REVIEW
Australian Dental Journal 2003;48:(3):156-168
Diagnosis and management of unusual dental abscesses in
children
WK Seow*
Abstract
Although the majority of dental abscesses in children
originate from dental caries or trauma, a few are
associated with unusual conditions which challenge
diagnosis and management. Recent research findings
have shed light on these unusual entities and greatly
improved understanding of their clinical
implications. These conditions include
developmental abnormalities such as dens
invaginatus in which there is an invagination of
dental tissues into the pulp chamber and dens
evaginatus in which a tubercle containing pulp is
found on the external surface of a tooth crown. In
addition, inherited conditions which show abnormal
dentine such as dentine dysplasia, dentinogenesis
imperfecta, and osteogenesis imperfecta predispose
the dentition to abscess formation. Furthermore,
‘spontaneous’ dental abscesses are frequently
encountered in familial hypophosphataemia, also
known as vitamin D-resistant rickets, in which there
is hypomineralization of dentine and enlargement of
the pulp. In addition to developmental conditions,
there are also acquired conditions which may cause
unusual dental abscesses. These include pre-eruptive
intracoronal resorption which was previously
known as ‘pre-eruptive caries’ or the ‘fluoride
bomb’. In addition, some undiagnosed infections
associated with developing teeth are now thought to
be the mandibular infected buccal cysts which
originate from infection of the developing dental
follicles. In the present paper, these relatively
unknown entities which cause unusual abscesses in
children are reviewed with the aim of updating the
general practitioner in their diagnosis and
management.
Key words: Dental abscess, dens invaginatus, dens
evaginatus, hypophosphataemia, pre-eruptive intracoronal
resorption, mandibular infected buccal cyst.
(Accepted for publication 13 March 2003.)
INTRODUCTION
In the paediatric patient, dental abscesses are not
uncommon. Despite the decline in dental caries in past
decades, many young children are still at risk for dental
decay, and pulpal infections from caries are commonly
*School of Dentistry, The University of Queensland, Brisbane.
156
encountered in primary teeth.1 In addition, dental
abscesses resulting from trauma are also encountered in
young children. In most children, these infections
usually present as chronic inflammation which is
localized to the offending tooth. In such cases,
management of localized pulpal infections in the
primary dentition includes root canal treatment or
extraction and space maintenance. On the other hand,
the treatment of a spreading, acute dental abscess
centres on pain control, antibiotics, surgical drainage
and removal of the source of infection, which may
include endodontic treatment or extraction of the
tooth. The antibiotic which is usually used for acute
oral infections in children is oral amoxicillin, usually
prescribed at doses of 20-40mg/kg/day, in three divided
daily doses for five days.2 For the children who are
allergic to penicillin, oral clindamycin at doses of 15-
25mg/kg/day in three or four equal daily doses is an
effective alternative.2 Hospitalization and parenterally-
administered antibiotics may be required for children
who show spread of the dental infection.
However, some pulp infections have unusual origins
which challenge diagnosis and management. Some of
these infections have been referred to ‘spontaneous
abscesses’ because of the lack of apparent aetiological
factors. Many of these unusual abscesses are associated
with developmental anomalies of the teeth, either as a
local aberration of tooth development, or a general
manifestation of systemic conditions. In contrast, other
abscesses are related to acquired conditions such as
those caused by infection of the pulp due to extensive
coronal destruction from pre-eruptive resorption.
Occasionally, an oral abscess may result from infection
of the follicle of a developing tooth through infection of
the operculum or pericoronitis. As many of these
unusual dental abscesses are associated with developing
or newly erupted teeth, they are usually encountered in
children.
As the prevention of dental abscesses plays a central
role in the management of these unusual entities, it is
useful for the clinician to be aware of their clinical
implications and the methods of abscess prevention.
Recent research on these unusual conditions has greatly
improved the understanding of their aetiology and
Australian Dental Journal 2003;48:3.
Table 1. Developmental and acquired conditions associated with dental abscesses in children
Developmental
Abnormal morphology of crown
• Dens invaginatus
• Dens evaginatus
Abnormal structure of dentine
• Dentine dysplasia (Type I)
• Dentine dysplasia (Type II)
• Dentinogenesis imperfecta
• Osteogenesis imperfecta
• Familial hypophosphataemia
Pathological features Teeth most commonly affected
Invagination of tooth structure into the pulp through a Maxillary lateral incisors
palatal pit. Invaginated part may contain enamel, dentine
and pulp which communicates with the main pulp chamber.
Cusp-like evagination of tooth structure on the occlusal Maxillary and mandibular
surface. The evaginated cusp usually contains pulp tissue premolars, predominantly
which communicates with the main pulp chamber. in Asiatic races
The pulp is filled with calcifications which resemble a Primary and permanent dentition
mixture of cementum, bone and globular dentine.
