceptible to MS infection
Transmission of MS Why is mother the culprit?
• Most intimate contact (sharing utensils, kissing, etc) • Immunologic factors transferred from mother to child (in utero and through breast feeding) • Spends the most time with the child
Transmission of MS Mother - child • Mother-child pairs are found to harbor the same S. mutans strains • Quantitative amounts positively correlated between mother and child pairs • Children whose mothers are the primary caretaker during the 1st 2years of life are found to have more MS than children with other caretakers
Transmission of MS Li & Caufield (1995) • DNA fingerprinting of 34 mother-infant and of 7 fathers who lived in the same household 24/34 (70.6%) infants harbored identical genotypes of MS identical to mothers • None of the infant DNA fingerprint patterns matched the fathers’ strain • MS transmission from mother to child
• Female offspring 88% • Male offspring 53%
NEW THOUGHTS Milgrom. P. CDOE 1998
The problem begins long before the baby is born: high risk community will show infections with cariogenic organisms earlier in the development of the dentition than previously thought.
Lactobacilli
Lactobacilli constitute a low or negligible portion of plaque microbiota. They are found in relatively high proportions in cavitated lesions indicating their role in dental caries lies in the progression rather than in the initiating of the disease. LB levels in saliva reflect total carbohydrate consumption, not necessarily sucrose consumption only. Children from whom both MS & LB were isolated, exhibit greater caries experience whereas in those in whom neither organism is found, often have the lowest caries score.
Host - salivary factors
Provides the main host defense system against dental caries. Clearance of foods and the buffering of acids generated in dental plaque. Mediates selective adhesion and colonization of bacteria on tooth surface. contains several antimicrobial systems which may aid in the elimination of bacteria.
Antimicrobial proteins include lysozyme, lactoferrin, peroxidase enzymes, agglutinins, histidine rich protein which work synergistically, but the clinical significance of individual microbial systems is not well defined.
Agglutinins Agglutinate oral bacteria and enhance their removal (MS). -Mucins, agglutinating glycoproteins, fibronectin, beta-2 macroglobulin, lysozyme, secretory immunoglobulin A pH buffering systems – carbonic acid - bicarbonate (most active during stimulated salivary flow), phosphate and proteins (active during resting periods) Continuous feeding of sugars at night time when the flow rate of saliva is lowest increases the caries risk of the infant significantly.
Immunological factors
Saliva – secretory immunoglobulin A
GCF – immunogluobulin G
Non-specific antimicrobial systems – saliva and phagocytic cells through GCF
there is little direct evidence of beneficial effects on caries in humans In young children antibody levels and caries prevalence are of limited value
Psycho-social & Behavioral issues in ECC
Putting a child to bed with a baby bottle is a wide spread behavior, with a prevalence far in excess of that for ECC.
Length of the contact with bottle at night time is important . Greater lengths of bottle contact appears to be positively associated caries. Children with caries eliminate bottle use 4-7 months later than those without caries.
However sleeping with a bottle is not more common in children with maxillary anterior caries. Studies have shown that night-time bottle use appears to be prevalent in children both with caries and without caries.
But Serwint reports no difference in the percentage of children with and without maxillary anterior caries using the bottle at 18 months. The average age of weaning in those with and without maxillary anterior caries to be either not different or greater in those without caries.
O’sullivan, Tinanoff (Pediatr Dent 1993)
86% of children with max. ant caries – bottle during night 69% without max. ant. caries also took bottle to bed. In another study 90% children with or without caries bottle fed between 12-18 months showed a prevalence of only 20%. Use of a bed time bottle appears to be highly prevalent in children with and without maxillary anterior caries and there is little evidence to support the conclusion that use of bottle beyond the age of 1 is a major caries risk factor
Prolonged / at-will breast feeding
May cause maxillary anterior caries (Roberts et al,Wiliams & Hergreaves, Gardner et al ) Allowing children to nurse at will during the night is associated with the presence of caries. Derkson GD & Ponti P reports 6% of caries free children and 22% of caries positive children were exposed to prolonged night time breast feeding at 6 months of age. Caries not specifically to max. ant. can develop in children who are exclusively breast fed. (Roberts GJ et al, Silver DH ). They are highly susceptible to caries.
AAP – “breast feeding ensures the best development and psycho-social out comes for the infant.”
