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Early Childhood Caries, Nursing
Caries and Rampant Caries
Group A
BDS 02/18
BDS 03/18
BDS 09/18
Outline
• Introduction
• Early Childhood caries
• Nursing Caries
• Rampant Caries
• Diagnosis of caries
• Management of Caries in Pediatric patients
• Prevention strategies
Introduction
• The WHO Global Oral Health Status Report (2022) estimated that oral
diseases affect close to 3.5 billion people worldwide, with 3 out of 4 people
affected living in middle-income countries.
• Globally, an estimated 2 billion people suffer from caries of permanent
teeth and 514 million children suffer from caries of primary teeth.
• Dental caries is a microbial disease of the calcified tissues of the teeth,
characterized by demineralization of the inorganic portion and destruction
of the organic substance of the tooth.
• The World Health Organization (WHO) defines caries as a localized post-
eruptive, pathological process of external origin involving softening of the
hard tooth tissue and proceeding to the formation of a cavity.
Early Childhood Caries
Definition
• Early childhood caries (ECC) is defined as the presence of one or more
decayed (noncavitated or cavitated), missing (as a result of caries), or
filled tooth surfaces in any primary tooth in a child 71 months of age
or younger. (American Academy of Pediatric Dentistry (AAPD)
(Adopted in 2003, Revised in 2007, 2008).
History
• Dr. Ellias Fass, 1962 – 1st published comprehensive description of
caries in infants and termed as “ Nursing bottle caries”.
• In 1978, the American Academy of Pedodontics released “Nursing
Bottle Caries”, a joint statement with the American Academy of
Pediatrics, to address a severe form of caries associated with bottle
usage.
• Initial policy recommendations were limited to feeding habits.
• Over the next 2 decades, however, recognizing that this distinctive
clinical presentation was not consistently associated with poor
feeding practices and that caries was an infectious disease, AAPD
adopted the term “early childhood caries” (ECC) to reflect better
multifactorial etiology.
• Current definition of ECC was released by AAPD in 2002.
Severe ECC
• AAPD specifies that, in children younger than 3 years of age, any sign
of smooth-surface caries is indicative of severe early childhood caries
(S-ECC)
• From ages 3 through 5, 1 or more cavitated, missing (due to caries),
or filled smooth surfaces in primary maxillary anterior teeth;
or
• a decayed, missing, or filled score of ≥4 (age 3), ≥5 (age 4), or ≥6 (age
5) surfaces also constitutes S-ECC
Classification of ECC by Wayne
Type I
(mild to moderate)
• Isolated caries lesions involving molars and incisors
• Cause is a combination of cariogenic semi-solid or solid food and poor oral
hygiene
• Seen in 2-5 years old
Type II
(moderate to severe)
• Labiolingual carious lesion affecting maxillary incisors-with or without the
molars depending on age
• Mandibular incisors are not affected
• Cause is use of feeding bottle or at will breast feeding or a combination of
both with or without poor oral hygiene
• Seen soon after eruption of teeth
Type III
(severe)
• Carious lesion involve almost all the teeth including mandibular incisors
• Usually seen in 3-5 years of age
• Cause is a combination of factors and a poor oral hygiene
• Rampant in nature and involves immune tooth surface
TYPE I TYPE II TYPE III
Clinical & Radiographic examples of ECC
Nursing Caries
• Nursing caries is a unique pattern of dental caries in very young
children due to prolonged and improper feeding habits
Etiologic agents
• Bovine milk, milk formula and human breast milk have all been
implicated due to their lactose content
• Juices, honey dipped pacifiers have also been implicated
• Basic mechanism of caries initiation is same however; so all the 4
variables-pathogenic micro-organisms, substrates, host factor(tooth)
and time are essential in causing demineralization
1. Pathogenic micro organism
• Streptococcus mutans is the principal organism that colonizes the
tooth after it erupts into the oral cavity
• Transmitted to infants mouth from mother
• It is considered more virulent for the following reasons
• It colonizes the teeth
• It produces large amount of acid
• It produces large amount of extracellular polysaccharides which favour
plaque formation
• S.mutans is more commonly evident in rapid and smooth surface
caries and less common in pit and fissure caries
2. Substrate-fermentable carbohydrate
• Carbohydrates are utilized by microorganisms to form dextrans which;
• Adhere organisms to tooth surface
• Cause organic acid to demineralize the tooth
• In infants and toddlers the main sources of carbohydrates are
1. Bovine milk and formula
2. Human milk
3. Fruit juices
4. Sweet syrups e.g.. Vitamin preparations
5. Pacifiers dipped in honey or sugar solution
6. Sweets and chocolate
3. Host
• Teeth act as the host of the microorganism
• Hypomineralization or hypoplasia-increases susceptibility
• Thin enamel of deciduous teeth make the spread of lesions faster
• Developmental grooves acts as plaque retentive areas.