The roots are short and blunted.
The pulp is totally calcified in primary dentition. Primary and permanent dentition
In permanent dentition coronal pulps are calcified with
remaining narrow channels.
Bluish, brown discolouration may be noted in both Primary and permanent dentitions
dentitions. The crowns are bulbous, with short affected
roots. Calcification of the pulp may be complete.
Some types of Osteogenesis imperfecta Primary and permanent dentitions
(Types III and IV) show features of dentinogenesis affected
imperfecta. Other types, e.g., Type I may show enlarged
pulp chambers.
The dentine is hypomineralized, and presents histologically Primary and permanent dentitions
as globular dentine. In addition, there are voids and affected
channels within dentine which run from the dentine-enamel
junction to the pulp.

Acquired conditions
Pre-eruptive intracoronal resorption
Mandibular infected buccal cyst
Resorption within the crown of an unerupted tooth which Primary and permanent teeth
usually begins after crown formation. When the tooth
erupts into the oral cavity, it usually becomes infected and
resembles a large carious lesion.
Infection of the follicle of a developing, partially-erupted First and second permanent
tooth may occur from the infected operculum or pericoronitis. molars, and third molars

management. Although a few of these entities are rare,
others are increasingly recognized to be much more
common than previously thought because they are
often undiagnosed. Hence, the aim of this paper is to
review these unusual conditions which are commonly
associated with pulpal abscesses in children, in order to
update the dental practitioner in the diagnosis and
management of these entities.
Developmental abnormalities of crown
Table 1 presents a list of developmental and acquired
conditions which are often associated with dental
abscesses. As can be seen from Table 1, the
abnormalities of crown morphology which are well
known to cause pulpal abscesses include both
invaginations and evaginations of the surface.
Dens invaginatus (Dens-in-dente)
Clinical and pathological features
Dens invaginatus is estimated to affect about
1-2 per cent of the population, and is mainly seen
in the maxillary permanent lateral incisors although it
can also be located in other teeth such as
supernumeraries, mandibular incisors, premolars, and
molars.3-5 Occasionally, it occurs with other dental
anomalies.6,7
Dens invaginatus is a developmental aberration in
which an enamel-lined sac is found within a tooth
Australian Dental Journal 2003;48:3.
crown or root. The sac is usually filled with pulp tissue,
may be blind-ended or exits into the periodontal
ligament, and causes the crown or root to be dilated.3
The abnormality is formed by invagination of the inner
enamel epithelium into the dental papilla before
mineralization of the crown. The site of invagination
may be marked by a deep pit, usually the palatal pit of
a maxillary lateral incisor, or the tip of a molar cusp.8,9
Figure 1a-1c show an abscess associated with a conical
maxillary permanent lateral incisor which has a large
dens invaginatus in an 11-year-old child.
Pulpal infection commonly occurs when there is
communication of the invaginated pulp with the oral
environment. This presents soon after dental eruption
in those cases which have preformed openings into the
exterior, or may occur later in those teeth in which
caries in the pits leads to pulpal exposure. In the case of
abscesses occurring in maxillary lateral incisors without
obvious causes, the presence of a dens invaginatus
should always be considered.
As the invagination is usually deep within the crown
or root, diagnosis is usually determined only after
detailed radiographic exposure.10 The periapical film
may reveal an enamel-lined sac within the pulp which
may appear dilated. The most challenging types of dens
invaginatus are those which are small, and rotated in
their long axes, so that classical radiographic
appearances are not seen.
157
Fig 1a. Anterior dentition of an 11-year-old boy whose maxillary left
lateral incisor became abscessed due to the presence of a dens
invaginatus (see Fig 1b and 1c).

Fig 1c. Radiograph of the tooth in Fig 1b. Note the thin enamel and
dentine layers forming the walls of the dens invaginatus.

Fig 1b. A large dens invaginatus was found within the crown of a
conical maxillary permanent lateral incisor of the patient in Fig 1a.
The tooth became abscessed and was extracted because of the
severity of the defect which made endodontics extremely difficult.

Management
Management of dens invaginatus includes prevention
of pulpal infection through early diagnosis.11 In this
regard, it is recommended that all deep palatal pits on
maxillary lateral incisors be investigated using
periapical radiography to exclude the possibility of
dens invaginatus. Figure 1d shows a double dens
invaginatus discovered in the maxillary lateral incisor
Fig 1d. Periapical radiograph showing double dens invaginatus in a
in a 13-year-old boy when the tooth was maxillary permanent lateral incisor in a 13-year-old boy.
radiographically exposed to investigate the deep palatal
pits. Before pulpal infection has occurred, such palatal
pits may be cleaned, and protected with a double seal composite resin. Although prophylactic removal of the
consisting of glass-ionomer cement, followed by dens invaginatus has been suggested by some authors,12
158 Australian Dental Journal 2003;48:3.
Fig 2a. A maxillary second premolar which has a dens evaginatus on
the occusal surface.