AAPD – “frequent breast feeding at night & on demand after eruption of teeth may be implicated in contributing to the development of ECC” The potential for ECC is related to extended and repetitive feeding times with prolonged exposure of teeth to fermentable carbohydrates without appropriate oral hygiene measures.
In a study using enamel powder calcium and phosphate were deposited onto the enamel when breast milk was present. However when supplemented with 10% sucrose, breast milk caused caries in 3.2 weeks.
Environmental factors influencing caries Environment Socio-economic status Ethnicity Culture
stress poverty health care delivery system
Race and ethnicity
prevalence Native American children and Canadian aboriginal children showed 70 – 80% ECC prevalence …..parents consider it as a normal childhood disease that affects children Investigators and clinicians had poor understanding of high ECC prevalence among these populations Whites had higher dfs scores than blacks but lower compared to Hispanics and Mexicans Ethnic minorities including the immigrant populations have increased rates of ECC (in Sweden children with immigrant background were three times more likely to have caries compared to other children.) …..concern for oral health, prenatal diet that could contribute to enamel hypoplasia, care of primary teeth, child rearing practices and access to dental and medical care.
Socioeconomic status
Individuals from lower SES experience financial, social and material disadvantages that compromise their ability to care for themselves, adequate nutrition, obtaining professional health care services and live in a healthy environment, all of which lead to reduce resistance to oral and other disease.
According to Chen low SES individuals -have more fatalistic beliefs about their health -lower perceived need for care leading to less self care -Lower utilization of preventive health services
The availability of dental care in low-income areas and reimbursements of dental services are limited.
Cariogenicity of sugars
Sucrose, fructose & glucose found in fruits juices & vitamin C drinks as well as in solids are associated with ECC
Sucrose: 1. small uncharged molecule that easily diffuses into dental plaque 2. highly soluble & acts as a substrate both for the production of extracellular polysaccharide & for acid production 3. it favours establishment of SM on teeth & high sucrose intake give rise to voluminous amount of plaque formation 4.it does not contain substances that can inhibit plaque bacteria or form a protective coating on the enamel surface of the teeth.
Diet
The relationship of dietary sugar and caries has been investigated using total weight of sugar intake and frequency of sugar intake.
In studies of preschool children, the total weight intake of sugary items does not vary between those with and without caries. However there is an association between the frequency of sugary intake and caries. Children who receive bottles containing sweetened milk or other sweet drinks have a higher prevalence of maxillary anterior caries than those whose bottle contain only milk or water.
Why milk may be less cariogenic than other sugar containing liquids
Phosphoproteins inhibit enamel dissolution
Antibacterial factors in milk interfere with oral microbial flora
Cariogenic bacteria may not be utilize lactose for energy source as readily as sucrose
Remineralizes artificially demineralized enamel invitro
It may be the vehicle for more cariogenic substances as parents combine milk or milk formula with other food products or sugars. The majority of 6months – 5 year old children are put to bed with a bottle other than water.
Children who consumed beverages containing sucrose in their baby bottle had levels of MS four times the level of those who consumed milk in their bottle.
The potential cariogenicity of most common bottle contents - milk & infant formulas remain unclear.
Studies have failed to identify a unique family profile that predisposes to this condition. Parental concern is evident, but it is a problem of overindulgence or lack of parental restraint rather than one of neglect. Even though parents know the harmful effects of putting the baby to sleep with the bottle they still do it. Once a feeding pattern is established it tends to remain fixed, not because of parents but because of the baby. If parents attempt to alter the pattern, the baby rebels and the parent relent
Diet Diet is critical to ECC
Early dietary habits are continued into adulthood High consumption of salty and sugary snack food snacks lead to lifelong dental problems. Lack of transition of structured meal and snack results in a grazing meal pattern. Malnutrition can delay the eruption and composition of primary teeth and bone. Salivary gland function is impaired by iron deficiency and prenatal exposure to lead.
Tooth brushing
Increased frequency and better oral hygiene levels are associated with lower caries levels in preschool children. Studies show that increased tooth brushing frequency and parental involvement decrease carious lesions on smooth surfaces. Acc. Winter et al absence of tooth brushing is not associated with a greater prevalence of incisor caries, others find no relationship between tooth brushing frequency and caries. The age of initiation of tooth brushing demonstrate few associations with caries status.
