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Diagnosis and Management of Unusual Dental Abscesses in
Diagnosis and Management of Unusual Dental Abscesses in
Diagnosis and Management of Unusual Dental Abscesses in
Acquired conditions
Pre-eruptive intracoronal resorption 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.
Mandibular infected buccal cyst 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, crown or root. The sac is usually filled with pulp tissue,
others are increasingly recognized to be much more may be blind-ended or exits into the periodontal
common than previously thought because they are ligament, and causes the crown or root to be dilated.3
often undiagnosed. Hence, the aim of this paper is to The abnormality is formed by invagination of the inner
review these unusual conditions which are commonly enamel epithelium into the dental papilla before
associated with pulpal abscesses in children, in order to mineralization of the crown. The site of invagination
update the dental practitioner in the diagnosis and may be marked by a deep pit, usually the palatal pit of
management of these entities. a maxillary lateral incisor, or the tip of a molar cusp.8,9
Figure 1a-1c show an abscess associated with a conical
Developmental abnormalities of crown maxillary permanent lateral incisor which has a large
Table 1 presents a list of developmental and acquired dens invaginatus in an 11-year-old child.
conditions which are often associated with dental Pulpal infection commonly occurs when there is
abscesses. As can be seen from Table 1, the communication of the invaginated pulp with the oral
abnormalities of crown morphology which are well environment. This presents soon after dental eruption
known to cause pulpal abscesses include both in those cases which have preformed openings into the
invaginations and evaginations of the surface. exterior, or may occur later in those teeth in which
caries in the pits leads to pulpal exposure. In the case of
Dens invaginatus (Dens-in-dente) abscesses occurring in maxillary lateral incisors without
Clinical and pathological features obvious causes, the presence of a dens invaginatus
Dens invaginatus is estimated to affect about should always be considered.
1-2 per cent of the population, and is mainly seen As the invagination is usually deep within the crown
in the maxillary permanent lateral incisors although it or root, diagnosis is usually determined only after
can also be located in other teeth such as detailed radiographic exposure.10 The periapical film
supernumeraries, mandibular incisors, premolars, and may reveal an enamel-lined sac within the pulp which
molars.3-5 Occasionally, it occurs with other dental may appear dilated. The most challenging types of dens
anomalies.6,7 invaginatus are those which are small, and rotated in
Dens invaginatus is a developmental aberration in their long axes, so that classical radiographic
which an enamel-lined sac is found within a tooth appearances are not seen.
Australian Dental Journal 2003;48:3. 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 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.
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
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.
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.
Fig 6d. Orthopantomogram of an XLH patient who had prophylactic
stainless steel crowns placed on the permanent first molars to prevent With regard to other aspects of dentistry, recent
pulpal abscesses. Note the periapical and furcation radiolucencies on reports suggest that orthodontic treatment may be
the primary mandibular second molars which had not been protected successful in children with XLH57 and implants may be
with steel crowns.
also be cautiously used.58
junction so that when the enamel is lost through Acquired conditions associated with dental abscesses
attrition or caries, oral micro-organisms enter the pulp Pre-eruptive intracoronal resorption of dentine
through these channels.45,49,54 Furthermore, the Occasionally, the dental practitioner encounters an
incompletely mineralized dentine exists in the form of apparently intact, recently emerged tooth which has
globular dentine or calcospherites which trap micro- become abscessed, and there is a negative history of
organisms, and impedes mechanical endodontic trauma or caries. Typically, such a tooth shows an
cleaning (Fig 6b).49,55 Other endodontic difficulties are ostensibly intact surface, and a large cavity within the
caused by the thin dentine which perforates easily and coronal dentine just below the amelodentinal junction.
does not support restorative posts for prosthetic Such teeth have been known by a variety of names such
crowns. as ‘occult caries’, ‘hidden caries’, ‘fluoride bombs’, and
The degree of dentine mineralization in XLH and ‘fluoride syndrome’.59 The terms ‘hidden caries’ or
hence the risk for developing dental abscesses varies ‘occult caries’ refer to the fact that such lesions are
from patient to patient. Usually males are affected to a thought to have originated as carious lesions, and have
greater extent, as would be expected of an X-dominant eluded discovery during clinical examination.60-63 On
condition, and tend to show the most severe dental the other hand, the terms ‘fluoride bombs’ or ‘fluoride
changes, including taurodontism.53,56 The risks of an syndrome’ suggest that fluoride is an aetiological
individual to dental abscess formation may be assessed factor64,65 (Fig 7a). This theory states that fluoride has
by history and dental radiographic signs.45 Usually, the encouraged remineralization and the slowing of caries
younger the patient when the first abscesses occur, the process in the surface enamel, masking the cavitation
more severe the dental manifestation. In addition, the which progresses in dentine. In some teeth, such lesions
sizes of the pulp chambers of the teeth and the have been discovered incidentally on radiographs
radiodensity of the dentine may also be determined before their eruption into the oral cavity and these are
from radiographs (Fig 6c). In the most severe cases in often erroneously referred to as ‘pre-eruptive caries’.66
which the risk of abscesses is highest, the pulps are More recently, the term ‘pre-eruptive intracoronal
extremely large, with the pulp horns reaching the resorption’ (PEIR) is used to apply to teeth showing
Australian Dental Journal 2003;48:3. 163
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
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 condition, the majority of lesions remain undetected
typical appearance of a ‘fluoride bomb’ (arrow). Histologic until there is pulpal involvement or fracture of the
examination of the tooth showed that it to be a pre-eruptive cusps from extensive cavitation.68 Thus, PEIR may be
intracoronal resorption lesion. (Radiograph courtesy of Dr Scott
Smith.) an important cause of unusual pulpal abscesses in
children that present within a short period of time of
tooth eruption.