Fig 3a. The mandibular second premolar shows remnants of a

fractured dens evaginatus.

Fig 2b. In the maxillary second premolar depicted in Fig 2a, the dens
evaginatus was protected by composite resin, which was placed
before the tooth achieved contact with the opposing tooth.

the unpredictable results of such treatment in immature

teeth do not justify this procedure as routine treatment.
When pulpal involvement has occurred in a tooth
with dens invaginatus, treatment options include
endodontic treatment and root canal filling. The
endodontic treatment may be limited to the invaginated
section or extended to involve the entire pulp.5,13,14
Ultrasonic débridement has been found to be highly
useful for endodontic treatment of dens invaginatus.13
For young teeth with incompletely formed root apices,
which have become abscessed due to dens invaginatus,
apexification using calcium hydroxide therapy has been Fig 3b. Radiograph of the tooth in Fig 3a, showing a large diffuse
periapical radiolucency associated with an incompletely calcified
reported to be successful.15 Surgical root sectioning and apex. Apexification using calcium hydroxide was successfully
retrograde root canal therapy has also been reported as performed on the tooth before root canal filling.
an alternative if conventional endodontic therapy is
unsuccessful.16 form an accessory tubercle or cusp which is composed
of enamel and dentine, and enclosing pulp tissue, which
Dens evaginatus (Evaginated odontome) communicates with the main pulp of the tooth.18 As the
Clinical and pathological features tubercle is usually fragile, and fractures easily, the pulp
Dens evaginatus presents as a tubercle which is frequently exposed within a short time of tooth
protrudes from the occlusal surface of a premolar emergence.19 Figures 2a, b show dens evaginatus on the
tooth, or the lingual surface of an anterior tooth. This maxillary second premolar which had recently erupted.
anomaly has been reported mainly in the Asiatic races, The defect is difficult to diagnose once the tubercle
where the prevalence rate is thought be as high as 2 per has fractured or abraded.17,18,20 In many cases, the defect
cent.17 The defect is thought to be due to an outflow of is discovered only after a dental abscess has occurred,
the dental epithelium during tooth development to such as the case depicted in Fig 3a and 3b. Diagnosis
Australian Dental Journal 2003;48:3. 159
Fig 4a. Clinical presentation of the primary dentition in a child with
dentine dysplasia type I. Note the severe periodontal bone loss and
abscess on the buccal of the mandibular right second primary molar.
Fig 4b. Panoramic radiograph of the child depicted in Fig 4a. Note
the severe calcification of the pulps in the entire primary dentition.
may be aided by the presence of the same anomaly in
other parts of the mouth, and the exclusion of other
aetiological factors such as trauma or caries.
Management
As in other types of crown anomalies, prevention of
pulp infection can be achieved only through early
diagnosis. When the characteristic tubercles or
accessory occlusal cusps are noted in premolars, they
should be further investigated with periapical
radiographs which may show a tubercle containing
enamel, dentine and pulp. If the tubercle is fractured,
periapical radiolucencies are usually present (Fig 3b).
The pulpal status of the teeth may be determined by the
usual vitality tests.
If diagnosis is made before pulpal infection has
occurred, protection of the tubercle should be
performed by the placement of composite resins around
and on top of the tubercle (Fig 2b).21-23 This method
should afford protection from cuspal wear and
fracture, and should ideally be performed prior to the
tooth reaching full occlusal function. Although
suggested by some authors, the radical procedure of
prophylactic tubercle fracture, Cvek partial pulpotomy,
160
Fig 4c. Histologic section of an exfoliated tooth from the child in
Fig 4a. Note the obliteration of the pulp chamber with calcified
structures resembling bone and dentine.
and calcium hydroxide direct pulp capping17,24 is
difficult to justify due to the unpredictable outcomes of
these procedures.
As the majority of dens evaginatus is diagnosed after
pulpal infection occurred, the management options are
usually full endodontic therapy or extraction.25 As is the
case with dens invaginatus, apexification of the
immature tooth using calcium hydroxide is often
required before root filling can be performed as pulpal
infection usually occurs before root development is
complete.26
Structural abnormalities of dentine
As the physiology of dentine is intimately linked with
the pulp, structural changes in dentine are often
associated with pulp changes. Such abnormalities may be
observed in children with inherited disorders of dentine
such as dentine dysplasias, dentinogenesis imperfecta or
mineralization defects such as rickets. In these
conditions, dental abscesses are a common feature.