4. Time
• The more time baby is asleep with the bottle in the mouth there is higher risk
as salivary flow rates decrease
Clinical features
It affects the primary teeth in the following sequence
• Maxillary central
• Maxillary lateral
• Maxillary first molars
• Maxillary canine and second molars
• Mandibular molars at later stage
• Mandibular anterior teeth are usually spared because of protection from the
tongue and the proximity of lingual gland saliva ducts
Progression of the lesion
Implications
• Increased risk of developing caries in permanent dentition
• Child at risk of other health hazards
• Financial burden to parents
Rampant Caries
• There is no complete agreement on the definition of rampant caries
or on its clinical picture.
• Rampant caries has been defined by Massler as a “suddenly
appearing, widespread, rapidly burrowing type of caries, resulting in
early involvement of the pulp and affecting those teeth usually
regarded as immune to ordinary decay.”
• There is no evidence that the mechanism of the decay process is
different in rampant caries or that it occurs only in teeth that are
malformed or inferior in composition.
• On the contrary, rampant caries can occur suddenly in teeth that
were previously sound for many years.
• The sudden onset of the disease suggests that an overwhelming
imbalance of the oral environment has occurred, and some factors in
the caries process seem to accelerate it so that it becomes
uncontrollable.
Etiology
• Rampant caries is multifactorial in etiology
• Its not limited to poor feeding habits like nursing caries
• Poor salivary flow
• Systemic conditions e.g.. Sjogren’s, immunodeficiency
• Genetic factors-predisposition
• There is considerable evidence that emotional disturbances may be a
causative factor in some cases of rampant caries.
Clinical features
• Rampant caries occurs rapidly
• There is therefore early pulpal involvement
• Surfaces considered to be ‘immune’ are also affected e.g.. Mandibular
incisors (as opposed to nursing caries)
• Young teenagers seem to be particularly susceptible to rampant
caries, although it has been observed in both children and adults of
all ages
Davies believed that rampant caries should be
coined to a condition where…
• Lesions are more than 10
• High caries experience for the child age
• Sudden characteristic feature
• Caries developing in otherwise immune surfaces
• Extensive loss of tooth structure (particularly dentin) even though
enamel shows little defect
• Soft, mustly, ivory coloured dentin consistency indicating rapid
progession of disease
Diagnosis of Caries
• The process of diagnosing all these carious conditions is dependent
on proper history taking and examination
• This may be sufficient in some cases but in others diagnostic aids will
be needed e.g.. radiographs
• Visual-tactile-radiographic has been the traditional sequence used by
most clinicians
• This procedure involves the visual identification of demineralized areas
(typically white spots) or suspicious pits or fissures
• Also involves use of the dental explorer to determine the presence of a loss
of continuity or breaks in the enamel and assess the softness or resilience
of the enamel.
• Interproximal caries has generally been detected with the use of bite-wing
radiographs.
Other Developments…
• Fiber-optic Trans illumination
• Electric Resistance Measurement
• Ultrasonics
• Dyes
Management of Caries in Pediatric Patients
Management carried out in phases with the following Treatment
aims:
• To deal with any existing emergency
• To Arrest and control disease progression; and institute preventive
measures
• To restore all carious lesions
Emergency phase
• Management of any existing emergency: pain and infection
a) Pain-prescribe analgesics, teeth needing immediate attention
should be extirpated
b) Infection-Drainage of abscess and prescription of anti-biotics to
manage infections
Prevention & Arrest of Disease process.
• After the emergency has been taken care of the clinician should start
instituting prevention measures to limit further disease progression
• Measures to arrest disease process are key
• An individualized caries risk assessment is an important step in the
management
• It aims to modify the risk factors
• Oral Hygiene Instruction and Motivation should be done
• Parents should be asked to wean off the child from using a bottle
while in bed.
• In case of considerable emotional dependence on the bottle, suggest
the use of plain water.
• Parents are instructed to brush child’s teeth last thing at night with
fluoride toothpaste
• For children aged 3-6 years, chair-side topical fluoride varnish
(2.2% F) application to teeth should be carried out
Stabilization of carious process
• If the carious lesion is arrested, it should be monitored to ascertain
that it remains in non-progressive stage until exfoliation.
• For non-cavitated proximal enamel lesions, a resin infiltration system
used in conjunction with fluoride therapy can be used to control
caries progression
• Pits and fissure sealants where necessary/indicated
Fluoride varnish application
• Teeth that require temporization are excavated with spoon
excavators and glass ionomer cement is used to seal the teeth.
