3. • Pulp therapy for young permanent teeth:
Apexogenesis (vital pulpotomy):
• Indications:
1. Treatment of young permanent teeth with
carious exposures.
2. Exposed teeth with no symptoms of painful
pulpitis.
3. Pulp exposure resulting from crown fracture.
4. Permanent teeth with immature root
development but with healthy pulp tissue.
3
4. • The goal of apexogenesis is to maintain the
radicular pulp vital to allow the complete
development of the root. Calcium hydroxide
placed directly on the radicular pulp stump
stimulates a calcific response immediately
adjacent to it, which is seen later on as a
radiographic "bridge" over the amputation site.
If degenerative and irreversible coronal pulp
changes have not progressed into the radicular
pulp, successful root closure can progress to
completion. So, a periodic radiograph should be
taken to confirm that no pathologic periapical
changes are present, also periodic clinical
evaluation is mandatory.4
6. Apexification (Root end closure in non vital
tooth):
If a young permanent tooth has a pulp with
extensive degeneration or necrosis throughout,
the pulp should be totally debribed and the
canal treated with calcium hydroxide.
Apexification is used to promote root
elongation and/or a calcific root closure. Even
though the pulp has been necrotic and is
removed, Hertwig's epithelial root sheath is
tough to persist and be capable of generating
the response.
6
8. • A conventional endodontic procedure is done
after apexification is complete. In
apexification, the entire pulp contents are
removed to the level of the radiographic apex,
using endodontic broaches & files. Calcium
hydroxide is placed at the apical end of the
radicular canal. The Ca (OH)2 gradually
washes out; therefore, it must be replaced
every several months until apical closure
occurs.
8
10. • There is no complete agreement on the
definition of rampant caries or on the clinical
picture of this condition. 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.
10
12. • The distinguishing characteristics of rampant
caries are the involvement of proximal surfaces
of the lower anterior teeth and development of
cervical type of cavities. 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. Some factor in the caries process
seems to accelerate the process to the extent that
it becomes uncontrollable and it is then referred
to as rampant caries.
12
13. • When a patient has what is considered an
excessive amount of teeth decay, it must be
determined whether that person actually has a
high susceptibility and truly rampant caries of
sudden onset or the oral condition represents
years of neglect and inadequate dental care.
The term rampant caries should be applied to a
caries rate of 10 or more new lesions/year.
13
14. • Etiology:
There is considerable evidence that emotional
disturbances may be the causative factor in some
cases of rampant caries. Depressed emotions and
fears, dissatisfaction with achievement, rebellion
against a home situation, a feeling of inferiority,
traumatic school experience and continuous
general tension and anxiety have been observed in
children and adults who have rampant caries.
14
15. • An emotional disturbance may initiate an
unusual craving for sweets or the habit of
snacking, which might in turn influence the
incidence of dental caries. On the other hand, a
noticeable salivary deficiency is common in
tense, nervous or disturbed persons. Some
believe that rampant caries is attributable to
primary and secondary nutritional inadequacies.
However, it is not a deficiency disease or one
associated with malnutrition.
15
16. • There are sufficient clinical and laboratory
findings to indicate that sucrose is more likely
to cause rampant multi surface cavitation this
is related to high molecular weight dextrans
that are formed during the metabolism of
sucrose by streptococcus mutans.
16
18. • Terminology:
The most commnonly used name is
"Nursing-Bottle Caries". Other names mentioned
in the literatures are; Baby-bottle caries, Nursing
bottle syndrome, Baby-bottle tooth decay,
Nursing caries and recently Early Childhood
Caries.
• Definition:
It is a specific pattern of rampant caries
affecting the primary teeth of an infant during
the first three years of age.
18
19. • Etiology:
1. Inappropriate nursing habits, involving either
the breast or the bottle-feeding.
2. The regular use of a sweetened comforter (a
bottle containing sweet beverages of any kind or
breast-feeding at night) at bedtime and/or
during the day.
3. Breast-feeding prolonged beyond the normal
age for weaning.
4. Falling asleep with pacifier covered with honey
or jam.
5. The regular use of syrups for therapeutic
reasons during chronic or recurring illnesses.19
20. • Mechanism:
When the child falls asleep, the milk or the
sweetened liquid becomes pooled around the
maxillary anterior teeth. The carbohydrate
containing liquid provides an excellent media for
acidogenic bacteria (S.mutans and Lactobacilli).