Dentine dysplasias
Clinical and pathological features
The dentine dysplasias consist of a group of fairly
rare conditions involving dentine only, and are often
associated with abscesses.27 While dentine dysplasia is
often inherited as genetic conditions involving only the
teeth,28,29 a few rare dysmorphic syndromes have dental
features similar to dentine dysplasia. These include
tumoral calcinosis (extensive calcification of joints and
teeth), and brachio-skeleto-genital syndrome (mental
Australian Dental Journal 2003;48:3.
retardation, abnormal ribs, bone sclerosis and
hypospadias).30 In dentine dysplasia, while there are
overlapping features in the different variants, these are
usually classified as Type I, or radicular dentine
dysplasia and Type II or coronal dentine dysplasia to
denote the respective location of the primary defect.27
The predisposition to dental abscesses in both types
of dentine dysplasia is related to the pulpal obliteration
found in these conditions.27 In Type I, the clinical
crowns are of normal colour in both dentitions, the Fig 5a. Anterior permanent teeth of a child with dentinogenesis
coronal dentine is normal, and the pulp obliteration imperfecta showing typical discolouration.
which usually is mainly confined to the root, is severe
except for thin, cresent-shaped pulpal remnants parallel
to the cemento-enamel junction.27,31 The roots which are
usually short, conical or absent, is associated with
mobility and early exfoliation.27,32 On radiographs,
there are often periapical radiolucencies, which may be
granulomas or cysts.31,33 Figure 4a and 4b show the
typical clinical manifestations of a child affected with
Type I dentine dysplasia, while Fig 4c depicts the severe
calcification of the pulp of an exfoliated primary tooth
from the same child.
In Type II dentine dysplasia, the primary dentition
usually has a bluish or amber discolouration, but the
permanent teeth are normal in colour.29,34 The primary
teeth show total pulp obliteration as in Type II, but the
permanent teeth have less calcifications, and the pulps Fig 5b. Bitewing radiograph of the child in Fig 5a, showing complete
obliteration of the pulps at age 13 years. Note the radiolucency
classically show thistle-shaped configuration and pulp situated at the furcation of the mandibular first molar.
stones. Periapical abscesses are commonly encountered
in these teeth.34 used when this abnormality of dentine is inherited as an
The pathogenesis of the dental abscesses in dentine isolated defect of dentine.35 On the other hand, the term
dysplasia is the result of oral bacteria ingressing into ‘opalescent dentine’ is used when the dentine
the pulp through the dysplastic dentine after loss of abnormality is a feature of osteogenesis imperfecta or
enamel through caries, trauma or attrition. It is also OI.35-37 The dental abnormalities in DI and OI are
probable that the teeth in dentine dysplasia are more associated with specific molecular defects in connective
likely to suffer attrition of the enamel as a result of the tissues of dentine and bone.35,38-41
dysplastic dentine. Hence surface protection of the The typical features of DI include translucent, grey
teeth through fissure sealants and steel crowns may or brownish crown discolouration (Fig 5a), bulbous
help in preventing pulpal abscesses. In addition, pulpal crowns, short roots, fracturing away of enamel, severe
infection may also occur as endo-perio lesions through attrition, and pulp obliteration.42 Dental abscesses
severe loss of periodontal attachment in Type I dentine encountered in DI are thought to occur from the
dysplasia (Fig 4a). disruption of pulpal vascular supply associated with the
abnormal calcifications which result in pulp necrosis.
Management Diagnosis of DI depends on the clinical and
Prevention of periodontal attachment loss is difficult radiographic appearances (Fig 5a, 5b). Although both
in patients with dentine dysplasia due to the extremely dentitions are typically affected, occasionally, only the
short roots which result in poor periodontal support.27 primary dentition alone shows the discolouration. In
Meticulous oral hygiene has been shown to have some the case of opalescent dentine occurring with OI, the
success in preventing periodontal attachment loss and clinical appearances of the primary or permanent
pulpal abscesses. Root canal treatment of severely teeth dentition may be quite variable.43
calcified teeth is also difficult, and extraction may be
the only option in many cases.27 Management
Dental management of DI includes accurate
Dentinogenesis imperfecta diagnosis and assessment of the risk of attrition and
Clinical and pathological features abscess formation, and prophylactic capping of the
Dentinogenesis imperfecta (DI), is one of the most teeth.44 As there may be a spectrum of dental
common autosomal dominant genetic disorders manifestations in DI, sequential radiographic exposure
affecting human beings.35 According to current of the teeth at intervening periods may reveal whether
nomenclature, the term ‘dentinogenesis imperfecta’ is they are particularly prone to attrition or pulpal
Australian Dental Journal 2003;48:3. 161
Fig 6a. Longitudinal section of an exfoliated primary tooth from a
male child with XLH. Note the dentinal clefts and defects which
connect the pulp with the exterior.
obliteration. In a young patient in whom the attrition
rate is highly progressive, and radiographs reveal rapid
pulpal obliteration, prophylactic steel crowns should be
inserted on all the molars, and resin crowns on the
incisors to protect the teeth from further wear.44 The
posterior crowns may be inserted using a conservative
technique in which there is minimal removal of tooth
structure and separation of the teeth achieved by
separating elastics prior to crown insertion.45
In the patient who shows excessive attrition, overlay
dentures may restore occlusal vertical dimension,
prevent further tooth wear, and improve aesthetics.