• Temporization by sealing of the carious cavity after caries removal
reduces the load of bacterial colonization in tooth
Restorative Phase
• During this phase restorative procedures are perfumed and
completed i.e. simple fillings, pulp capping, pulpotomies,
pulpectomies and stainless steel
• Therefore ALL carious tissue has to be removed and final restorative
materials placed
• In young children with high risk of caries, there is good evidence that
stainless steel crowns function better than multi-surface intra-oral
restorations.
How about for non-restorable teeth?
• Extraction should be perfumed for teeth that can not be restored,
followed by space maintainer fabrication where appropriate
• Clinicians should try as much as possible to avoid extractions on the
child’s first visit
A, Restorable with resins. B, Restorable with crown forms
(possibly). C, Nonrestorable.
Maintenance Phase
• Patients must be reviewed to detect any changes and check status of
the restorations
• Recall intervals are based on the outcome of their caries risk
assessment:
a) Patients with obvious signs of active oral disease or its predisposing
factors should be reviewed at 3 monthly intervals until well
controlled
b) Recall visit of low caries risk children;6 months and should not
exceed 12 months.
Prevention strategies-AAPD
Recommendations
• Avoiding frequent consumption of liquids and/or solid foods containing sugar, in particular:
a. Sugar-sweetened beverages (e.g., Juices, soft drinks, sports drinks, sweetened tea) in a baby bottle or no-
spill training cup.
b. Ad libitum breast-feeding after the first primary tooth begins to erupt and other dietary carbohydrates
are introduced.
c. Baby bottle use after 12-18 months.
• Implementing oral hygiene measures no later than the time of eruption of the first primary tooth. Tooth
brushing should be performed for children by a parent twice daily, using a soft toothbrush of age-
appropriate size. In children under the age of three, a smear or rice-sized amount of fluoridated toothpaste
should be used. In children ages three to six, a pea-sized amount of fluoridated toothpaste should be used.
• Providing professionally-applied fluoride varnish treatments for children at risk for ECC.
• Establishing a dental home within six months of eruption of the first tooth and no later than 12 months of
age to conduct a caries risk assessment and provide parental education including anticipatory guidance for
prevention of oral diseases.
• Working with medical providers to ensure all infants and toddlers have access to dental screenings,
counseling, and preventive procedures.
• Educating legislators, policy makers, and third-party payers regarding the consequences of and preventive
strategies for ECC.
Caries risk & risk factors
Introduction
Risk Factor
• An environmental, behavioral or biological which if present directly
increases the probability of disease occurring and if absent or
removed reduces the probability.
Venn Diagram showing
caries risk factors
Caries risk factors include;
• Host-tooth factor and saliva
• Plaque
• Microbes
• Diet(substrate)
• Hereditary/Genetics
1.Host Factors
a)Tooth factor
Morphology and position in arch
• Deep pits and fissures can retain food debris and bacteria,
making them difficult to clean, thereby causing them to be
more susceptible to dental caries.
• The permanent mandibular first molars followed by the
maxillary first molars and mandibular and maxillary second
molars .
• Position of the tooth in the arch has a heavy bearing on the
incidence of carious lesions.
• Irregularities in the arch form, crowding and overlapping of
the teeth also favor the development of caries as these
regions provide an excellent environment for plaque
accumulation.
• Partially impacted third molars are more prone to caries
and so are the buccally or lingually placed teeth.
lower anterior crowding
Chemical nature
• Dicalcium phosphate dihydrate and fluorapatite make
the enamel resistant to carious attack to a certain
extent.
• The presence of mineral ions such as Ca, F, Zn and Fe in
higher concentrations, decreases the enamel solubility.
• Higher the solubility of the enamel surface greater is
the possibility of caries development. Hence, they can
be seen in case of enamel hypoplasia.
• The mineral content of enamel tends to increase with
advancing age. Such teeth have an increased resistance
to carious attack.
b)Saliva
Flow rate
• Adults have rates of 1-1.5 ml/ minute, values below 0.7 ml/minute
are low an indicate risk for caries
• In children the values depend on age and cooperation.
• Preschoolers have secretion rates of 0.5 ml for stimulated and 0.3ml/
min for unstimulated saliva.
• An unstimulated rate of 0.1ml/min is considered a risk value.
pH and Buffering capacity
• The buffer capacity of both unstimulated and
stimulated saliva involves three major buffer systems:
i. the bicarbonate (HCO−3), (6.1-6.3)pH
ii. the phosphate, and the (6.8-7.0)pH
iii. protein buffer systems.
• The bicarbonate is the main system
• pH should be above 5.5 (critical pH) below which
there is higher risk of caries
Viscosity
• Increased viscosity of saliva may hinder its natural
cleansing action thereby promoting the deposition of
plaque on the tooth surface.
• Likewise when the salivary viscosity is low, the
amount of minerals and bicarbonates are inadequate
thereby limiting its anticaries activity.