28. Thyagarajan T, Sreenath T, Cho A, Wright JT, Kulkarni AB. 51. Seow WK, Needleman HL, Holm IA. Effect of familial
Reduced expression of dentin sialophosphoprotein is associated hypophosphatemic rickets on dental development: a controlled
with dysplastic dentin in mice overexpressing transforming longitudinal study. Pediatr Dent 1995;17:346-350.
growth factor-beta 1 in teeth. J Biol Chem 2001;276:11016- 52. Carpenter TO. New perspectives on the biology and treatment of
11020. X-linked hypophosphatemic rickets. Pediatr Clin North Am
29. Dean JA, Hartsfield JK, Wright JT, Hart TC. Dentin dysplasia, 1997;44:443-466.
type II linkage to chromosome 4q. J Craniofac Genet Dev Biol 53. Holm IA, Nelson AE, Robinson BG, et al. Mutational analysis
1997;17:172-177. and genotype-phenotype correlation of the PHEX gene in X-
30. Witcher SL Jr, Drinkard DW, Shapiro RD, Schow CE Jr. Tumoral linked hypophosphatemic rickets. J Clin Endocrinol Metab
calcinosis with unusual dental radiogrphic findings. Oral Surg 2001;86:3889-3899.
Oral Med Oral Pathol 1989;68:104-107. 54. Murayama T, Iwatsubo R, Akiyama S, et al. Familial
31. Shankly PE, Mackie IC, Sloan P. Dentinal dysplasia type I: report hypophophataemic vitamin D-resistant rickets: dental findings
of a case. Int J Paediatr Dent 1999;9:37-42. and histologic study of teeth. Oral Surg Oral Med Oral Pathol
Oral Radiol 2000;90:310-316.
32. Kosinski RW, Chaiyawat Y, Rosenberg L. Localized deficient root
development associated with taurodontism: case report. Pediatr 55. Hillmann G, Geurtsen W. Pathohistology of undecalcified
Dent 1999;21:213-215. primary teeth in vitamin D-resistant rickets: review and report of
two cases. Oral Surg Oral Med Oral Pathol Oral Radiol
33. Ansari G, Reid JS. Dentinal dysplasia type I: review of the
literature and report of a family. ASDC J Dent Child 1996;82:218-224.
1997;64:429-434. 56. Goodman JR, Gelbier MJ, Bennett JH, Winter GB. Dental
34. Brenneise CV, Conway KR. Dentin dysplasia, type II: report of 2 problems associated with hypophosphataemic vitamin D
new families and review of the literature. Oral Surg Oral Med resistant rickets. Int J Paediatr Dent 1998;8:19-28.
Oral Pathol Oral Radiol Endod 1999;87:752-755. 57. Kawakami M, Takano-Yamamoto T. Orthodontic treatment of a
35. International working group on constitutional diseases of bone. patient with hypophosphatemic vitamin D-resistant rickets.
International nomenclature and classification of the ASDC J Dent Child 1997;64:395-399.
osteochondrodysplasias (1997). Amer J Med Genet 58. Resnick D. Implant replacement and guided tissue regenration in
1998;79:376-382 a patient with congenital vitamin D-reistant rickets. J Oral
36. Malmgren B, Norgren S. Dental aberrations in children and Implantol 1998;24:214-218.
adolescents with osteogenesis imperfecta. Acta Odontol Scand 59. Seow WK. Pre-eruptive intracoronal resorption as an entity of
2002;60:65-71. occult caries. Pediatr Dent 2000;22:370-376.
37. Lindau B, Dietz W, Lundgren T, Storhaug K, Noren JG. 60. Sawle RF, Andlaw RJ. Has occlusal caries become more difficult
Discrimination of morphological findings in dentine from to diagnose? A study comparing clinically undetected lesions in
osteogenesis imperfecta patients using combinations of polarized molar teeth of 14-16 year old children in 1974 and 1982. Br Dent
light microscopy, microradiography and scanning electron J 1988;164:209-211.
microscopy. Int J Paediatr Dent 1999;9:253-261.