However, as overlay dentures are a high risk factor for
dental decay, extremely good preventive oral care,
including daily topical fluoride treatment will need to
be practiced by the patients.
As in dentine dysplasia, when abscesses occur,
endodontic treatment in either the primary or
permanent dentitions may be problematic if there is
extensive calcifications, and extractions may be the
only option in such teeth.46 However, if it is desirable to
retain a permanent tooth, endodontic surgery can be
undertaken on teeth with extensive calcific
metamorphosis, if the roots are sufficiently long, but
has a guarded prognosis. In permanent teeth that
require endodontic therapy and have minimal calcific
pulp changes, routine endodontics may be performed.
Familial hypophosphataemic rickets
Clinical and pathological features
X-linked hypophosphataemic rickets (XLH), also
known as vitamin D-resistant rickets is one of the most
common forms of rickets in developed countries.47 It is
162
Fig 6b. Histologic section of the tooth in Fig 6a. Note the globular
nature of the dentine which renders endodontic cleaning very
difficult.
a systemic disease of particular importance in the
aetiology of unusual dental abscesses.27,45,48-51 Dentists
should be alerted to this condition as the systemic
features may be mild, and dental abscesses may be the
first presenting signs.48 In fact, a few cases are first
diagnosed by dentists.
The prevalence rate is usually reported to be around
1:20,000.52 In this condition, there is deficient
mineralization of bone caused by a genetic defect in
renal transepithelial transport of phosphate, which
leads to decreased tubular reabsorption of phosphate
and persistent hypophosphataemia.47,52,53
The features of rickets are the main systemic signs,
but many children are not diagnosed until about 2-3
years of age when they begin to show typical features
such as bowing of the legs.52 The disease is treated with
large doses of oral replacement phosphate.52
Dental abscesses are frequently encountered in XLH
to the extent that some patients are first diagnosed
from the appearance of the ‘spontaneous’ dental
abscesses which are found in the absence of caries or
trauma.45,48,49,51 These abscesses are due to deficiencies of
dentine mineralization which results in large pulp
chambers and physical defects within the dentine, as
shown in Fig 6a. In many teeth, there are channels
which connect the pulp horns to the amelodentinal
Australian Dental Journal 2003;48:3.

Fig 6c. Bitewing radiograph of a male child who has XLH. The pulps
of the teeth are large and the radiodensity of dentine is reduced.
Fig 6d. Orthopantomogram of an XLH patient who had prophylactic
stainless steel crowns placed on the permanent first molars to prevent
pulpal abscesses. Note the periapical and furcation radiolucencies on
the primary mandibular second molars which had not been protected
with steel crowns.
junction so that when the enamel is lost through
attrition or caries, oral micro-organisms enter the pulp
through these channels.45,49,54 Furthermore, the
incompletely mineralized dentine exists in the form of
globular dentine or calcospherites which trap micro-
organisms, and impedes mechanical endodontic
cleaning (Fig 6b).49,55 Other endodontic difficulties are
caused by the thin dentine which perforates easily and
does not support restorative posts for prosthetic
crowns.
The degree of dentine mineralization in XLH and
hence the risk for developing dental abscesses varies
from patient to patient. Usually males are affected to a
greater extent, as would be expected of an X-dominant
condition, and tend to show the most severe dental
changes, including taurodontism.53,56 The risks of an
individual to dental abscess formation may be assessed
by history and dental radiographic signs.45 Usually, the
younger the patient when the first abscesses occur, the
more severe the dental manifestation. In addition, the
sizes of the pulp chambers of the teeth and the
radiodensity of the dentine may also be determined
from radiographs (Fig 6c). In the most severe cases in
which the risk of abscesses is highest, the pulps are
extremely large, with the pulp horns reaching the
Australian Dental Journal 2003;48:3.