2.Microbes
• The main etiological agent in occlusal and pit and fissure caries is the
S. mutans. Deep dentinal caries is commonly associated with
lactobacilli, certain gram-positive anaerobes and filaments such as
Eubacterium and Actinomyces.
• Root caries or cemental caries is predominantly associated with
Actinomyces viscosus. However other species of Actinomyces such as
A. naeslundii and A. nocardia have also been isolated.
3.Diet(substrate)
• The cariogenicity of a dietary carbohydrates varies
with frequency of intake, physical form, chemical
composition, route of administration and presence of
other food constituents
• Frequency of in-between meal snacks
• Frequent ingestion of sucrose even when with a
relatively low conc. of 1.25%.
• Solid and sticky form is more harmful
• Monosacchrides and disacchrides are more
harmful(easily fermantable)
4. Plaque
• Important to estimate
a) the number of surfaces affected
b) the amount of plaque accumulated
c) whether its presence is associated with carious lesions in those
same sites.
• Conditions that compromise the long term maintenance of good oral
hygiene are associated positively with caries risk.
5. Hereditary
• Racial characteristics predispose particular groups to
dental caries.
• Fissure pattern varies among populations as well as
within racial groups rendering teeth more or less
susceptible to dental caries.
Risk Indicators
• A factor or circumstance that is indirectly associated with the disease.
• Caries risk indicators include:
1. Past caries experience
2. Exposure to fluoride
3. Socioeconomic status
4. Chronic systemic diseases
1.Past caries incidence
• A strong predictor of future caries experience caries is past caries
experience
• A dental chart and history are important to assess attendance, how
often restorations and re-restorations have been required, and
whether teeth have been lost due to caries.
2.Exposure to flouride
• Use of fluorides can be considered as one of the most protective
factors when assessing patient’s caries risk.
• Fluoride exerts its anticariogenic effect predominantly by
becoming incorporated into the crystals in the dental hard
tissues making the enamel more resistant to the acid attack on
tooth surfaces.
• Fluoride decreases the solubility of enamel, promotes
remineralization and decreases acid generation by plaque
• All sources of fluoride exposure should be considered.
• Whether fluoride exposure has arrested the appearance or
progression of incipient caries lesions over time should be noted.
• If new lesions have appeared or existing lesions have progressed,
then the patients fluoride exposure may be inadequate
3. Socio-economic status
• It is a stronger predictor of caries risk in children (than in adults) as
individuals living in severe socioeconomic conditions often tend to
develop more lesions than those having a better situation.
4. Chronic Systemic Diseases
• The greatest caries risk is associated with conditions particularly
Sjogren’s syndrome
• Other systemic and chronic diseases that cause salivary gland
hypofunction and xerostomia and are thereby regarded as risk factors
e.g.. Early onset diabetes
IMPORTANCE OF SALIVA IN CARIES PREVENTION
a) Clears cariogenic foods from the mouth
b) Buffering power-prevents PH in plaque from falling to low levels
c)Secondary mineralization
d)Serves as a vehicle for fluoride
e)IgA in saliva prevents bacterial species from colonizing plaque
Key Risk Age Groups
Key-risk age group 1: Ages 1 to 2 years
• Studies by Kohler et al (1978,1982) showed that
mothers with high salivary mutans streptococci levels
frequently transmit mutans streptococci to their
babies as soon as the first primary teeth erupt,
leading to greater development of caries
• It was also shown that the practice of giving infants
sugar containing drinks in nursing bottles at night
increases the development of caries (Wendt and
Birkhed, 1995).
Key-risk age group 2: Ages 5 to 7 years
• In a study by Carvalho et al (1989), plaque reaccumulation was heavy
on the occlusal surfaces of erupting maxillary and mandibular molars,
particularly in the distal and central fossae
Key-risk age group 3: Ages 11 to 14 years
• Normally, the second molars start to erupt at the age
of 11 to 11 1/2 years in girls and at around the age of
12 years in boys(eruption time is 16- 18 mon.)
• During this period, the approximal surfaces of the
newly erupted posterior teeth are most caries
susceptible
Key-risk age groups in young adults and adults
• Under certain circumstances, young adults (19 to 22 year olds) may
also be regarded as a risk age group.
