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Case 56

Rapid breakdown of first

permanent molars
A 7-year-old boy presents with first permanent molar
teeth which his parents say have decayed rapidly,
starting immediately on eruption. Identify the cause
and discuss the treatment options.

The child complains of pain from his back teeth on both
sides. The pain is worse with sweet foods and cold liquids
and persists for several minutes after stimuli. Toothbrushing with cold water is also painful but the teeth do not cause
pain on biting.

History of complaint
The pain has been present for a few months and has
increased in severity over the last month. The child now
reports that one of his back teeth feels broken. The first
permanent molars erupted on time and his mother noticed
that some of them appeared to crumble as soon as they
emerged through the gum. She has read in magazines that
fluoride can damage teeth and has switched to a toothpaste
without fluoride on the assumption that this is the cause.

Medical history
The patient is a healthy child, the only history of note being
neonatal jaundice.

Dental history
The child has no experience of operative dental care. A diet
history reveals a reasonably well-balanced diet, with limited
consumption of refined carbohydrates and carbonated
beverages. Toothbrushing has been performed with adultformula fluoride-containing toothpaste, starting at approximately 1 year and continuing until 7 years of age.

Extraoral examination
The child has no facial swelling or asymmetry and no lymph
nodes are palpable.

Intraoral examination

Fig. 56.1 The upper left first permanent molar.

He is in the early mixed dentition stage. All four first permanent molars have areas of brown, rough, irregular
enamel. The severity varies between the teeth and the worst
affected are the maxillary molars whose enamel appears to
be completely absent in some areas. These teeth have soft
dentine exposed occlusally. The lower right first permanent
molar is the least severely affected with only a small localized brown enamel defect on the buccal aspect. This is hard
on probing. In addition, there are areas of white enamel
opacity in the incisal third of the labial surface of all permanent central and lateral incisors, which are most pronounced
in the maxillary central incisors. The remaining primary
dentition is caries free, and appears normal in structure and
morphology. Oral hygiene appears good. The appearances
of the dentition are shown in Figures 56.1 and 56.2.

On the basis of what you know already, what do you

Fig. 56.2 The central incisors.

The defects appear to be hypoplasia or hypomineralization of

the enamel which has either become carious or taken up




Rapid b r e a k d o wn o f f i r s t p e r m an e n t m o la r s
extrinsic stains. The molars are so severely affected that
diagnosis is difficult, but the opaque white zones on the
central incisors are characteristic of enamel hypoplasia.
Hypoplasia is the result of reduced ameloblast numbers or
activity. Enamel is missing so that the surface contour is
abnormal. A hypomineralized enamel usually has normal
contour initially but is softer than normal and may be worn

Differential diagnosis
What is the likely cause of the childs pain?
The hot and cold sensitivity is characteristic of pain mediated
by a vital pulp. It could be a result of caries in the dentine or
exposed occlusal dentine. Molarincisor hypoplasia is
frequently associated with pain and sensitivity.

What is your initial differential diagnosis for the enamel

Do the enamel defects follow a chronological pattern, and

if so, at what time was the affected enamel formed?


Almost, the incisal and occlusal parts of the permanent

central incisors and first molars form at about the same time,
starting to mineralize just before birth. The affected enamel
would have been formed after birth and during the first 12
years of life. This may be seen by consulting Figure 56.3.

Dental caries is the commonest cause of destruction of first

permanent molars and should be considered, even though
the appearances would be very unusual. Enamel hypoplasia is
more likely and developmental, acquired, generalized and
localized forms are recognized. The most likely cause is
enamel hypoplasia due to neonatal illness. Other causes
which might be considered are amelogenesis imperfecta,
fluorosis and cytotoxic chemotherapy for malignant disease.
In many cases no cause is found and the term idiopathic
enamel hypoplasia is used.

This distribution of hypoplasia is often referred to as molar

incisor hypoplasia. There is some evidence that molar-incisor
hypoplasia is not completely chronological. The occlusal and
buccal surfaces tend to be worst affected. Canines and
premolars are unaffected despite mineralizing at the same
time. Defects may be asymmetrical and enamel loss may be a
secondary phenomenon.

What additional questions would you ask, and why?