As salivary flow is decreased during sleep, the
clearance of the liquid from the oral cavity is
slowed. The lactose content of the milk (Human
or bovine) can be cariogenic as the milk is
allowed to stagnate on the teeth for long time.
20
21. • Clinical picture:
1. Teeth affected:
The four maxillary incisors are most affected
while the four mandibular incisors usually
remain sound. Probably because the body of the
tongue lies over the lower teeth during sucking
which limits the exposure of the mandibular
incisors to cariogenic substrate.
The other primary teeth, the canines, first
molars and the second molars may exhibit
caries involvement depending upon how long
the carious process remains active, but the
extensiveness of the lesions usually is not as
severe as those of the maxillary incisors.21
23. 2. Clinical pattern:
Initially, the maxillary incisors develop a
band of dull white demineralization along the
gum line that goes undetected by the parents.
As the condition progresses, the white lesions
develop into cavities that circle the necks of
the teeth in a brown or black collar. In
advanced cases, the crowns of the four
maxillary incisors may be destroyed
completely leaving decayed brownish-black
root stumps. Conversely, the four mandibular
incisors remain unaffected.
23
24. • The reason for the unique distribution of
caries between the maxillary and mandibular
incisors and the unequal severity of the
lesions between the incisors and the other
teeth is related to three factors:
A. The chronology of primary teeth eruption.
B. The muscular pattern of infant sucking.
C. The duration of the deleterious habit.
24
25. • Developmental stages:
I. Initial stage:
Cervical opaque, chalky white
demineralization of the tooth substances.
Pain is not felt at this stage.
25
26. II. Damaged stage:
The carious lesion extends into the dentin
and shows marked discoloration on the
labial, lingual and inter-proximal surfaces.
Parents can spot the condition at this stage
due to the discoloration of the teeth and the
child starts complaining about toothache
when cold foods are ingested.
26
27. III. Deep lesion stage:
Lesions in the maxillary incisors are larger
and the first primary molars are all
affected.
Complaints of pain during tooth brushing
or eating, especially when biting is
frequent.
Pulpal problems in the maxillary incisors
can occur (spontaneous pain during the
night; and pain after cold or hot drinks).
27
28. IV. Traumatic stage:
Maxillary incisors become so weakened
by caries that relatively small forces suffice
to fracture them.
V. Arrested caries:
In all the previous stages arrested caries
might occur, when the cause of the dental
caries is eliminated. The lesions might get a
dark brown to black appearance.
28
29. • Management of Early Childhood Caries:
Prevention.
Treatment.
29
30. A. Prevention of Early Childhood Caries:
There are three general approaches that
should be followed to prevent Early
Childhood Caries.
I. Community-based strategy:
Which relies on:
1. National educational program for mothers and
caregivers to influence their dietary habits as
well as those of their infants.
2. Personal and community preventive
programs.
3. Water fluoridation.
30
31. II. Professional examination and preventive care
in the dental clinic:
1. Early dental examination at or before the age
of 1 year.
2. Parents counseling:
A. From birth, the infant should be held while
feeding.
B. The child who falls asleep while nursing
should be burped and then placed in bed.
31
32. C. The mother should wean the child as soon
as he can drink from a cup at approximately
12-15 months of age.
D. Parents should be cautioned about
prolonged and frequent infant feeding
habits.
3. Professional application of topical fluoride,
chlorohexidine varnishes and fissure sealant.
32
33. III. Development of appropriate dietary and
self-care habits at home:
1. Oral hygiene.
2. Uses of fluoride supplements (according to
area need).
3. Uses of fluoridated dentifrice.
4. Dietary habits.
33
34. B. Treatment of Early Childhood Caries:
The treatment of children with Early
Childhood Caries depends upon the extent
of the lesions, the age and the behavior of
the child, and the degree of the cooperation
of the parents. Regardless these factors, the
steps in treating the child is divided into:
I. Cessation of habit.
II. Sealing all caries-free pits and fissures.
III. Fluoride application.
34
35. IV. Gross excavation of carious lesions and filling
of the cavities with zinc oxide-eugenol or
glass-ionomer cement. This will arrest the
caries process and prevent its rapid
progression to the dental pulp.
V. Pulp therapy and buildups of restorable teeth.
This may involve compomer, composite filling
and stainless steel crowns.
VI. Treatment under general anesthesia is often
required for small children with extensive
carious lesions.35