• Most have erupting or newly erupted third molars without full
chewing function and with highly caries-susceptible fissures
Caries Risk Assessment
• Is the determination of the likelihood of the incidence of caries (ie,
the number of new cavitated or incipient lesions) during a certain
time period.
or
• the likelihood that there will be a change in the size or activity of
lesions already present. With the ability to detect caries in its earliest
stages (ie, white spot lesions), health care providers can help prevent
cavitation
Caries risk assessment tools
American Academy of Pediatric Dentistry Caries-risk Assessment Tool
•THANK YOU

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1 - ECC, Nursing Caries and Rampant Caries.pptx

  • 1. Early Childhood Caries, Nursing Caries and Rampant Caries Group A BDS 02/18 BDS 03/18 BDS 09/18
  • 2. Outline • Introduction • Early Childhood caries • Nursing Caries • Rampant Caries • Diagnosis of caries • Management of Caries in Pediatric patients • Prevention strategies
  • 3. Introduction • The WHO Global Oral Health Status Report (2022) estimated that oral diseases affect close to 3.5 billion people worldwide, with 3 out of 4 people affected living in middle-income countries. • Globally, an estimated 2 billion people suffer from caries of permanent teeth and 514 million children suffer from caries of primary teeth. • Dental caries is a microbial disease of the calcified tissues of the teeth, characterized by demineralization of the inorganic portion and destruction of the organic substance of the tooth. • The World Health Organization (WHO) defines caries as a localized post- eruptive, pathological process of external origin involving softening of the hard tooth tissue and proceeding to the formation of a cavity.
  • 4. Early Childhood Caries Definition • Early childhood caries (ECC) is defined as the presence of one or more decayed (noncavitated or cavitated), missing (as a result of caries), or filled tooth surfaces in any primary tooth in a child 71 months of age or younger. (American Academy of Pediatric Dentistry (AAPD) (Adopted in 2003, Revised in 2007, 2008).
  • 5. History • Dr. Ellias Fass, 1962 – 1st published comprehensive description of caries in infants and termed as “ Nursing bottle caries”. • In 1978, the American Academy of Pedodontics released “Nursing Bottle Caries”, a joint statement with the American Academy of Pediatrics, to address a severe form of caries associated with bottle usage. • Initial policy recommendations were limited to feeding habits.
  • 6. • Over the next 2 decades, however, recognizing that this distinctive clinical presentation was not consistently associated with poor feeding practices and that caries was an infectious disease, AAPD adopted the term “early childhood caries” (ECC) to reflect better multifactorial etiology. • Current definition of ECC was released by AAPD in 2002.
  • 7. Severe ECC • AAPD specifies that, in children younger than 3 years of age, any sign of smooth-surface caries is indicative of severe early childhood caries (S-ECC) • From ages 3 through 5, 1 or more cavitated, missing (due to caries), or filled smooth surfaces in primary maxillary anterior teeth; or • a decayed, missing, or filled score of ≥4 (age 3), ≥5 (age 4), or ≥6 (age 5) surfaces also constitutes S-ECC
  • 8. Classification of ECC by Wayne Type I (mild to moderate) • Isolated caries lesions involving molars and incisors • Cause is a combination of cariogenic semi-solid or solid food and poor oral hygiene • Seen in 2-5 years old Type II (moderate to severe) • Labiolingual carious lesion affecting maxillary incisors-with or without the molars depending on age • Mandibular incisors are not affected • Cause is use of feeding bottle or at will breast feeding or a combination of both with or without poor oral hygiene • Seen soon after eruption of teeth Type III (severe) • Carious lesion involve almost all the teeth including mandibular incisors • Usually seen in 3-5 years of age • Cause is a combination of factors and a poor oral hygiene • Rampant in nature and involves immune tooth surface
  • 9. TYPE I TYPE II TYPE III
  • 10. Clinical & Radiographic examples of ECC
  • 11.
  • 12. Nursing Caries • Nursing caries is a unique pattern of dental caries in very young children due to prolonged and improper feeding habits
  • 13. Etiologic agents • Bovine milk, milk formula and human breast milk have all been implicated due to their lactose content • Juices, honey dipped pacifiers have also been implicated • Basic mechanism of caries initiation is same however; so all the 4 variables-pathogenic micro-organisms, substrates, host factor(tooth) and time are essential in causing demineralization
  • 14. 1. Pathogenic micro organism • Streptococcus mutans is the principal organism that colonizes the tooth after it erupts into the oral cavity • Transmitted to infants mouth from mother • It is considered more virulent for the following reasons • It colonizes the teeth • It produces large amount of acid • It produces large amount of extracellular polysaccharides which favour plaque formation • S.mutans is more commonly evident in rapid and smooth surface caries and less common in pit and fissure caries
  • 15. 2. Substrate-fermentable carbohydrate • Carbohydrates are utilized by microorganisms to form dextrans which; • Adhere organisms to tooth surface • Cause organic acid to demineralize the tooth • In infants and toddlers the main sources of carbohydrates are 1. Bovine milk and formula 2. Human milk 3. Fruit juices 4. Sweet syrups e.g.. Vitamin preparations 5. Pacifiers dipped in honey or sugar solution 6. Sweets and chocolate
  • 16. 3. Host • Teeth act as the host of the microorganism • Hypomineralization or hypoplasia-increases susceptibility • Thin enamel of deciduous teeth make the spread of lesions faster • Developmental grooves acts as plaque retentive areas. 4. Time • The more time baby is asleep with the bottle in the mouth there is higher risk as salivary flow rates decrease
  • 17. Clinical features It affects the primary teeth in the following sequence • Maxillary central • Maxillary lateral • Maxillary first molars • Maxillary canine and second molars • Mandibular molars at later stage • Mandibular anterior teeth are usually spared because of protection from the tongue and the proximity of lingual gland saliva ducts
  • 18.