amelodentinal junction, and the radiodensity of dentine
approaches that of bone. Medical therapy with
phosphate supplementation does not seem to have
positive effects on the teeth.50
Management
The main management strategy for the dental
manifestations of XLH is the prevention of pulpal
abscesses. In the young patient, this may be achieved
through prophylactic coverage of the teeth with steel
crowns in the molar teeth and composite resins in the
incisor teeth. As the placement of steel crowns using
conventional techniques requires removal of relatively
large amounts of tooth structure, the risk of pulp
exposure is high in those patients where the pulp
chambers are large. To prevent this, a conservative
crown technique employing the use of separating
elastics and non-removal of tooth structure has been
recommended for the insertion of prophylactic steel
crowns for children with rickets.45 In severe cases it may
be necessary to protect the occlusal surfaces of partially
erupted molars with composite resins prior to insertion
of steel crowns which is performed when the teeth are
fully erupted.45 The steel crowns may be converted to
full gold or porcelain crowns when adulthood is
reached. Figure 6d shows the orthopantogram (OPG)
of a child with XLH who had stainless steel crowns
inserted in the permanent first molars to prevent dental
abscesses.
With regard to other aspects of dentistry, recent
reports suggest that orthodontic treatment may be
successful in children with XLH57 and implants may be
also be cautiously used.58
Acquired conditions associated with dental abscesses
Pre-eruptive intracoronal resorption of dentine
Occasionally, the dental practitioner encounters an
apparently intact, recently emerged tooth which has
become abscessed, and there is a negative history of
trauma or caries. Typically, such a tooth shows an
ostensibly intact surface, and a large cavity within the
coronal dentine just below the amelodentinal junction.
Such teeth have been known by a variety of names such
as ‘occult caries’, ‘hidden caries’, ‘fluoride bombs’, and
‘fluoride syndrome’.59 The terms ‘hidden caries’ or
‘occult caries’ refer to the fact that such lesions are
thought to have originated as carious lesions, and have
eluded discovery during clinical examination.60-63 On
the other hand, the terms ‘fluoride bombs’ or ‘fluoride
syndrome’ suggest that fluoride is an aetiological
factor64,65 (Fig 7a). This theory states that fluoride has
encouraged remineralization and the slowing of caries
process in the surface enamel, masking the cavitation
which progresses in dentine. In some teeth, such lesions
have been discovered incidentally on radiographs
before their eruption into the oral cavity and these are
often erroneously referred to as ‘pre-eruptive caries’.66
More recently, the term ‘pre-eruptive intracoronal
resorption’ (PEIR) is used to apply to teeth showing
163

Fig 7a. An OPG of a 12-year-old boy who developed an abscess
related to the mandibular right second molar. The tooth showed the
typical appearance of a ‘fluoride bomb’ (arrow). Histologic
examination of the tooth showed that it to be a pre-eruptive
intracoronal resorption lesion. (Radiograph courtesy of Dr Scott
Smith.)
Fig 7b. An OPG of a 5-year-old child with a pre-eruptive intracoronal
resorption lesion in the mandibular left first permanent molar
(arrow). The lesion appears as a radiolucent defect resembling caries
in the dentine beneath an intact occlusal surface.
such lesions to denote the aetiology and nature of these
lesions.59,67-69 Figure 7b shows typical features of a PEIR
lesion in the unerupted, mandibular left first permanent
molar in a 5-year-old girl.
Prevalence
The prevalence of PEIR can be determined using
radiographs of unerupted teeth, and different
prevalence figures have been reported, depending on
the type and quality of radiographic exposure. In
studies involving nearly 2000 OPGs and 1200
bitewings, PEIR has been found to occur in about 2-6
per cent of children and adolescents with unerupted
teeth, and a tooth prevalence of about 1-2 per cent.69,70
Although any tooth in the permanent and primary
dentition may be affected by PEIR, previous case
reports have indicated a predominance of premolars,
and second and third molars, probably due to the fact
that these teeth are those most frequently observed in
their unerupted states when children first present for
their OPGs. In recent years, as more panoramic
164
radiographs are exposed in younger subjects, an
increased number of first permanent molars have also
been reported to show PEIR.71,72
In the primary dentition, the prevalence is unknown
as radiographs of unerupted primary teeth are seldom
available. Seow and Hackley reported a 2-year-old
child with an abscess in a recently erupted primary
second molar which showed an intact occlusal surface,
and a large resorption lesion within the coronal
dentine.67 The authors suggested that it was likely to
have originated as PEIR. No other cases have been
reported in the primary dentition.
In spite of the relatively high prevalence of this
condition, the majority of lesions remain undetected
until there is pulpal involvement or fracture of the
cusps from extensive cavitation.68 Thus, PEIR may be
an important cause of unusual pulpal abscesses in
children that present within a short period of time of
tooth eruption.