Regular tooth brushing may counteract the effects of a diet.
In a study children who reported high snack diet but regular toothbrushing had a dmfs score of 2.2 compared with a dmfs score of 3.0 in those with low snack diet and no tooth brushing
Studies have found a positive and significant association between gingivitis, mutans streptococci levels and caries.
Dental knowledge
Understanding the relationship between the microbiology of caries, the role of cariogenic foods and use of the baby bottle is necessary for the prevention of ECC.
Studies have shown that caregivers usually know that bottle use and high sugar intake increase the risk of caries in their children, tooth brushing prevents caries.
But parents who have high scores on dental knowledge usually have children with high caries level.
These studies confirm the generally agreed principle that education alone is insufficient to produce behavior change.
Implications of ECC
High risk for developing new lesions both in primary and permanent dentition.
increased treatment costs and time. may require GA or deep sedation in young children.
requires extensive restorative treatment & extraction of teeth at an early age.
Children with ECC weigh less than 80% of their ideal weight.
Poor nutritional practices may be responsible for both the reduced weight and caries.
Loss of school days and increased days with restricted activity.
Diminished ability to learn
Diminished oral health-related quality of life
Diagnosis
To identify the high caries-risk subjects before the clinical manifestations of the disease and to give individual protection to maintain a satisfactory dental health status.
Anamnestic phase
socioeconomic status medical problems Pharmacological treatments Dietary habits Dental health education Oral hygiene habits
Clinical examination
Oral hygiene caries experience Aspect of the lesions Localization of the lesions Previous restorative treatment Need for orthodontic treatment
Microbiologic and biochemical tests caries risk (MS salivary levels) CHO consumption Saliva buffer capacity
diagnosis
high risk
low risk moderate risk
Risk Assessment
Risk assessment for transmission of SM from caregiver to child
Refer to “dental home”
Teach proper oral hygiene with demonstration (Lift The Lips)
Discuss feeding and behavior guidance
Examine teeth for demineralization/decay
Review proper hygiene techniques
Caries –risk assessment tool (CAT) AAPD
Caries risk indicators
Clinical conditions
No carious teeth in past 24 months No enamel demineralization No visible plaque; no gingivits
Optimal systemic and topical fl exposure Consumption of foods strongly associated with caries initiation primarily at meal times
Environmenta
l characteristics
Low risk
Moderate risk
Carious tooth from past 24 months One area of demineralization Gingivitis
Suboptimal systemic fl exposurewith optimal topical exposure Occasional between exposures to simple sugars
High risk
Carious tooth from past 24 months One area of demineralization Radiographic enamel caries Visible plaque on anterior teeth High titers of MS Orthodontic appliances Enamel hypoplasia Suboptimal topical fl exposure Frequent meal exposures to simple sugars or foods strongly associated with caries Low level care giver SES No usual source of dental care
Caries risk indicators
Low risk
Moderate risk
Environmental characteristics
High caregiver socioeconomic status Regular use of dental care in an established dental home
General health conditions
High risk
Irregular use of dental services Midlevel caregiver SES
Active caries present in the mother Children with special health care needs Conditions impairing saliva composition/flow
Preventive action taken after caries risk assessment of infants and toddlers
Diet
Low risk At risk
Signs of ECC
Advice
Changing feeding pattern Counseling, Sugar substitutes xylitol
Education counseling
Oral Review Education hygiene practices Motivation training Fluoride Fluoride Fluoride tooth tablets or paste drops
Professional tooth cleaning Fluoride tablets or drops Fluoride varnish
Microbiological Monitoring •Determine MS levels of children and their mother/father • Information provides the dentist with the basis for implementing a prevention program for high-risk families • Microbiological-based intervention can influence the level and timing of MS colonization
• 10% povidine iodine • Chlorhexidine varnish or gel
Microbial sampling
Young child : Tongue impression with wooden spatula technique (Kohler & Bratthall) Dentocult SM strip (Orion)
Infants:
cotton swab
Barriers to childhood caries treatment
Child Not able to cope very well with dental treatment
parents Parents cannot control frequency of between meal sugary foods and drinks
Dentist further training in pediatric dentistry
Health care systems payment, insurance
Interventions