  • 20. Implications • Increased risk of developing caries in permanent dentition • Child at risk of other health hazards • Financial burden to parents
  • 21. Rampant Caries • There is no complete agreement on the definition of rampant caries or on its clinical picture. • Rampant caries has been defined by Massler as a “suddenly appearing, widespread, rapidly burrowing type of caries, resulting in early involvement of the pulp and affecting those teeth usually regarded as immune to ordinary decay.”
  • 22. • There is no evidence that the mechanism of the decay process is different in rampant caries or that it occurs only in teeth that are malformed or inferior in composition. • On the contrary, rampant caries can occur suddenly in teeth that were previously sound for many years. • The sudden onset of the disease suggests that an overwhelming imbalance of the oral environment has occurred, and some factors in the caries process seem to accelerate it so that it becomes uncontrollable.
  • 23. Etiology • Rampant caries is multifactorial in etiology • Its not limited to poor feeding habits like nursing caries • Poor salivary flow • Systemic conditions e.g.. Sjogren’s, immunodeficiency • Genetic factors-predisposition • There is considerable evidence that emotional disturbances may be a causative factor in some cases of rampant caries.
  • 24. Clinical features • Rampant caries occurs rapidly • There is therefore early pulpal involvement • Surfaces considered to be ‘immune’ are also affected e.g.. Mandibular incisors (as opposed to nursing caries) • Young teenagers seem to be particularly susceptible to rampant caries, although it has been observed in both children and adults of all ages
  • 25.
  • 26. Davies believed that rampant caries should be coined to a condition where… • Lesions are more than 10 • High caries experience for the child age • Sudden characteristic feature • Caries developing in otherwise immune surfaces • Extensive loss of tooth structure (particularly dentin) even though enamel shows little defect • Soft, mustly, ivory coloured dentin consistency indicating rapid progession of disease
  • 27. Diagnosis of Caries • The process of diagnosing all these carious conditions is dependent on proper history taking and examination • This may be sufficient in some cases but in others diagnostic aids will be needed e.g.. radiographs
  • 28. • Visual-tactile-radiographic has been the traditional sequence used by most clinicians • This procedure involves the visual identification of demineralized areas (typically white spots) or suspicious pits or fissures • Also involves use of the dental explorer to determine the presence of a loss of continuity or breaks in the enamel and assess the softness or resilience of the enamel. • Interproximal caries has generally been detected with the use of bite-wing radiographs.
  • 29. Other Developments… • Fiber-optic Trans illumination • Electric Resistance Measurement • Ultrasonics • Dyes
  • 30. Management of Caries in Pediatric Patients Management carried out in phases with the following Treatment aims: • To deal with any existing emergency • To Arrest and control disease progression; and institute preventive measures • To restore all carious lesions
  • 31. Emergency phase • Management of any existing emergency: pain and infection a) Pain-prescribe analgesics, teeth needing immediate attention should be extirpated b) Infection-Drainage of abscess and prescription of anti-biotics to manage infections
  • 32. Prevention & Arrest of Disease process. • After the emergency has been taken care of the clinician should start instituting prevention measures to limit further disease progression • Measures to arrest disease process are key • An individualized caries risk assessment is an important step in the management • It aims to modify the risk factors
  • 33. • Oral Hygiene Instruction and Motivation should be done • Parents should be asked to wean off the child from using a bottle while in bed. • In case of considerable emotional dependence on the bottle, suggest the use of plain water. • Parents are instructed to brush child’s teeth last thing at night with fluoride toothpaste • For children aged 3-6 years, chair-side topical fluoride varnish (2.2% F) application to teeth should be carried out
  • 34. Stabilization of carious process • If the carious lesion is arrested, it should be monitored to ascertain that it remains in non-progressive stage until exfoliation. • For non-cavitated proximal enamel lesions, a resin infiltration system used in conjunction with fluoride therapy can be used to control caries progression • Pits and fissure sealants where necessary/indicated
  • 36. • Teeth that require temporization are excavated with spoon excavators and glass ionomer cement is used to seal the teeth. • Temporization by sealing of the carious cavity after caries removal reduces the load of bacterial colonization in tooth
  • 37. Restorative Phase • During this phase restorative procedures are perfumed and completed i.e. simple fillings, pulp capping, pulpotomies, pulpectomies and stainless steel • Therefore ALL carious tissue has to be removed and final restorative materials placed • In young children with high risk of caries, there is good evidence that stainless steel crowns function better than multi-surface intra-oral restorations.