A chronological pattern suggests systemic illness which may
be identifiable in the history. Defining a possible cause may
allow others such as fluorosis to be excluded. You need to ask
further details about the prenatal and perinatal medical
history. The following conditions may be relevant and should
be specifically sought:
Preterm birth or low birth-weight baby
Rhesus incompatibility
Intubation as neonate
Maternal vitamin D deficiency.
These disturbances may manifest as enamel defects
distributed along the enamel formed around birth. You
should also enquire about all severe systemic disturbances in
the first 2 years of life, for example meningitis, encephalitis,
severe measles or pneumonia. Even relatively minor fevers or
infections, such as ear infections, are known to be associated
with similar enamel defects.

Justify this differential diagnosis.

Dental caries is the commonest cause of destruction
of the dental hard tissues. Newly erupted teeth are
particularly prone to dental caries until their enamel
maturation is completed in the oral environment. First
permanent molars are also prone to early caries because
of their deep fissures. However the possibility of caries
seems unlikely. Although there is no guarantee that the
diet history elicited is truly representative of the childs actual
diet, there are no restorations or caries in the deciduous
dentition. The molars have discoloured or absent enamel over
a wide area. This is not typical of dental caries unless
carbohydrate intake is excessive or the teeth have some other
predisposing factor such as enamel hypoplasia. The soft
dentine indicates that some caries is present but the pattern
of destruction suggests that this caries is secondary. The
zones of opacity on the incisors look like early white spot
demineralization but are at a site that is almost never affected
by caries.
Enamel hypomineralization and/or hypoplasia is the
most common developmental disorder observed in teeth.

Fig. 56.3 Time of mineralization of the

permanent dentition.









Rapid b r e a k d o wn o f f i r s t p e r m an e n t m o la r s


This child has a generalized defect with a chronological

pattern. The history of neonatal jaundice deserves some
consideration. It is capable of affecting amelogenesis but
rarely causes clinically evident hypoplasia and then only in
very severely affected individuals. Neonatal jaundice is a very
common condition and in almost all cases can be excluded
as a cause of enamel hypoplasia. In this child the position of
the enamel defects is inconsistent with a short period of
jaundice at birth.
Fluorosis where it is endemic is a common cause of enamel
opacities and enamel hypoplasia. The deciduous dentition is
usually much more mildly affected. The level of fluoride
required to cause enamel defects depends on concentration,
period and age of ingestion.
Fluorosis is almost certainly not the cause of the current
problem. The defects in the molars would result from only
very high fluoride concentrations, in excess of 25 parts per
million (p.p.m.). Such levels do not occur in the UK. In
addition, fluorosis of this severity is endemic and should not
follow a chronological pattern.
Mild fluorosis may be seen as a result of supplementation and
this is presumably what the parent has read. In such cases
there are usually fine opaque white lines following the
perikymata and small irregular enamel opacities or flecks with
or without staining. Such mild defects are also common in
normal teeth and increase in frequency when the fluoride
level is lower than 0.7 p.p.m. Although the severity of the
defects and distribution are incompatible with the diagnosis
of fluorosis, it needs to be considered because the child has
been using adult-formula fluoride-containing toothpaste from
an early age. Ingestion of adult-formula fluoride toothpaste
would be the most likely cause of mild fluorosis in the UK.
Amelogenesis imperfecta must be considered even
though it is rare. Amelogenesis imperfecta can cause enamel
hypoplasia, hypocalcification or hypomaturation and either of
the first two conditions could lead to the appearances seen in
the molar teeth. However, several factors indicate that this is
not amelogenesis imperfecta. There appears to be no family
history, the pattern appears chronological rather than
affecting all surfaces of all teeth equally and the deciduous
dentition is unaffected. While these features are not
conclusive because of the wide range of clinical presentations
seen in the many different types of this disease, they do make
the diagnosis most unlikely.
Idiopathic molarincisor hypoplasia is a convenient term
used to describe cases of enamel hypoplasia with this
distribution for which no cause can be ascertained.

What investigations are indicated and why?
Intraoral radiographs are indicated to assess the proximity of
the coronal defects to the dental pulp. A panoramic
tomograph is indicated, to ascertain the presence and stage
of development of the remaining permanent dentition, in
view of the possibly poor long-term prognosis of some of the
first permanent molars. The panoramic tomograph is shown
in Figure 56.4.

Fig. 56.4 Panoramic tomograph.

If there were extensive softening of the occlusal dentine of
the molars or if radiographs indicated deep caries, tests of
vitality would be required.

What does the panoramic tomograph show?

All permanent teeth with the exception of the third
permanent molars are present and the dental age is
consistent with the patients chronological age. The gross
structural defect in the first permanent molars is reflected in
their radiographic appearance. The worst affected teeth the
maxillary molars have irregular enamel outlines and there is
reactionary dentine in the distal pulp horns. The view is
unsuitable for detailed examination of the teeth, but no large
carious lesions are evident and the unerupted permanent
second molars appear to be of normal shape and to have a
normal enamel structure.