• Lower MS in mothers • Diet counseling • Chlorhexidine • Fluoride Regular oral hygiene and dental care • Educate family • Diet, oral hygiene, fluoride, transmission
Prevention Programs 1. Support and participation of the parents or caregiver
2. Must start early Three principles ways to prevent ECC
1.Community based measures 2.Professional measures
3.Home care methods
ECC prevention
Community Education Water fluoridation Community & personal development
professional
Early detection Diet counseling Fl, chlx,sealants
Home care Dietary habits Fl dentifrices Fl supplements Oral hygiene
Control of transmission of cariogenic bacteria
Community based education Goals: Increase the knowledge of mothers about ECC Improve the dietary and nutritional habits of infants and mothers Educational status of parents is inversely associated with the prevalence of appropriate use of baby bottle, especially at bed time The mean number of dmft at the age of 3 years
Significantly Mothers of children with ECC lack the knowledge of harmful effects of feeding bottle and the time when baby is weaned off the bottle than mothers of children without ECC
In a Canadian study, mothers were given hand made cradles – traditionally used for comforting the infants. In additional pamphlets, logos & posters, toothbrushes & tooth pastes were distributed. There was significant reduction in bottle use. In a study (in Alaska), the community was divided into high, medium and low intensity sites. The programme included one-one counseling, swap parties – where parents exchanged their child’s bottle for a cup. Logo used was “stop BBTD”. After 3 yrs, 33% in H-I, 18% in M-I & 27% in L-I reductions in ECC were recorded. But did not reach 50%.
Water fluoridation
Highly effective (40-60%) in reducing dental caries in primary dentition. More effective in reducing caries in children from low SES than from high SES. It is the only means of prevention that does not require a dental visit or parental motivation. However there is no direct evidence to its effect on ECC
FLUORIDE
Topical
Toothpaste Anti-Cavity Rinses
Fluoride Applications (Varnish)
(NOT Mouthwash)
Systemic
Water Tablets Drops In vitamins
Köhler (1994): preventive program with mothers and 1st born children until 3yrs old -Counseling, prophylaxis, fl-, OHI, Chlorhexidine • Study showed successful reduction of MS in mothers, during the eruption of primary dentition in child can prevent colonization of MS • Delayed in colonization can reduce the development of caries • Follow-up of children at 7yrs old showed long-term effects: less caries experience in test vs control group
Antimicrobial therapy An application of 10% povidine-iodine every two months reduced the risk of ECC in low income Puerto Rican children aged 12-19 months When women in their 7th month of pregnancy rinsed daily with NaF & Chlx , bacterial colonization in their children’s mouth was delayed by an average of four months
Oral application of genetically engineered antibodies also offers new prospects for passive immunization against dental caries. Oral passive administration of monoclonal to S.mutans prevented recolonization in humans who had been treated with chlx first. Protection against S.mutans colonization lasted upto two years although the monoclonal antibody was applied over a period of only three weeks.
Chlorhexidine
Loe et al., Possess stronger antimicrobial properties than fluoride but synergistic to physiochemical tooth properties. Anticaries effect of chlorhexidine in different forms – mouth rinses, gels, dentifrice & varnish.
Caries associated micro-organisms exhibit different degrees of natural susceptibility to chlx.
But lactobacillus species are less susceptible than MS -they survive the chlx levels at that kills MS. MS differential sensitivity to chlx makes selective chemotherapeutic treatment of caries possible
Prevention Prevention of ECC begins with the intervention in the prenatal and perinatal periods women should be advised to optimize nutrition during the third trimester and the infants first year. Mother needs to have a healthy mouth
Prevent transmission of infection
Dietary Guidance Dental disease (decay) is exacerbated by diet. Avoid prolonged breast- and bottle- feeding, especially at sleep times. Do not fill bottle/sippy cup with a sugarcontaining product, aviod extended and repetitive use of no-spill training cup Encourage cup use at 6 - 8 months. Limit sweet, starchy snack foods. Do not add sugar to solid foods.
Wipe infant’s gums with a wet cloth or gauze after each feeding. Wean around age one Brush baby teeth ~ 6 months in age - erupts. Use a half pea size amount of fluoridated toothpaste on the toothbrush.
See dentist when the first tooth erupts, or no later than age one Supplementing milk with vitamins during initial years reduces the prevalence of linear enamel hypoplasia Drink fluoridated water
Treatment
Treatment should be definitive yet specific for each individual patient.