  • 38. How about for non-restorable teeth? • Extraction should be perfumed for teeth that can not be restored, followed by space maintainer fabrication where appropriate • Clinicians should try as much as possible to avoid extractions on the child’s first visit
  • 39. A, Restorable with resins. B, Restorable with crown forms (possibly). C, Nonrestorable.
  • 40. Maintenance Phase • Patients must be reviewed to detect any changes and check status of the restorations • Recall intervals are based on the outcome of their caries risk assessment: a) Patients with obvious signs of active oral disease or its predisposing factors should be reviewed at 3 monthly intervals until well controlled b) Recall visit of low caries risk children;6 months and should not exceed 12 months.
  • 41. Prevention strategies-AAPD Recommendations • Avoiding frequent consumption of liquids and/or solid foods containing sugar, in particular: a. Sugar-sweetened beverages (e.g., Juices, soft drinks, sports drinks, sweetened tea) in a baby bottle or no- spill training cup. b. Ad libitum breast-feeding after the first primary tooth begins to erupt and other dietary carbohydrates are introduced. c. Baby bottle use after 12-18 months. • Implementing oral hygiene measures no later than the time of eruption of the first primary tooth. Tooth brushing should be performed for children by a parent twice daily, using a soft toothbrush of age- appropriate size. In children under the age of three, a smear or rice-sized amount of fluoridated toothpaste should be used. In children ages three to six, a pea-sized amount of fluoridated toothpaste should be used. • Providing professionally-applied fluoride varnish treatments for children at risk for ECC. • Establishing a dental home within six months of eruption of the first tooth and no later than 12 months of age to conduct a caries risk assessment and provide parental education including anticipatory guidance for prevention of oral diseases. • Working with medical providers to ensure all infants and toddlers have access to dental screenings, counseling, and preventive procedures. • Educating legislators, policy makers, and third-party payers regarding the consequences of and preventive strategies for ECC.
  • 42. Caries risk & risk factors
  • 43. Introduction Risk Factor • An environmental, behavioral or biological which if present directly increases the probability of disease occurring and if absent or removed reduces the probability.
  • 44. Venn Diagram showing caries risk factors Caries risk factors include; • Host-tooth factor and saliva • Plaque • Microbes • Diet(substrate) • Hereditary/Genetics
  • 45. 1.Host Factors a)Tooth factor Morphology and position in arch • Deep pits and fissures can retain food debris and bacteria, making them difficult to clean, thereby causing them to be more susceptible to dental caries. • The permanent mandibular first molars followed by the maxillary first molars and mandibular and maxillary second molars . • Position of the tooth in the arch has a heavy bearing on the incidence of carious lesions. • Irregularities in the arch form, crowding and overlapping of the teeth also favor the development of caries as these regions provide an excellent environment for plaque accumulation. • Partially impacted third molars are more prone to caries and so are the buccally or lingually placed teeth.
  • 47. Chemical nature • Dicalcium phosphate dihydrate and fluorapatite make the enamel resistant to carious attack to a certain extent. • The presence of mineral ions such as Ca, F, Zn and Fe in higher concentrations, decreases the enamel solubility. • Higher the solubility of the enamel surface greater is the possibility of caries development. Hence, they can be seen in case of enamel hypoplasia. • The mineral content of enamel tends to increase with advancing age. Such teeth have an increased resistance to carious attack.
  • 48. b)Saliva Flow rate • Adults have rates of 1-1.5 ml/ minute, values below 0.7 ml/minute are low an indicate risk for caries • In children the values depend on age and cooperation. • Preschoolers have secretion rates of 0.5 ml for stimulated and 0.3ml/ min for unstimulated saliva. • An unstimulated rate of 0.1ml/min is considered a risk value.
  • 49. pH and Buffering capacity • The buffer capacity of both unstimulated and stimulated saliva involves three major buffer systems: i. the bicarbonate (HCO−3), (6.1-6.3)pH ii. the phosphate, and the (6.8-7.0)pH iii. protein buffer systems. • The bicarbonate is the main system • pH should be above 5.5 (critical pH) below which there is higher risk of caries
  • 50. Viscosity • Increased viscosity of saliva may hinder its natural cleansing action thereby promoting the deposition of plaque on the tooth surface. • Likewise when the salivary viscosity is low, the amount of minerals and bicarbonates are inadequate thereby limiting its anticaries activity.