61. Creanor SL, Russell JI, Strang DM, Burchell CK. The prevalence
38. MacDougall M. Refined mapping of the human dentin of clinically undetected occlusal dentine caries in Scottish
sialophosphoprotein (DSPP) gene within the critical adolescents. Br Dent J 1990;169:126-129.
dentinogenesis imperfecta type II and dentin dysplasia type II
loci. Eur J Oral Sci 1998;106:227-233. 62. Kidd EAM, Naylor MN, Wilson RF. Prevalence of clinically
undetected and untreated molar occlusal dentine caries in
39. Lund AM, Jensen BL, Nielsen LA, Skovby F. Dental
adolescents in the Isle of Wight. Caries Res 1992;26:397-401.
manifestations of osteogenesis imperfecta and abnormalities of
collagen I metabolism. J Craniofac Genet Dev Biol 1998;18:30- 63. Weerheijm KL, Gruythuysen RJM, van Amerongen WE.
37. Prevalence of hidden caries. ASDC J Dent Child 1992;59:408-
412.
40. Thotakura SR, Mah T, Srinivasan R, et al. The non-collagenous
dentin matrix proteins are involved in dentinogenesis imperfecta 64. Page J. The ‘fluoride syndrome’: occult caries? Br Dent J
type II (DGI-II). J Dent Res 2000;79:835-839. 1986;160:228.
Australian Dental Journal 2003;48:3. 167
65. Ball IA. The ‘fluoride syndrome’: occult caries? Br Dent J 77. Craig GT. The paradental cyst. A specific inflammatory
1986;160:75-76. odontogenic cyst. Br Dent J 1976;141:9-14.
66. Skaff DM, Dilzell WW. Lesions resembling caries in unerupted 78. Ackermann G, Cohen MA, Altini M. The paradental cyst: a
teeth. Oral Surg Oral Med Oral Pathol 1978;45:643-646. clinicopathologic study of 50 cases. Oral Surg Oral Med Oral
67. Seow WK, Hackley D. Pre-eruptive resorption of dentin in the Pathol 1987;64:308-312.
primary and permanent dentitions: case reports and literature 79. Vedtofte P, Praetorius F. The inflammatory paradental cyst. Oral
review. Pediatr Dent 1996;18:67-71. Surg Oral Med Oral Pathol 1989;68:182-186.
68. Seow WK. Multiple pre-eruptive intracoronal radiolucent lesions 80. Lim AAH, Peck RHL. Bilateral mandibular cyst: lateral radicular
in the permanent dentition: case report. Pediatr Dent cyst, paradental cyst, or mandibular infected cyst? Report of a
1998;20:195-198. case. J Oral Maxillofac Surg 2002;60:825-827.
69. Seow WK, Lu PC, McAllan LH. Prevalence of pre-eruptive 81. Packota GV, Hall JM, Lanigan DT, Cohen MA. Paradental cysts
intracoronal dentin defects from panoramic radiographs. Pediatr on mandibular first molars in children: report of five cases.
Dent 1999;21:332-339. Dentomaxillofac Radiol 1990;19:126-132.
70. Seow WK, Wan A, McAllan LH. The prevalence of pre-eruptive 82. Thompson IO, de Waal J, Nortje CJ. Mandibular infected buccal
dentin radiolucencies in the permanent dentition. Pediatr Dent cyst and the paradental cyst: the same or separate entities. J Dent
1999;21:26-33.
Assoc S Afr 1997;52:503-506.
71. Wood PF, Crozier DS. Radiolucent lesions resembling caries in
83. Wolf J, Hietanen J. The mandibular infected buccal cyst
the dentine of permanent teeth: a report of sixteen cases. Aust
(paradental cyst). A radiographic and histological study. Br J
Dent J 1985;30:169-173.
Oral Maxillofac Surg 1990;28:322-325.
72. Walton JL. Dentin radiolucencies in unerupted teeth: report of
two cases. ASDC J Dent Child 1980;47:183-186.
73. Weerheijm KL, Kidd EAM, Groen HJ. The effect of fluoridation
on the occurrence of hidden caries in clinically sound occlusal
surfaces. Caries Res 1997;31:30-34. Address for correspondence/reprints:
74. Grundy CE, Pyle RJ, Adkins KF. Intra-coronal resorption of Associate Professor W Kim Seow
unerupted molars. Aust Dent J 1984;29:175-179. School of Dentistry
75. Rutar JE. Paediatric dentistry: coronal radiolucency: Case The University of Queensland
reports. Aust Dent J 1997;42:221-224.
200 Turbot Street
76. Thurnwald GA, Acton CH, Savage NW. The mandibular infected
buccal cyst – a reappraisal. Ann R Australas Coll Dent Surg Brisbane, Queensland 4000
1994;12:255-263. Email: k.seow@uq.edu.au