What is your diagnosis?
The patient has enamel hypoplasia that does not follow a
completely chronological pattern, and in the absence of a
known insult to account for the defects, idiopathic molar
incisor hypoplasia/hypomineralization is the most appropriate
working diagnosis. The diagnosis may need to be reviewed if
evidence of early illness can be obtained from the general
medical practitioner or if more teeth erupt with similar defects.
The diagnosis is sufficiently accurate to embark on treatment.

What treatment options are available for the molars?
The appropriate treatment for grossly hypoplastic first
permanent molar teeth is extraction, particularly when, as
here, caries is also present. Preservation of these molars
through adulthood would require provision of full-coverage
crowns. These have a finite lifespan and their intermittent
replacement, the risks of undetected leakage, caries and
pulpal involvement, localized periodontitis and the expense
and inconvenience would amount to significant morbidity in
the lifetime of the patient.

When should the molar teeth be extracted?

Timing of the extractions is important and several factors
must be taken into consideration, as shown in Table 56.1.






Rapid b r e a k d o wn o f f i r s t p e r m an e n t m o la r s
Table 56.1 Factors in the timing of extractions


Stage of dental development

Second permanent molars are most likely to erupt passively into a favourable position when there is radiographic evidence of calcification of a small
crescent of interradicular dentine (mineralizing of the furcation). This is the ideal time to extract the first molar and is generally between 8 12 and
10 12 years of age.

Presence of third molars

This must be assessed radiographically. Hard tissue formation should be visible at age 910 years. The crypt may be visible as early as 7 years.

Orthodontic analysis

A complete assessment must be made. The space gained might be utilized for active orthodontic treatment. Extraction of first permanent molars is
rarely ideal for orthodontic purposes and treatment may be complex. If no third molars are present, the need for orthodontic treatment may be critical
in deciding whether or not to extract the first molars.

Table 56.2 Possible restorative options for the incisors




Composite veneers

Not destructive of tooth tissue, reversible and generally well tolerated

even in anxious children.
Excellent cosmetic result possible and easy to maintain.

Discolour with time.

Tendency to fracture if placed at incisal edge.

Enamel microabrasion

Minimal destruction of enamel if carefully performed.

Technique well tolerated.

Unpredictable. Teeth may suffer postoperative sensitivity.

Accidental exposure of dentine is possible where enamel is very thin.

Localized composite restoration

Enamel destruction limited to defect and full thickness need not be

removed if opaque composites used.
Good cosmetic result possible.

Irreversible, weakens tooth structure and large areas of dentine may be uncovered.
Colour change and marginal discolouration with time.

Porcelain veneers

Good appearance

Contraindicated in this age group as gingival contour not mature and stable tooth
position not yet established.

Full crown restoration

Good appearance

Inappropriate until late second decade because immature pulp horns may be exposed.
Gingival contour not mature and stable tooth position not yet established.

How can the molar teeth be preserved until the patient is at

the optimal age for their extraction?
Preformed stainless steel crowns are a durable, cheap and
relatively simple restoration. Laboratory made nickelchrome
onlays have been advocated as a less destructive option,
should it be decided that the teeth are to be retained for full
coronal coverage restorations in later life. A preventive resin
restoration can be provided for the less severely affected
molar in the lower right quadrant.
Molars with molarincisor hypoplasia are often considered
highly sensitive to a variety of stimuli and have a reputation
for being difficult to anaesthetise.

What treatment options are available for the incisor teeth?

The areas of white enamel on the labial surface of the incisor
teeth do not require treatment at this age and they may
become less obvious with time. Should an interim cosmetic
improvement be required in the patients teenage years,

composite veneers applied by hand, with no tooth

preparation, provide a simple and effective solution. The
advantages and disadvantages of the possible restorative
solutions are listed in Table 56.2.

What advice would you give the mother with regard to

The misconception about fluorosis should be dispelled:
fluorosis can only develop while the teeth are forming.
Provided the child can rinse and spit out effectively it would
be appropriate for him to use an adult formulation fluoride
toothpaste. This would provide a significant caries benefit
(and the mother would also gain from using it). No fluoride
supplement is indicated for this child who, at least on the
basis of a preliminary analysis, eats little sugar and has no
caries. There might be a particular advantage in using fluoride
toothpaste during adolescence and early adulthood when
the diet often changes markedly.