  • 51. 2.Microbes • The main etiological agent in occlusal and pit and fissure caries is the S. mutans. Deep dentinal caries is commonly associated with lactobacilli, certain gram-positive anaerobes and filaments such as Eubacterium and Actinomyces. • Root caries or cemental caries is predominantly associated with Actinomyces viscosus. However other species of Actinomyces such as A. naeslundii and A. nocardia have also been isolated.
  • 52. 3.Diet(substrate) • The cariogenicity of a dietary carbohydrates varies with frequency of intake, physical form, chemical composition, route of administration and presence of other food constituents • Frequency of in-between meal snacks • Frequent ingestion of sucrose even when with a relatively low conc. of 1.25%. • Solid and sticky form is more harmful • Monosacchrides and disacchrides are more harmful(easily fermantable)
  • 53. 4. Plaque • Important to estimate a) the number of surfaces affected b) the amount of plaque accumulated c) whether its presence is associated with carious lesions in those same sites. • Conditions that compromise the long term maintenance of good oral hygiene are associated positively with caries risk.
  • 54. 5. Hereditary • Racial characteristics predispose particular groups to dental caries. • Fissure pattern varies among populations as well as within racial groups rendering teeth more or less susceptible to dental caries.
  • 55. Risk Indicators • A factor or circumstance that is indirectly associated with the disease. • Caries risk indicators include: 1. Past caries experience 2. Exposure to fluoride 3. Socioeconomic status 4. Chronic systemic diseases
  • 56. 1.Past caries incidence • A strong predictor of future caries experience caries is past caries experience • A dental chart and history are important to assess attendance, how often restorations and re-restorations have been required, and whether teeth have been lost due to caries.
  • 57. 2.Exposure to flouride • Use of fluorides can be considered as one of the most protective factors when assessing patient’s caries risk. • Fluoride exerts its anticariogenic effect predominantly by becoming incorporated into the crystals in the dental hard tissues making the enamel more resistant to the acid attack on tooth surfaces. • Fluoride decreases the solubility of enamel, promotes remineralization and decreases acid generation by plaque • All sources of fluoride exposure should be considered.
  • 58. • Whether fluoride exposure has arrested the appearance or progression of incipient caries lesions over time should be noted. • If new lesions have appeared or existing lesions have progressed, then the patients fluoride exposure may be inadequate
  • 59. 3. Socio-economic status • It is a stronger predictor of caries risk in children (than in adults) as individuals living in severe socioeconomic conditions often tend to develop more lesions than those having a better situation.
  • 60. 4. Chronic Systemic Diseases • The greatest caries risk is associated with conditions particularly Sjogren’s syndrome • Other systemic and chronic diseases that cause salivary gland hypofunction and xerostomia and are thereby regarded as risk factors e.g.. Early onset diabetes IMPORTANCE OF SALIVA IN CARIES PREVENTION a) Clears cariogenic foods from the mouth b) Buffering power-prevents PH in plaque from falling to low levels
  • 61. c)Secondary mineralization d)Serves as a vehicle for fluoride e)IgA in saliva prevents bacterial species from colonizing plaque
  • 62. Key Risk Age Groups Key-risk age group 1: Ages 1 to 2 years • Studies by Kohler et al (1978,1982) showed that mothers with high salivary mutans streptococci levels frequently transmit mutans streptococci to their babies as soon as the first primary teeth erupt, leading to greater development of caries • It was also shown that the practice of giving infants sugar containing drinks in nursing bottles at night increases the development of caries (Wendt and Birkhed, 1995).
  • 63. Key-risk age group 2: Ages 5 to 7 years • In a study by Carvalho et al (1989), plaque reaccumulation was heavy on the occlusal surfaces of erupting maxillary and mandibular molars, particularly in the distal and central fossae
  • 64. Key-risk age group 3: Ages 11 to 14 years • Normally, the second molars start to erupt at the age of 11 to 11 1/2 years in girls and at around the age of 12 years in boys(eruption time is 16- 18 mon.) • During this period, the approximal surfaces of the newly erupted posterior teeth are most caries susceptible
  • 65. Key-risk age groups in young adults and adults • Under certain circumstances, young adults (19 to 22 year olds) may also be regarded as a risk age group. • Most have erupting or newly erupted third molars without full chewing function and with highly caries-susceptible fissures
  • 66. Caries Risk Assessment • Is the determination of the likelihood of the incidence of caries (ie, the number of new cavitated or incipient lesions) during a certain time period. or • the likelihood that there will be a change in the size or activity of lesions already present. With the ability to detect caries in its earliest stages (ie, white spot lesions), health care providers can help prevent cavitation
  • 67. Caries risk assessment tools American Academy of Pediatric Dentistry Caries-risk Assessment Tool
  • 68.