Aetiology of pre-eruptive resorptive lesions
In unerupted teeth, diagnosis of PEIR is only possible
through radiographic exposure of the crowns of
developing teeth. In investigations which contain serial
radiographs of the same subject at different time
periods, it was established that cavitation of the
intracoronal dentine begins only after crown
development is complete.67 Thus it may be inferred
from these observations that the cavity is not the result
of an intrinsic disturbance of mineralization, rather it is
likely to be due to resorption of dentine tissue after
mineralization.
That the aetiology of the lesions is resorption of
dentine is deduced from histological examination of
affected teeth which often show classical signs of
resorption such as osteoclasts and scalloping of the
dentine margins.67,68 However, the origin of the
resorption cells, as well as their pathway of entry are
still unclear. It is speculated that the cells arise from
undifferentiated cells of the developing dental follicle,
or from the surrounding bone. They probably enter the
dentine through a break in the enamel surface, such as
hypoplastic pits or surface cracks or lamellae.
Controlled studies, as well as individual case reports
have not revealed any particular systemic factors which
may predispose a child to PEIR.69,70 In particular, there
is no gender or racial predilection to the condition. Also
of importance is the fact that fluoride does not appear
to have an aetiological role. Studies have shown that
the children who have PEIR do not have any history of
fluoride exposure through drinking water or fluoride
supplementation.71,72 These findings confirm that those
of Weerheijm et al. who showed that the prevalence of
‘hidden’ lesions in a fluoridated town in Holland was
over 30 per cent less compared to a non-fluoridated
town in the same country.73 These findings refute the
use of the term ‘fluoride bomb’ to describe these lesions.
Trigger factors for the resorption are also unknown,
although it has been found that teeth with pre-eruptive
Australian Dental Journal 2003;48:3.
resorption are a few times more likely to be associated
with ectopic eruption compared to teeth without the
condition.69,70 Infection of the predecessor primary
tooth has been suggested as another possible factor but
is unlikely as many affected permanent teeth do not
have primary predecessors.

Natural history of PEIR lesions

The progress of the resorption is usually slow before
the tooth erupts into the oral cavity, although some
lesions undergo periods of high activity. When the
tooth breaks through the mucosa, micro-organisms
may ingress into the resorbed cavity to cause further
breakdown, so that a large carious lesion results.68 The
disproportionate size of the cavity relative to the short
time the tooth has been in the mouth should alert the
clinician to the fact that the lesion is unlikely to be
caries. In some affected teeth, the pulp is encroached
soon after eruption, so that a dental abscess quickly
develops. The majority of case reports suggest that
there is no pain or other symptoms associated with the
lesion until the pulp becomes infected (Fig 7a and 7b).
If the lesion is surgically explored while the tooth is
still unerupted, the tissue found within the cavity is
usually connective tissue, which shows varying
numbers of inflammatory cells including
osteoclasts.67,68,74 In some cases, the soft tissue in the
lesion connects directly with the gingival tissues
through an external opening such as the buccal pit.
However, it is evident from several case reports that the
resorptive process usually stops when the tooth is fully
erupted, when the direct communication between the
lesion and the surrounding bone and soft tissues is
severed. Hence in cases where the cavity is uncovered
after the tooth is fully erupted, the lesion usually
appears relatively empty, or filled with a friable
material composed mainly decomposed dentine.75 On
the other hand, if the cavity has been naturally
uncovered through collapse of the cusps, the lesion
takes on the appearance of a large carious cavity as it
rapidly becomes colonized by the oral microbial flora.
Management
The management of PEIR should be centred on early
diagnosis and treatment. In addition to the usual
assessment of tooth presence and its position, the
author recommends that all unerupted teeth on
bitewings and other intra- and extra-oral radiographs
be routinely scrutinized for PEIR.69,70
If an intracoronal radiolucency is detected in an
unerupted, developing tooth, the tooth should be re-
exposed with a more detailed radiograph. For example,
if an intracoronal radiolucency is detected on a panorex
radiograph, an intra-oral periapical film would be
required to accurately confirm the diagnosis. If the
lesion is confirmed, its size and the projected time of
tooth eruption should be determined. If a relatively
small lesion is found in a tooth which is about to
emerge, it may be monitored carefully until after tooth
Australian Dental Journal 2003;48:3.
Fig 8a. An OPG of a 5-year-old child with a mandibular infected
buccal cyst. Typical features of the condition include a partially
erupted permanent molar, and the sclerotic buccal margin of the
lesion. (Radiograph courtesy of Dr Paul Monsour.)
Fig 8b. Computerized tomography imaging scan of the mandible in
the case depicted in Fig 8a, showing the buccal location of a
mandibular infected buccal cyst in the buccal position, (arrow) and
displacement of the molar tooth to the lingual. A similar condition
may be developing on the contralateral side. (Radiograph courtesy of
Dr Paul Monsour.)
eruption when the cavity may be restored using routine
restorations. On the other hand, some lesions may be
seen to be encroaching on the pulp even prior to tooth
eruption. In these cases, it may be necessary to
surgically expose the unerupted tooth to curette and
restore the lesion.67 In these cases, it is recommended
that the soft tissue within the lesion be sent for
histopathological investigation.