Conventional restorative approaches may not arrest the disease. ART techniques using GIC should be used both as preventive and therapeutic. Supplemented with regimented applications of topical fluoride . Employ advanced behaviour management techniques – immobilization, sedation or GA Stainless steel crown – aggressive therapy
Repeated restoration cycle
Elderton “chain of events that constitute traditional restorative treatment is referred to Repeated restoration cycle”
Restorative treatment is assumed to be cyclic phenomenon.
dentist
pain Pt not satisfied does not go to dentist
Dentist detects only caries Caries risk uninvestigated
Treatment cost increases
Lesions restored acute symptoms removed
Dentition become deteriorated Reasons for failed restoration not identified
Treatment ends with OHI
Recalls not regular Secondary lesions appear
Restorative strategies
Early caries with minimal loss of enamel
professionally applied fluoride therapy Extensive cavitation with no pulpal involvement Anterior teeth Acid etch composite resin technique Pedo strip crown GIC restorations Posterior teeth Posterior composite restorations GI ceremet restorations Stainless steel crown Extensive cavitation with pulpal involvement Pulpotomy/pulpectomy followed by permanent restorations Extraction followed by space maintainer / partial or complete denture
Fluoride Varnish Most effective on early white spot lesions
Fluoride Varnish Fluoride varnishes are intended to remain in close contact with enamel for several hours. Toothbrushing is sufficient to clean the teeth before application.
How Does FV Work?
The lacquer-based product releases fluoride ions into the dental enamel in high concentrations.
Adheres to the dental enamel forming a depot from which fluoride is slowly released.
Extends the exposure time of fluoride in the mouth compared to other topical fluorides.
Advantages of Fluoride Varnish
Apply in less than one minute Does not require special equipment or the need for a prophylaxis prior to application
Sets on contact with saliva
Neutral taste
Delay caries progression
Advantages of Fluoride Varnish
Safety
Application in Orthodontics
As much as 50% reduction in demineralization (1)
Applications for handicapped, mentally and medically compromised patients
Fluoride Varnishes Available .
Duraphat®
Duraflor®
Fluor Protector
(Colgate Oral Pharmaceuticals)
(Medicom® Inc.)
(Ivoclar-Vivadent)
5% NaF - 10 ml tube 5% NaF - 10 ml tube 1% Difluorsilane (unit-
dose)
CavityShield® (OMNII )
5% NaF(unit-dose)
Safety and Convenience Unit-dosed for asepsis control Applicator brush for convenience & cost savings • CavityShield® Dosage Applied – 0.25 ml for primary dentition – 0.40 ml for mixed dentition
– 0.65 ml for permanent dentition
Fluoride Varnish Supplies
Inherently Inconsistent Dosage Delivery 1st Application of Duraphat
Varnish
Sodium Fluoride/ Sweetener
2nd Application of Duraphat
Fluoride Varnish Application
Fluoride Varnish Application 1. Position Child – child’s head onto your lap
Fluoride Varnish Application Prepare the Fluoride Varnish
Fluoride Varnish Application 4. Dry the tooth
Fluoride Varnish Application 5. Apply varnish – posterior teeth
Fluoride Varnish Application 5. Apply varnish – anterior teeth
Fluoride Varnish Application 7. Give Child a Drink of Water
SUMMARY
EARLY MONITORING – 1 year
FLUORIDE VARNISH for at-risk kids
DIET COUSELING
SEALANTS
EDUCATION
HOME CARE -toothbrushing/ flossing
REGULAR DENTAL VISITS
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www.dentistpro.org to find more
Fluoride Varnish Supplies Fluoride varnish armamentarium : Gloves Toothbrush Fluoride Varnish & Applicator 2x2 gauze sponges and/or cotton rolls Paper Towel for a bib Disposable Mouth mirror (optional)
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references
Pediatr Dent 26, 5. 2004 Pediatr Dent 2004- 2005 ref manual Pediatr Dent 19:1,1997 Pediatr Dent 13:1991 Pediatr Dent 15, 1993 Community Dent Oral Epidemiol 26 1998 Community Dent Oral Epidemiol 22,1994 Community Dent Oral Epidemiol 17, 1989 J Public Health Dent 56: 1996 J Public Health Dent 52: 1992 J Dent child 1996 J Dent child 1996 DCNA 2000, 1996, 2004,
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