The prognosis of teeth affected by PEIR will depend
on the size of the lesion at the time of discovery,
whether there is pulpal involvement and the extent of
root development. A large cavity which has encroached
onto the pulp of an immature tooth with wide open
root apices probably has a poor prognosis in terms of
the extensive endodontic and restorative work which
will be required. On the other hand, a fairly mature
tooth with a PEIR lesion which is small to moderate-
sized should have good prognosis. These lesions may be
easily restored using routine restorations. Recurrence of
the resorption after curettage and restoration of the
cavity has not been reported.
Mandibular infected buccal cyst
Clinical and pathological features
The mandibular infected buccal cyst (MIBC), also
known as the inflammatory paradental cyst is another
165
unusual cause of dental abscesses in children and
adolescents with partially erupting permanent molars.76
Since Craig first described this condition in 1976, and
suggested the term ‘paradental cyst’,77 there has been
debate regarding the appropriate name for this entity,
although most authors agree to the term ‘mandibular
infected buccal cyst’. The prevalence rate of 3 per cent
reported by Ackerman et al. is probably an
underestimate as many cases of MIBC are either not
recognized or diagnosed as dentigerous cysts.78 Nearly
all reported cases of MIBC involve the mandibular
permanent first, second or third molars, although
rarely, the condition may be encountered in the
maxilla.79 While most cases occur unilaterally, bilateral
MIBC has also been reported. In the case of the first
molars, a buccal or distal location is most frequently
encountered whereas in the case of third molars, the
location is usually distal.79,80
In the case of the first and second permanent molars,
symptoms often developed within a year of their
emergence into the oral cavity. There is usually
buccolingual tilting of the crown of the affected tooth,
and there may be distal displacement of the crypt of the
posterior adjacent tooth81 (Fig 8a and 8b). Pain, swelling
and localized deep periodontal pocketing on the buccal
or distal aspects are the most common symptoms in
these teeth. In contrast, in the case of third molars, the
time lapse between symptoms and emergence can be
variable. These teeth are usually impacted and
associated with previous histories of pericoronitis, and
there is severe pain, swelling and trismus.81
On radiographs, the lesion usually presents as a cyst-
like, well-defined buccal or distal radiolucency of
around 1-2cm in diameter, with a thin sclerotic rim81
(Fig 8a and 8b). Depending on the chronicity of the
lesion, varying degrees of reactive bone may be seen at
the margin. There is usually loss or attenuation of the
lamina dura surrounding the root apices or a furcation
radiolucency. In addition, there may a radiopaque
inferior margin of the cyst, and attenuation of the
cortical boundary of the crypt of the adjacent posterior
tooth. Figure 8a shows typical radiographic features of
the MIBC. In recent years, diagnosis of MIBC is further
enhanced by computed tomography imaging (CT)
scans82 (Fig 8b).
In MIBC, the dental follicle surrounding a
developing tooth, usually a mandibular molar,
undergoes cystic changes due to inflammatory
stimulation of the reduced enamel epithelium or the
epithelial cell rests of Malassez.83 The source of the
inflammation is usually the infected operculum or
pericoronitis around an erupting tooth. In histologic
sections, the MIBC may be distinguished by its lining of
thick, proliferating, non-keratinized, stratified
squamous odontogenic epithelium, and a wall
composing of dense, mature fibrovascular connective
tissue with an intense inflammatory cell infiltrate.78 The
connective tissue of the cyst is found to be continuous
with the follicle of the tooth in the majority of cases.78
166
Management
Although infected first and second molars were
previously treated by extraction and cystic removal, a
more conservative approach is currently recommended,
employing antibiotics, curettage and removal of cystic
contents. Retention of the affected tooth is associated
with good success rates and normal healing in the
majority of cases, although recurrent infection may
occur in a small percentage of subjects.79
CONCLUSIONS
In conclusion, although the majority of dental
abscesses in children results from caries or trauma, a
percentage originate from unusual conditions which
range from developmental abnormalities to acquired
conditions. These abscesses may be prevented by timely
and accurate diagnosis and appropriate preventive
measures. Knowledge of these conditions would aid the
general practitioner in the differential diagnosis and
treatment of these entities.
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Address for correspondence/reprints:
Associate Professor W Kim Seow
School of Dentistry
The University of Queensland
200 Turbot Street
Brisbane, Queensland 4000
Email: k.seow@uq.edu.au
Australian Dental Journal 2003;48:3.